Of all cephalic injuries caused by the trauma of birth those affecting the contents of the skull, brain and meninges are most important.
This fact is duly appreciated in older medical literature. It always seemed obvious that all severer injuries of the cranial bones, such as deep indentations and guttered fractures, as a rule, will also damage intracranial structures. It is more surprising that it has been known for a very long time that serious intracranial lesions, especially meningeal hemorrhages, not so rarely are encountered in autopsies of newborn infants even in the absence of any evidence of traumatism.
As early as 1832 Cruveilhier offered excellent illustrations of intracephalic hemorrhages of the newborn in his pathologic-anatomic atlas. This condition has been discussed thoroughly from the anatomic point of view by Weber and also by Virchow in 1852. The description of the pathologic anatomy of these subdural hematomas furnished by Kundrat in 1890 up to the present time has been changed merely in certain details.
In considering this topic historically it seems striking that it was not the obstetrician but the neurologist who first manifested interest in the clinical aspect of the problem.
Little of London, in 1843, in his first paper dealing with cerebral spastic paralysis in young children asserted that the condition is due to a lack of development of cerebral tissues and also to a meningitis, and mentions rather casually that this type of paralysis seems to follow difficult and prolonged labor with or without the use of instruments. He expresses the opinion that palsy subsequent to an abnormal labor is due to an intracranial hemorrhage. In a second paper, published in 1862, he asserts that cerebral spastic palsy in children is the result of an intracranial birth hemorrhage in about three-fourths of all instances.
There will be opportunity to quote later in detail the views of other neurologists concerning the possible or probable relation of brain trauma at birth to the later physical and mental development of the child. It, therefore, will suffice to state in this connection merely that the neurologist has manifested a keen interest in this problem early and has maintained it ever since. In chronological order, probably the pediatrician has to be mentioned next as concerning himself with the question.
A short monograph of Finkelstein, published in 1902, reveals a keen appreciation of the outstanding importance of birth trauma in the health and physical development of the infant.
The last to enter the field was the obstetrician. It can be trustfully asserted that his researches have finally led to a better understanding of the etiology and pathology of intracranial birth lesion and are directly responsible for the general interest of late visible evidenced in the numerous scientific contributions to this subject.
The impetus for this renewed and keener interest, it seems, has been furnished by the classic paper of Seitz (published in 1907 dealing in the main with the symptomatology of brain hemorrhage in the newborn, and the paper of Beneke (1910) on lacerations of the tentorium. It is a fact, historically interesting, that solely the new method of opening the infant’s skull at autopsy (described by Beneke) has permitted us to form a definite and clear conception of the exact pathology and actual frequency of intracranial injuries caused by the birth trauma.
The student of the extensive literature devoted to these lesions must keep in mind the important fact that exact and reliable knowledge concerning the intracranial hemorrhages of the newborn infant has been gained only within the last ten years, and that many of the older contributions, still extensively and rather Indiscriminately quoted by recent writers, often express nothing but mere surmise or theory.
It Is a deplorable fact that modern textbooks of obstetrics in this question of the cranial birth trauma express entirely erroneous views and in elaborate statistics of neonatal mortality practically never mention or classify the one important and common cause ; viz., intracranial traumatic lesions.
It seems appropriate to begin the discussion of the pathology with a description of those methods of autopsy which alone permit exact determination of the existing intracranial conditions.
Seitz suggested for all cases of suspected intracranial lesions, whenever possible, severing the head immediately after death and hardening it in a freezing mixture before opening the skull. The cadaver, however, must not be permitted to lie any length of time in the usual dorsal position because gravitation invariably will cause some of the blood to flow backwards and, as has been pointed out, by Henschen, to actually reach the spinal canal after death. This method furthermore is not entirely satisfactory because it does not preclude the disappearance of flattening of convolutions under increased intracranial pressure. It, therefore, seems preferable to open the skull immediately in accord with the method devised by Beneke. The customarily employed technic destroys the tentorium and for this reason heretofore has not permitted a proper appreciation of the frequency and character of tentorium Injuries. Beneke opens the skull in the sagittal suture and carefully pulls the parietal bones down on either side. Rough manipulation may result in injury to the underlying dura mater, and, indeed, might cause a tear in the tentorium. However, in the case of such an artefact, no hemorrhage will be found associated with the visible injury. Both hemispheres of the brain then are ablated and the tentorium thus laid free for inspection. In a later paper Beneke and Zausch suggested a slight modification of this technic for certain cases. In the execution of the older method the vena magna Galeni is severed, and thus the anatomic evidence of the source of the hematoma might be destroyed, e.g., in a ventricular hemorrhage. In such cases the typical Beneke method must be changed so that each hemisphere is removed separately under careful preservation of the corpora quadrigemina and of the large ganglia. Next the cover of the third ventricle is lifted. Only in this manner the location of a tear in the vena magna Galeni can be rendered visible.
In order to avoid an injury to the longitudinal sinus, it has been suggested that incisions be made on either side of and parallel to the sagittal suture through the edges of the parietal bones by means of sharp scissors before the parietals are carefully bent down on either side.
CLASSIFICATION AND PATHOLOGY OF INTRACRANIAL TRAUMATIC LESIONS
For practical purposes intracranial birth lesions most conveniently are divided into those characterized by a large hemorrhage and those in which but little or no blood is extravasated. Further subdividing these two groups, we arrive at the following classification :
A . Hemorrhages
(1) Cephalhematoma internum
(2) Subarachnoidal hemorrhages
(3) Dural hematoma
(c) Mixed type
(4) Brain hemorrhages
(b) Diffuse (Couvelaire) or circumscribed (Kruska)
B . Lesions without Hemorrhage
(1) Contusion cerebri
(2) Ischemic areas (Kruska)
(3) Slight tentorial lacerations.
Cephalhematoma Internum. In dealing with the cephalhematoma externum we had occasion to point out certain features in the embryonic development of the cranial bones which explain the fact that some of the vessels of the cranial periost pass directly through the skull bones into the firmly attached dura mater. Therefore, even in the absence of definite bone lesions external traumatism in the newborn may cause the formation of an epidural hematoma. It seems likely that in many instances an external cephalhematoma thus will be accompanied by an internal cephalhematoma. The fact is occasionally mentioned in clinical reports (e.g., by Sidbury). The opportunity for more exact study of this type of intracranial hemorrhage is but rarely offered since the firm attachment of the dura to the skull bones apparently prevents the formation of an epidural hematoma large enough to cause the infant’s death.
Leaving out of consideration in this connection epidural hemorrhages incident to injury of a cranial bone, we can state that the typical cephalhematoma internum, as a rule, represents only an accidental finding at autopsy, and so far as known, is void of any clinical significance also in the later life of the child.
Subarachnoidal Hemorrhages. Hematomas in the subarachnoidal space, so-called leptomeningeal hemorrhages, lie on the convex surface of the brain hemisphere, more frequently near the midline. Occasionally they are bilateral, when they will be more pronounced on one side. There is ample pathologic evidence available for the conclusion that after breech and forceps extractions minute subarachnoidal hemorrhages are not by any means rare. Ziehen thought they may occasionally be responsible for convulsions of the Jacksonian type. In accordance with their more common distribution spasmodic contractions released by them would be more pronounced in, or may be limited to, the lower extremities. At necroscopy of a premature infant, born after an easy spontaneous labor and dying thirty-six hours later, Beneke and Zausch found a large subpial hematoma in the posterior portion of the brain covering the cerebellum on both sides.
In the opinion of Reus, however, in this type of intracranial hemorrhage in the overwhelming majority of instances definite clinical symptoms fail to appear.
Dural Hematomas. Though much rarer than the subarachnoidal hematomas, subdural hemorrhages are of decidedly greater clinical significance. Indeed, they represent from a practical point of view the most important group of all intracephalic parturitional hemorrhages.
When writers without further qualification still speak of cranial birth hemorrhages, they are actually referring solely, to the supra- and infratentorial subdural hemorrhages of the newborn.
In marked contrast to conditions in the adult, in the newborn infant, dural hemorrhages with but rare exceptions are of venous origin, and arise from their median meningeal artery only in some cases of guttered skull fracture after forcible delivery. Statistical proof of the prevalence of the subdural type among fatal Intracranial hemorrhages can be found in the study of Kowitz, based on six thousand autopsies of newborn or very young children. In accordance with their respective frequency in the cadaver he arranges these hemorrhages as follows : subdural, subarachnoidal, ventricular, and strictly cerebral.
Seitz’s first investigations seemed to confirm the older view that subdural hemorrhages in the newborn He most commonly over the convex surface of the brain hemispheres underneath the parietal bones. The error of this conception is evident in the light of our more recent information concerning tentorial tears, which had been entirely overlooked and were practically unknown up to the first studies of Beneke. Today authorities seem to agree that intracranial hemorrhages of clinical importance in the newborn most often are situated just above or below the tentorium.
The tentorium, as pointed out by Beneke, consists of an upper and a lower blade. The upper blade is the one more commonly torn, usually at its free edge. The tear varies in extent and shape, but in general indicates a tearing of the fibers perpendicularly across their direction. In the depth of the opening the thinner, and transparent lower blade is seen intact, covering the cerebellum.
Pott differentiates three types of typical lacerations of the tentorium. The first and worst form is a tear through the free edge, usually lying about in the middle, but often it is bilateral and through both blades of the tentorium. The torn edges are ragged, fringed, covered with thick coagula of the blood which has escaped from the injured veins running along the free margin. The blood escapes downward and upward, as a rule, apparently more of it spreading above the tentorium forward into the temporal fossa, or rising laterally over the surface of the occipital lobe. Less frequently blood flows downward and covers the cerebellum and medulla, finally also passing into the spinal canal.
In the second, milder type, so accurately described by Beneke, the laceration involves only the upper blade. The resulting hemorrhage is likely to be less severe.
In the third and least serious type, in all probability the most common type, the hemorrhage often seems limited to a small hematoma between the blades of the tentorium or at the end of the falx.
This type apparently in most instances is clinically without importance and is likely to be overlooked even in a careful autopsy.
Beneke emphasizes the striking fact that this pathology of the tentorium was known to Cruveilhier almost ninety years ago and was the subject of a paper published by Virchow in 1850. It has been forgotten, apparently on account of the faulty post-mortem technic generally employed in which the tentorium is severed from the pars petrosa of the temporal bone before it can be inspected.
In hemorrhages of the frankly infratentorial type, especially in the cases in which the large veins emptying into the sinus transversus are torn, the cerebellum and the adjoining portions of the medulla are found more or less completely covered by extravasated blood. Usually some of the blood flows down into the upper portion of the spinal canal.
In some of the cases of tentorial lacerations a mixed form of hemorrhage is produced by some of the blood escaping upward above the tentorium.
Infratentorial hemorrhages, arising as a rule from tentorial tears, but occasionally also from lacerations of the intervertebral joint capsules of the upper vertebrae (Henschen), in general are less extensive
than the supratentorial hemorrhages.
Seitz, who has given us the most elaborate study of the subdural hemispheric hematoma, gives credit to Kundrat (1890) for the first information concerning this type of intracranial hemorrhage. He had found them often in autopsies of young infants with small heads, born after short normal labors.
This hematoma between dura and arachnoidea, as a rule, lies only over one hemisphere. It varies considerably in size. If extensive, it may, in caplike fashion, cover the entire hemisphere. The quantity of extravasated blood has been estimated by various authorities between 40 and 90 cubic centimeters. Of great clinical importance is the fact that a large hematoma of one side distinctly compresses also the other hemisphere.
To avoid repetition, it will prove more convenient to mention anatomic details in reference to the source of the extravasated blood later in the chapter while discussing the mechanical causes held responsible for the injury of certain vessels.
Hemorrhages in the Lateral Ventricles. Hemorrhages in the lateral ventricles apparently do not occur often. As a rule, the hemorrhage is excessive, and the blood flows through all the ventricles towards the medulla and into the spinal canal.
A case of this sort is graphically described by Beneke and Zausch and may serve as illustration. Dura and pia on the convexity of the brain were found normal in appearance over both hemispheres. The left lateral ventricle was filled with blood. The clot continued through the interventricular foramen (of Monro) into the third ventricle and from there extended through the aqueduct (of Sylvius) and the foramen of Magendie into the fourth ventricle. A thick layer of blood lay under the cerebellum, surrounded the medulla oblongata and extended along the cervical cord down to the middle of the thoracic cord. Injuries to the brain tissue itself could nowhere be discovered. The extent of the hemorrhage left no doubt that it was the result of the rupture of a very large vein, situated so that the blood escaped first into the lateral ventricle. Since there was no tentorial tear, the rupture, in the belief of the writers, must have occurred in the vena magna Galeni, or in one of the main trunks of the vena cerebri interna, though this latter explanation seemed less acceptable.
The very method of autopsy of the head devised by one of the two authors (Beneke), made it impossible to establish in this instance the actual source of this profuse hemorrhage. It is in this connection that Beneke suggests the modification of his post-mortem technic already described in this chapter.
It will be shown later that other investigators incline to the belief that at least in some cases the tela choriodea must be regarded as the source of a ventricular hematoma.
Hemorrhages in the Brain Substance. True intracerebral hemorrhages are decidedly rare in the newborn. In a series of autopsies recorded by Couvelaire, the five hemorrhages discovered within the brain tissue were all found in premature fetus, weighing less than 3,000 grams. He pointed to the interesting fact that in six other premature infants weighing, however, more than 3,000 grams, diffuse tissue hemorrhage were situated in the medulla and spinal cord. These observations of Couvelaire permit the deduction that intracerebral hemorrhages are mor likely to occur in the soft brain of premature infants.
Leclerq and Paput emphasized that in the traumatic hemorrhages of the cerebrospinal system of the newborn, quite unlike the adult, the meningea hemorrhages are so decidedly more frequent than hemorrhages in the substance of the brain or cord;=. Of 14 intracranial hemorrhages found by them in 30 autopsies of newborn infants, but one was discovered in the substance of the cerebellum.
An ischemic necrosis of the brain tissue as the immediate cause of secondary hemorrhage into the degenerated tissue is strongly suggests in a case described by Beneke and Zausch. The infant died twelve day after version and extraction. At autopsy they found in the right temporal lobe of the brain a large blood coagulum. After its removal an irregular cavity remained. Both macroscopically and microscopically the clot proved to be fresh, certainly less than twelve days old. By exclusion the authors arrived at the final deduction that the hemorrhage occurred in a primarily softened area of brain tissue.
The problem of ischemic necrosis has been thoroughly investigated by Kruska. He described 20 instances of localized brain lesions, discovered at autopsy, which were not caused by hemorrhage. In his opinion, they represent ischemic foci produced by the spastic contraction of blood vessels.
Necrotic areas of this sort vary in size from very small ones to extensive destruction of brain tissue. They were found either solitary or multiple. As the only possible explanation of such a vessel spasm, Kruska could suggest a reflex from an intense mechanical skin irritation.
Beneke and Zausch accepted this explanation of a reflex origin of these lesions, but suggested that possibly also the sudden change of temperature might represent the required intense external irritation.
From this point of view, the ischemic necrosis of the brain cannot be properly classed a traumatic birth injury of the newborn. It represents, however, a type of those intracranial lesions developing in connection with birth, which are characterized by the absence at least of an immediate hemorrhage.
INTRACRANIAL LESIONS WITHOUT HEMORRHAGE
In the majority of cases of ischemic necrosis of the brain a hemorrhage fails to occur. In 3 of 20 cases described by Kruska the softened area had become infected and changed into a typical abscess. It is a mooted question whether such an ischemic necrosis might, at least in some instances, account for a porencephaly.
A contusion of the brain during labor has been described by Seitz. The mobility of the skull bones against each other, this faculty of the skull to be molded, as a matter of fact, actually protects the skull contents against the external trauma incident to labor. While the skull is being compressed a corresponding amount of cerebrospinal fluid is pressed into the spinal canal. Thus the skull cavity is actually, though not greatly, reduced without any compression of the brain itself. Under exceptional conditions, Seitz assumed, the brain in this manner may be contused or concussed. The newborn then exhibits symptoms, including convulsions, characteristic of intracranial hypertension, which, however, quickly disappear. Seitz acknowledged that such fleeting signs of an intracranial lesion might, however, also be produced by a slight and transient edema, or, as is claimed by other authors, even by small hemorrhages. It is worthy of note that Seitz’s suggestion of a possible concussion of the brain during labor was offered at a time when knowledge concerning intracranial lesions was practically limited to the subdural hematoma and there was nothing known concerning the frequent injuries of the tentorium.
The fact is now firmly established that in a considerable number of lacerations of the tentorium discovered at autopsy no hemorrhage at all or but bare traces of extravasated blood are found. Such tears represent definite parturitional traumatic lesions which, though insufficient to cause the death of the infant, may give rise to only temporary symptoms immediately at birth.
The extensive literature which in the past decade has accumulated on the question of the causation of intracranial birth injuries shows a bewildering confusion of ideas. Their frequent combination with external traumatic lesions, their anatomic characteristics, and their location brought mechanical factors as the immediate cause of their production into the foreground. The normal physiological reduction of intracranial space during molding, but especially forced and exaggerated compression in the cases of mechanical dystocia or of operative delivery, always seemed most obviously to represent the mechanical factors responsible for the intracephalic injuries. Further studies, however, revealed the fact, quite evident now, that extensive intracranial destructions often are discovered within the skulls of infants that were born spontaneously after easy and quick labors and even in children delivered in cesarean section.
An explanation of the intracranial traumatism on the basis of mechanical influences at least for such cases seemed unsatisfactory. Thus writers added as causative factors, prematurity, syphilis, asphyxiation, and more recently hemorrhagic diathesis.
Probably all these elements enter into the etiology of the various intracranial birth lesions and especially of hemorrhages, but on more careful study one can easily see that in the individual case they vary greatly among each other in significance.
Mechanical factors, probably almost always, are the immediate and direct causes of the traumatic injury. It seems plausible, however, that the effect of the trauma is likely to be severer if the brain is unusually soft or the vessel walls unusually fragile. Prematurity or lues then will represent definite etiological factors which predispose the intracranial tissues to more extensive damage. Again, if the infant’s blood is lacking in its normal ability to coagulate, or if an infant with but a slight intracranial injury is roughly handled during resuscitation (swinging after the method of Schultze!), then hemorrhagic diathesis and violent efforts at resuscitation obviously contribute in the origin of serious and fatal intracranial birth injuries.
Asphyxiation of the newborn, to which many writers assign a most important etiological role, probably acts both as a predisposing and a contributory factor, because an engorged sinus or vein not only is more prone to rupture, but also to extravasate more blood.
In accord with his own theory, each writer gives particular prominence to the one or the other of the many factors which undoubtedly enter into the etiology of these lesions. In my belief they are more appropriately grouped as immediate, predisposing, and contributory causes.
Immediate Causes. Immediate causes of intracranial lesions in the main are undeniably of a mechanical nature. The mechanical origin of an intracranial injury is obvious in the presence of extensive or deep depressions and fractures of skull bones, the result of severe pressure, either exerted directly by a forceps blade,’ or produced indirectly by forcible traction of the head along protruding portions of the rigid pelvic canal (promontory, symphysis, exostosis, etc.). These injuries have been adequately discussed in a preceding chapter.
Less apparent is the mechanical cause of the traumatization of certain structures within the skull in the absence of any evident mechanical obstruction to the passage of the fetal head.
A definite compression with reduction of the volume of the skull represents an integral element of every normal labor. Experience proves that in general this compression is free of any noteworthy harmful effect on the newborn child. This forces the conclusion that under normal conditions a process is at work which precludes a pathologic increase of intracranial pressure. As now understood, this protection of the skull contents, and, most important, of the brain tissue, against compression is procured by the escape of a small amount of cerebrospinal fluid toward the spinal canal, and furthermore by a reduction of the volume of the blood within the brain. This automatic adjustment of skull contents to the changed skull volume during the second stage of labor is so very satisfactorily accomplished in the overwhelming majority of instances because the actual diminution of the intracephalic space is comparatively insignificant. During the process of molding, as a matter of fact, the reduction in the length of certain diameters, chiefly of the lateral, is accompanied by a corresponding increase of others, chiefly the longitudinal. It will be shown later how important a role is played by this lengthening of the anterior-posterior diameters in the causation of injuries to the tentorium. Here it will suffice to emphasize that experience shows that the elastic brain easily adapts itself to the altered configuration of the head.
There still remains the question to be answered, why these mechanical factors, at play in all labors, only at times should become responsible for serious intracephalic injuries.
The explanation formerly given, and accepted as entirely satisfactory, was to the effect that serious damage is done only if either molding is excessive or is accomplished too quickly by an artificial or operative delivery in those cases in which the dystocia is due to a disproportion between the fetal head and the pelvis.
Thus developed the conception, still all too prevalent, that the infant’s brain is seriously damaged only in a difficult labor or by an instrumental delivery. A thorough modification of this view is required. The fact is now firmly established, that also the physiological traumatism of a normal labor is sufficient to lead to serious consequences if other coincident conditions supply those predisposing and contributory elements which will cause the normal physiological effects of the birth trauma to attain pathological importance.
Following approximately the classification adopted in preceding pages for the discussion of the pathology of intracranial traumatic lesions, we shall, in a similar manner, group direct mechanical factors responsible for the pathology into those causing hemispheric hemorrhages, tentorial tears and ventricular hemorrhages.
Mechanical Causes of Subdural Hematomas. When the head is fully molded the effected change in the relative position of adjoining cranial bones is most pronounced in the sagittal suture. As the result of this overriding of the edges of the parietals the subjacent dura is both folded and stretched. Only if the dura is abnormally fragile and the overlapping excessive, or very suddenly accomplished, does the dura break and the longitudinal sinus itself tear open. More commonly, as demonstrated by Kundrat and Seitz, under these conditions only the veins of one side are torn, exactly at the site of their entrance into the sinus. They give way to the combined effect of traction and distention, the latter being either due to local congestion from partial compression of the vessels, or, in cases of asphyxiation, being the local expression of a general venous congestion.
Exaggerated overlapping of the parietals over the squama of the occipital bone, in the beUef of many writers, in an identical manner is prone to cause rupture of the veins emptying into the transverse sinus, or laceration of the sinus itself, especially in breech extractions.
Subdural hematomas have been discovered at autopsy in babies born in a state of beginning or advanced maceration. In them the hemorrhage clearly antedates birth. In cases of evident congenital syphilis the explanation seems admissible that the hemorrhage has been caused by the destruction of vessels by a syphilitic process. In other instances a definite history of a severe trauma of the pregnant uterus by a blow or fall suggests strongly the traumatic origin of the lesion, but in neither case can we speak of a parturitional injury in the stricter sense.
Mechanical Causes of Tentorial Lacerations. As the result of a very thorough study of the problem, Beneke, as the first, was able to offer a most acceptable explanation of the exact mechanism of laceration of the tentorium. It is generally believed that certain histological structural details of such tissues as bones or ligaments permit reliable conclusions in regard to the functional purpose of these textures. The longitudinal direction of the fibers in the falx and their lateral extension on either side into the tentorium then would indicate that it is the chief mechanical task of the falx to prevent an abnormal extension of the long diameters of the cranium, i.e., to counteract during molding the effect of lateral compression.
Sudden or severe lateral compression through the compensating elongation of the cranium thus might exert on the falx a strain severe enough to cause it to tear. Presumably the tear would occur at the weakest point, and this is where the falx fibers diverge to form the upper blades of the tentorium.
Beneke’s conclusion that lateral compression represents the primary mechanical factor in the causation of tentorial injuries has been fully confirmed by the observations of Bauereisen, Herfif, Pott, and many others.
Experimental investigations (Moreno, L. Meyer and Hauch, etc.) have demonstrated furthermore that a comparatively slight pressure is sufficient to injure the tentorium in the newborn. Therefore, some of these investigators feel justified in asserting that in some of the cases seen at autopsy the tentorial tear might well have been caused by unskillful manipulation during resuscitation, as, e.g., by too firm a fixation of the infant’s head between both wrists, an almost unavoidable procedure during swinging.
This apparent vulnerability of the tentorium, even of the normal full-term infant, has been convincingly demonstrated in L. Meyer’s and Hauch’s experiments. They discovered that also compression of the head lengthwise readily causes the tentorium to tear. Further enlightenment concerning the mechanism of the origin of these tears is offered by Benthin. He observed that after a left-occipito anterior delivery in case of a unilateral tear the injury was on the right side, and in the case of a bilateral tear the damage was more extensive on the right side. The stronger pressure against the left parietal and the resulting flattening of the bone in this presentation causes a sharper dent in the right parietal with corresponding increased tension on the falx fibers running over to the right. Pressure in a lateral direction, he reasons, increases the vertical diameters of the cranium, and the falx thus is pulled upward, as easily demonstrated on a specimen. Traction is exerted on the fibers running transversely in the tentorium. This traction in the LOA position is stronger on the right side and, therefore, is more prone to be harmful on this side.
All these observations and experimental studies tend to show that compression of the head, especially in a lateral direction, plays no less important a role as a mechanical factor in the causation of tentorial lacerations than we have shown it to play in the origin of lacerations of the veins emptying into the longitudinal sinus. However, there is the one important difference, that the tentorium apparently proves decidedly more vulnerable than the dura. It undeniably can be severely traumatized by a quick compression of so short a duration that the infant’s head even immediately after birth will fail to exhibit such characteristics of prolonged compression as persisting overlapping of the parietals in the sagittal suture, or a large caput succedaneum. In view of these facts it becomes plausible that the tentorium occasionally is torn simply as the result of the forced passage of the fetal head through an incompletely dilated cervix or a rigid vulvar ring.
During the second stage of labor, in a general way, lateral compression prevails, but near its end, when the occiput of the fully rotated head is pressed against the symphysis during deflexion, a definite pressure is exerted in an antero-posterior direction. Benthin, and also Seitz, based on this fact the claim that most likely tentorial lacerations are produced by improper efforts to protect the perineum against injury. This seems particularly applicable to the attempt of delivering the head in the interval between uterine contractions by exerting strong pressure against the forehead of the fetus either over the perineum or by means of a finger introduced into the rectum. In this effort the infant’s occiput is forcibly pushed against the pubic arch. During such manipulations an asymmetric lateral pressure exerted with greater strength over the one frontal or parietal bone must prove particularly dangerous to the falx.
It is worthy of special emphasis that observations and experiments prove that the soft portions of the birth canal, an incompletely dilated cervix, or the rigid perineum of the primigravida, represent definite mechanical obstacles which may lead to serious intracranial traumatism.
It is a matter of conjecture whether or not pituitrin from this point of view plays a direct role in the causation of parturitional injuries of the newborn. As a matter of fact, by a larger dose of pituitrin, the fetal head is often quickly forced through a not fully effaced cervix. In studying the numerous detailed records of severer brain injuries in literature, one cannot fail to notice the frequency with which the administration of pituitrin is mentioned in these histories.
This might solely express the widespread use of pituitrin as an oxytocic, but in at least some of the cases a close relation of pituitrin to the brain injury might well be surmised, e.g., in a case of Lippman : A premature child weighing five and a half pounds developed typical convulsions 48 hours after delivery. One half ampule of pituitrin had been injected every thirty minutes during the entire labor. We find Sidbury, Neff, and Porter, among others, expressing their belief that pituitrin was undeniably responsible for many fatal hemorrhages that they had seen in newborn infants.
A study of these recorded cases of fatal intracephalic injuries, the majority to be found in German literature, also reveals the frequent mention of twilight sleep. Again this might be only the incidental result of the greater popularity of twilight sleep a decade ago among some of the German obstetricians.
The fact, however, cannot be overlooked that this method of pain relief lengthens the second stage of labor and in a large number of cases requires termination of labor by forceps. In the opinion at least of Neustaedter, twilight sleep may impair the life or future health of the child in that it supplies two definite factors which are commonly held responsible for intracranial injuries.
Kuestner, Demelin, Herff, Meyer and Hauch, Fischer, and others have placed on record observations of serious intracranial hemorrhages seen in infants delivered in cesarean section. For some of these cases it seems plausible that the injury occurred before delivery as the result of the efforts of the uterus to press the head into the narrowed pelvis.
But this explanation certainly does not apply to a case like the one reported by Kuestner, in which the indication for cesarean delivery was furnished by an advanced cervical carcinoma.
For some of the cases, therefore, it is evident that the head was severely traumatized solely by its forced extraction through a uterine incision of insufficient length.
Still another mechanical explanation for the causation of tentorial tears has been advanced by Wilke and Seitz. If in a breech delivery the occiput of the aftercoming head is sharply pressed against the symphysis, the force with which the cerebellum thus is pushed upward against the overlying tentorium, may be sufficient to cause its laceration.
It is approximately in the same manner that Bauereisen, Mayer, Meyer, and Hauch, etc., account for the particularly injurious effect on the tentorium of the Veit-Smellie maneuver.
We may quote here as an instructive illustration of the vulnerability of the tentorium of an aftercoming head a case described by Mayer :
Eighth child delivered in breech presentation without the slightest difficulty. First symptoms of an intracranial injury noticeable on third day. Autopsy shows an extensive laceration of the tentorium and the sinus rectus with excessive hemorrhage both above and underneath the tentorium.
Causes of Ventricular Hemorrhage. Most writers seem to assume that the ventricular hemorrhage is the result of a congestion in the vessels of the plexus chorioideus and, therefore, as a rule, is seen only in connection with deep asphyxiation of the newborn. Beneke and Zausch, and others are unwilling to accept this explanation for all cases. The usual profuseness of the hemorrhage in these cases would rather suggest the rupture of veins larger than those of the plexus. Beneke feels that in their rupture mechanical factors would seem to play the same important role now vindicated for all other meningeal hemorrhages of the newborn. He offers the following explanation : with the heightening of the vertical diameters of the head as the result of its lateral compression, the falx is pulled upward, and with it also the sinus rectus. Under exceptional conditions in this way not the tentorium ; as is more commonly the case, but the vena cerebri magna is torn where it connects with the sinus.
Syphilis. Little need be said in regard to the actual relation of syphilis to intracranial birth traumatisms. Lues is mentioned and stressed as a causative factor chiefly in the older writings. Weyhe’s figure of 18 per cent is still carelessly copied by those who overlook the important fact that Weyhe’s paper was published in 1889, 18 years before the discovery of the Wassermann reaction. All recent contributors, who base the diagnosis of syphilis on a positive Wassermann reaction, practically concur in the opinion that this disease has significance in the etiology of birth trauma, if not entirely so, chiefly only in so far as it is responsible for prematurity of the newborn.
Other Diseases of the Mother. There are sporadic observations on record which seem to suggest an increased susceptibility of the brain for traumatization in cases in which the mother during pregnancy was suffering from an acute infectious disease, plumbism, alcoholism, advanced arteriosclerosis, nephritis, etc. However, ever since it has been shown that even in cases of eclampsia the convulsions of the newborn more likely are the sequela of an intracranial lesion, caused by the forced delivery, than due to the maternal toxemia, writers have placed but little importance on maternal diseases as direct or even only as predisposing factors in the causation of intracephalic birth traumatisms.
Prematurity. All modern statistics of cephalic birth injuries point clearly to the etiologic significance of prematurity. The percentage of premature infants is high in all the various types of intracranial parturitional lesions, being the highest in the hemorrhages occurring within the substance of the brain or cerebellum. This fact is generally ascribed to an abnormal fragility of the vessel walls, of the dura and of the brain tissue itself, the result of incomplete development.
The premature infant proves remarkably vulnerable to the traumatisms of birth, and an analysis of the birth histories shows that in a large percentage of the fatal intracranial hemorrhages of prematurely born infants the labor was definitely recorded as normal and spontaneous. It was thought that such intracranial damage was due to the lessened protection offered by soft skull bones. But, indeed, investigations carried out by Kretz, forced him to the conclusion that there actually is more danger to the child from a far advanced ossification with corresponding narrowing of the open sutures. In these cases the molding of the head leads to a wider overlapping of the parietals with increased tension and pressure on the underlying dura and the veins emptying into the sinus.
An evident susceptibility to traumatization of the skull contents in the premature child fully justifies the assertion of various writers that serious intracephalic damage can result under these conditions even if the compression is not exaggerated and only of short duration, as might be caused alone by rigid soft portions of the birth canal. Thus Meyer and Hauch found an extensive bilateral laceration of the tentorium in a child, weighing but 2150 grams, delivered by cesarean section. Beneke and also Pott described tentorial lacerations discovered in small fetus of four and five months.
Quick Release of the Molded Head. Abels assumes that in the second stage of labor, with the well-molded head deep in the pelvis, every uterine contraction temporarily raises the fetal blood pressure.
A coincident rise of pressure also in the intracranial blood vessels is precluded by the equalizing counterpressure of pelvic and uterine walls and, in part, of the cervix. Within the area of the dilated cervix, where the compensatory outer pressure is wanting, the caput succedaneum forms. In this same region, in normally flexed occipital presentations, the sagittal suture and underneath it the longitudinal sinus is exposed to an abnormal internal pressure and becomes engorged. Sudden release of all counterpressure, by a precipitate passage of the head through the vulva, thus may cause the rupture of the engorged sinus. It is his belief that this theory satisfactorily explains the comparative frequency of intracranial hemorrhages after easy and precipitate -labors, especially in small and premature babies (pituitrin !). On the basis of Abels theory, which in general is identical with the accepted explanation of the so-called caisson disease, various writers have emphasized specific but commonly disregarded dangers of a quick forceps extraction or possibly even of the vaginal cesarean section. However, it seems that Abels theory has not met with much favor. At least some of the observations, cited by him in its support, in the light of newer information permit of a different and more acceptable interpretation.
Quick release is likely to prove more often detrimental because it causes a sudden change in the configuration of the skull. The quick release in a precipitate labor was preceded by a quick compression which is actually responsible for the intracephalic damage.
Asphyxiation. To asphyxiation as a direct cause of brain injuries of the newborn a decidedly more important role is assigned in the writings of older, than of more recent, authors. These older writers were acquainted only with the hemispherical subdural and strictly cerebral hemorrhages in which a congested condition of the injured sinus or veins offered a most obvious explanation for their rupture. A change of views had to come inevitably when autopsies performed after Beneke’s method began to establish the great frequency of tentorial lacerations, and this new knowledge led to a proper appreciation of mechanical factors in the direct causation of intracranial birth traumatisms, many of which are not associated with noteworthy hemorrhage.
To-day we are well fortified in the assertion that in very many of the seemingly asphyxiated newborn infants the asphyxia is rather the result than the cause of the intracephalic lesion, and we shall show later how efforts to overcome this presumptive asphyxiation tend to aggravate the consequences of the existing lesion.
One of the most important arguments in favor of the etiologic relation of asphyxia to intracranial hemorrhages is the irrefutable fact that in many infants, evidently the victims of a cerebral hemorrhage, small petechial hemorrhages are also found in the various serosas of the pleural and the abdominal cavity, generally held as characteristic of the death from suffocation.
These coincident ecchymoses as will be shown presently are now more acceptably explained, presumably in the majority of cases, as caused by a hemorrhagic diathesis.
The etiological significance of asphyxia cannot be proved any longer by reference to statistics. Even elaborate tabulations of the immediate causes of infant mortality within the first few days of life, practically without any exceptions, still fail to mention as a cause a parturitional intracephalic trauma.
The number of these deaths, as now is well known, is not small. In these statistical tabulations of clinical diagnosis the deaths from intracephalic lesions in part are included in the mortality figures for the various obstetrical operations, but presumably to the larger extent the traumatic deaths, especially subsequent to spontaneous labors, are counted as asph3’xias. Both morbidity and mortality figures for asphyxiation of the newborn are misleading and grossly incorrect. If writers employ these figures of a clinical diagnosis of asphyxiation together with the correct figures concerning injuries as established at post-mortem in calculating a percentage relation between asphyxia and intracranial birth lesions, their method is faulty and their deductions therefore unacceptable.
Anatomic facts lead to the conception that parturitional traumatic injuries of almost every type are primarily due to definite mechanical conditions.
There is no positive scientific evidence available even for the contention that congestion alone does cause rhexis of the vessels in the chorioidal plexus. Asphyxiation positively cannot have any direct bearing on the lacerations of the tentorium which, as definitely established, represent the most common type of all intracranial birth injuries.
Etiologic relation “of asphyxiation to intracephalic parturitional lesions, therefore, in the light of our present information, is practically limited to the plausible assumption that a congested sinus or vein is more likely than an empty one to rupture both under pressure or strain. Asphyxiation at best can be regarded only as a predisposing cause, and under certain conditions, as a contributory factor in so far as the congestion is likely to result in the extravasation of a larger amount of blood.
Hemorrhagic Diathesis. Robert M. Green, apparently as the first, in 1914 expressed the thought that intracephalic birth hemorrhages might be solely the local manifestation of a hemorrhagic tendency which so often can be noticed in the newborn.
Further investigations, all so far carried on only in this country, have furnished ample evidence for the validity of this interpretation of the hemorrhage in a number of instances. Foote dwells on the fact often mentioned in literature that in autopsies of newborn infants with intracranial hemorrhages smaller and larger hemorrhages commonly are also seen in the mucosas and especially in the serosas of various organs all through the body. As already mentioned, these petechial hemorrhages used to be considered indicative of the asphyxia responsible for the cranial lesion. More likely all the hemorrhages in such a case are due to a common cause, a hemorrhagic diathesis. Recently Rodda published his extensive studies of coagulation and bleeding time for the newborn. He found that there exists normally a delay in coagulation, the time being for the apparently normal healthy infant immediately after birth between five and nine minutes, with an average of seven minutes.
The bleeding time, ascertained with Duke’s method, he established as normal in a range between two and five minutes, with the average at about three and a half minutes. Infants with evidences of abnormal hemorrhages showed a coagulation time around eleven to twelve up to thirty-two minutes.
The conclusion thus seems inevitable that a congenital anomaly of blood coagulability plays a significant role in serious intracranial hemorrhages, at least as a contributory factor. This anomaly probably accounts for the presence of smaller petechial hemorrhages and ecchymoses also in other parts of the body where the direct traumatic cause for their development evidently could have been only of limited importance.
Rodda cites a most illuminating observation. In a case of twins the first child was delivered by means of forceps. The second smaller child followed easily in a breech presentation and died, as shown at necropsy, from an intracranial hemorrhage. The coagulation time of the surviving first child was found to be fifteen minutes, of the second child thirty-two minutes. In the second child the presumably smaller trauma incident to birth resulted in a fatal hemorrhage evidently on account of the hemorrhagic diathesis which permitted a slight, under normal conditions insignificant, intracranial lesion to extravasate a large amount of blood.
Warwick in a very recent report comments on the fact that of 53 cases of intracranial hemorrhage discovered in 136 consecutive necropsies only 12 were stillborn babies, while 41 lived for some time. In many cases the histories showed that the infants were seemingly normal at the time of birth, pathologic symptoms often not appearing for several days.
In 20 of the cases the hemorrhage over the brain was associated with hemorrhages in other organs, strongly suggesting the syndrome now generally known as hemorrhagic disease of the newborn. “This at once brings up the question of the decreased coagulability of the blood being intimately associated with the etiology of the cerebral hemorrhages. One is justified in such an assumption when one finds that nearly one half of the cases of intracranial hemorrhage are associated with hemorrhages in other organs.”
It is surprising that this literature does not take into consideration certain information available in surgical literature concerning the evident relation of chronic asphyxiation to a decreased blood coagulability. Investigations along these lines in regard to asphyxia of the newborn would seem most promising. They may lead to a better understanding of the hemorrhagic disease of the newborn and thus of the significance of asphyxiation as a predisposing factor in the causation of intracranial hemorrhages.
In a later chapter dealing with the treatment of these lesions we shall have opportunity to demonstrate that the therapeutic effect of blood and serum injections has furnished important clinical support for the contention that a decreased coagulability of the blood predisposes the formation of intracranial hematomas.
A delayed clotting time necessarily proves particularly serious in combination with the contributory factor to be considered next.
Manipulations During Resuscitation. In many of the customary procedures applied during resuscitation of the asphyxiated newborn, most typically in the swinging after the method of Schultze, the infant’s shoulders are grasped on either side and the head fixed between the balls of the thumbs or between the wrists. These swingings have been denounced by many authors as objectionable for various reasons. The fact, however, seems almost generally overlooked that still another danger lies in this inevitable lateral compression of the head, which in the excitement of the occasion easily might be exerted too sharply. Bauereisen’s experiments leave no doubt that such compression by itself may cause a serious tentorial tear.
Since the infant manipulated in this manner is asphyxiated and its blood vessels engorged, even a small tentorium injury produced in this state is prone to cause a noteworthy extravasation of blood. Theoretically, at least, it can be assumed that a concomitant abnormal coagulability of the blood under these conditions will result in a fatal hemorrhage. A combination of conditions of this sort, probably not uncommon, seems to explain plausibly a clinical picture which is almost typical. The infant is slightly asphyxiated. It seems to be normal immediately after resuscitation, but gradually develops the characteristic signs of an intracranial hemorrhage, to which it succumbs within the next few days.
All vigorous manipulations during resuscitation, especially those in which the baby is swung or held suspended with its head downward, necessarily will favor the escape of blood even from very small ruptured vessels. In this connection reference to the fact cannot be omitted that many of the infants born after twilight sleep require efforts to overcome their seeming asphyxiation.
SUMMARY OF ETIOLOGY OF INTRACRANIAL BIRTH INJURIES
In a large number of the cases the very obvious cause for the intracranial lesion is an external cranial trauma, evidenced by a deep indentation or a guttered fracture. Almost without exception these infants succumb immediately to the injury. Of much greater practical importance are internal injuries not so clearly established by external evidence.
For the majority of them the responsible mechanical cause is recognized in definite anomalies of labor, breech labors, extraction of the aftercoming head after version, difficult forceps extractions, especially in the cases of mechanical dystocia, etc. There still remains, then, a fairly large group of cases in which labor was easy, spontaneous, often precipitate, the child small, frequently premature. Also in these cases the immediate cause of the injury is a mechanical one, the compression of the head on its passage through the birth canal, both through its bony and its soft portions. Asphyxiation and, especially, prematurity render the infant abnormally susceptible to the trauma even of normal labor, and thus predispose it to serious injury. In the presence of only slight intracephalic traumatic lesions, a decreased coagulability of the blood and inappropriate manipulations during resuscitation necessarily tend to hasten or to prolong the escape of blood from injured vessels, though small, and thus represent important contributory factors in the causation of cerebral hemorrhages.
Certain mechanical factors cause intracranial tissues to be crushed or torn in the course of labor. The immediate consequences of these injuries in the main depend upon the injury to blood vessels.
Blood vessels, not fully developed, diseased or engorged, are more likely to be traumatized. The escape of blood is determined by the size of the injured vessel, but is exaggerated by congestion and unduly prolonged by a hemorrhagic tendency.
Frequency. The consideration of the question of frequency of intracephalic birth lesions, contrary to more common practice, here is placed after the thorough discussion of the pathology and etiology of these injuries. It is assumed that familiarity with the anatomy and causation of these injuries is requisite for the appropriate appreciation of the relevance of certain facts here presented.
Since accurate information concerning the incidence of intracranial lesions of all types, and especially of tentorial lacerations, became available only after the general adoption of Beneke’s special technic of post mortem examination of the skull, older statistics have become practically valueless. I, therefore, shall limit myself to quotations from the more noteworthy publications beginning with the year 1911.
Pott (1911) : When Pott became interested in this problem he discovered 14 tentorial tears in 101 autopsies. With a more careful technic and with minuter study of the findings he found the evidences of tentorial injuries in 6 out of the last 15 autopsies. He states in his conclusions : the fact that some residue of a dura hemorrhage can be discovered in a considerable number of the children coming to post mortem up to the age of six months, proves that the percentage of tentorial tears with some hemorrhage must be very great.
Bauereisen (1912) : In 667 consecutive deliveries, some of them premature, 47 infants were stillborn or died soon after birth. In all these cases, the head was severed from the body and hardened before being opened. All hemorrhages thus were fixed in their exact anatomic relations. Tentorial lesions were found in 11 instances, at times associated with other intracranial lesions. Of these 11 babies, all were born asphyxiated, in 9 the attempts at resuscitation had failed, 2 had lived two days. All were operative cases, forceps, and breech extractions.
Benthin (1912) : In a series of 1239 consecutive labors (including premature) 107 infants were stillborn or died soon. Of these, 73 came to autopsy, showing 8 tentorial teers evidently responsible for death (11 per cent of all autopsies).
Meyer and Hauch (1913) : In 64 necropsies of newborn infants tentorial injuries were found in 28 instances, but only in 12 of them the tear itself was responsible for the death. Since these 12 severe lacerations were observed in a series of 1200 labors, the authors calculate for fatal tentorial tears an incidence of i in every 100 labors, with both slight and serious tears in over 2 per cent of all labors.
Leclerq and Paput (1913): Of 30 newborn infants coming to autopsy, in 14 an intracranial hemorrhage was found.
Henschen (1913): Of 1277 infants examined post mortem, 29 (2.27 per cent) had died from intracephalic birth hemorrhages, which represents a death rate of 0.2 per cent from such hemorrhages in all labors.
Kowitz (1914): In an exhaustive study dealing with the etiology of hemorrhagic pachymeningitis, based on 6000 autopsies of young children, the author states that fatal intracranial hemorrhages, both after spontaneous and artificial deliveries, arranged in the order of their relative frequency, involve most often the dura and least frequently the cerebral tissue itself, with hemorrhages of the arachnoidea and into the ventricles ranging between them.
Moreno (1915) : In 40 necropsies of newborn babies the tentorium was found torn in 10 cases, 5 times the tear involving also the falx. This is an incidence of tentorial tears of 25 per cent in all autopsies and of l per cent in all deliveries. However, not in all instances had the tentorial injuries caused the death.
Hedren (1918) : In a total of 700 necropsies, excluding all macerated infants, 65 (9.3 per cent) cases showed intracranial hemorrhages. In 50 of these 65 cases, the reliable obstetrical records showed that the labor was spontaneous, in most instances normal in every respect, only 23 of them occurring at full term, being premature in the remaining 27 cases. Hedren gives the details of each case and presents the most exact study of the problem extant. Of these 50 intracranial hemorrhages, 42 were meningeal and only 5 of the strictly cerebral type. It seems also noteworthy that out of 27 subdural hemorrhages over the convexity of the brain he found some hemorrhages also on the other side in 21 cases. There were 6 purely ventricular hemorrhages and 2 ventricular hemorrhages combined with cerebellar hemorrhages, all 8 occurring in spontaneous labors. Hedren considers syphilis a predisposing factor of some importance, but lays particular stress on the striking frequency of coincident ecchymoses in serous membranes. They prove to him the significance of asphyxiation in the etiology of the intracranial hemorrhages.
Vischer (1919) : In 186 autopsies of newborn infants and infants up to the age of one month, performed exactly in accord with the method of Beneke, 74 brain hemorrhages were found, among them 51 tentorial tears. This means almost 40 per cent of hemorrhages and over 27 per cent of tentorial injuries of all autopsies. In this group of 51 tentorial tears, the hemorrhage was considerable in 27 cases ; it was slight or nearly absent in the other cases. Only in 23 cases of the whole group of 74 hemorrhages, the tentorium was found intact.
Warwick (1919) : In 36 routine autopsies of stillborn infants and those dying in early infancy 18 (50 per cent) showed definite evidence of a hemorrhage either somewhere over the brain surface or in ventricles. Of these 18 cases only 2 represented long labors. Both were twin labors, and in both instances it was the second born of the twins who succumbed to an intracephalic hemorrhage. There was in this group only 1 case of forceps extraction, performed on a six months fetus. Of the 18 babies, 2 were stillborn, 4 were asphyxiated at birth and the remaining 12 seemed at first perfectly normal, born after spontaneous labors. In 8 of the 18, at post-mortem, macroscopic hemorrhages were discovered in other organs, forcing the conclusion that the intracranial hemorrhages were only incidental to that syndrome of symptoms usually grouped as hemorrhagic disease of the newborn. Five of these 8 vomited blood before death and exhibited a marked delay in the coagulation time of their blood.
Bailey (1920) : In 100 autopsies performed in the Manhattan Maternity Hospital in New York, intracranial hemorrhages were found in 40 cases, of which 30 were stillborn infants, the others having died within four days after birth, which in 17 instances was spontaneous and normal.
Rodda (1920) : Statistics from post-mortem examinations made in the Newborn Clinic of the University of Minnesota reveal the noteworthy fact that more than 50 per cent of all infants that die intrapartum or during the first days of life, even after easy delivery, but frequently after breech and premature labors, have succumbed to intracranial hemorrhages.
Schaefer (1921) : In 680 autopsies were found 140 definite hemorrhages, 114 being supratentorial, 9 infratentorial, the remaining of a mixed type. Of 43 infants born after difficult forceps extractions, 39 had serious tentorial tears. In a large number of the fatal cases the labor was spontaneous. In about one-half of the spontaneous cases, in which the infants were premature and small, the tentorium was found injured.
This wealth of statistical material, representing but a selection from the more important contributions of the past decade, does not permit accurate calculations in regard either to the total frequency of intracranial birth injuries or the relative frequency of the various types. The reasons are obvious. In some instances percentage figures are given on the basis of all post mortems including young infants, in others the stillborn or macerated feti are excluded. Again, most writers employ the term “cerebral” or “brain” hemorrhages for all intracranial hemorrhages, while but a few distinguish clearly between the various types.
However, the references quoted here are entirely sufficient to permit the following conclusions : intracranial lesions as the result of the birth trauma are very common. They are discovered with ever-increasing frequency. The chronological arrangement of the foregoing quotations from literature clearly demonstrates this fact.
The percentage figures for intracranial birth injuries as cause of infantile death are growing, not because these injuries are becoming more frequent, but because more investigators are looking for them.
Among all the intracranial birth lesions hemorrhages rank first as causing death, while to tentorial lacerations must be assigned the first place in regard to mere frequency. Serious and fatal lesions occur frequently in the course of spontaneous and easy labors, especially in premature infants. In a considerable percentage of the autopsies definite intracranial lesions, especially subarachnoidal hemorrhages, and tentorial tears, without any or with but slight hemorrhage, represent only accidental findings. This proves that many infants necessarily survive though they have sustained definite intracephalic lesions during birth. The important bearing of this evident fact on the later physical and mental development of the child will be discussed later in this chapter.
The fact now firmly established by anatomic investigations, that intracranial birth traumatisms occur with great frequency, places on the clinician the pressing obligation to provide a clearer picture of their clinical symptomatology than that available at this time. Most of the recent writers still are quoting Seitz, the recognized pioneer in the study of the pathology and symptomatology of subdural birth hemorrhages, but, as a rule, fail to appreciate that our information in regard to lesions other than subdural hematoma, and especially concerning tentorial tears, is of more recent date, and that, therefore, some of the phenomena and symptoms so precisely determined and so well described by him, call for a different interpretation.
There are various reasons which prompted me to offer in the subsequent pages so detailed a discussion of the symptomatology of cranial birth lesions. As at present, so probably also in the future, the overwhelming majority of all confinements will be managed by general practitioners. Very few newborn infants at birth or even soon afterward are seen by expert neurologists. Effective therapy, often life saving, however, is plainly dependent upon early diagnosis.
Therefore, the most important of all efforts to alleviate the effects of cranial birth traumatisms, must be to familiarize the practitioner with the symptomatology of these lesions, so that he will be able actually to diagnose or at least to suspect such injuries.
In the attempt to render this detailed description of the symptomatology particularly useful to the practitioner, a classification of symptoms has been adopted which is based rather on the requirements for a prompt clinical diagnosis, than on the anatomic-pathologic conditions which, indeed, determine the specific symptoms :
Intracranial Hypertension. A marked dissimilarity between the symptomatology of intracranial lesions and, in special, of hemorrhages of the newborn, and those commonly seen in the adult, is plainly the result of anatomic differences in their respective skulls. Within the rigid adult skull, with the exception of a deep depressed fracture, hypertension is produced by an increase in the contents of the skull capsule. In the case of the fetus, we have to take into consideration an actual reduction of the skull volume from molding during labor, and after delivery an ability of accommodation to an increase of skull contents through yielding of sutures and fontanels.
The compression of the head during labor, if not excessive, or abnormal in other respects, apparently causes no signs of hypertension.
The reduction of the skull capacity from molding probably is small, and adequately compensated by the escape of some of the cerebrospinal fluid into the spinal canal, presumably also by a hastened absorption of the fluid into lymph vessels, and possibly by a reduction of the blood volume within the cranium. This escape of cerebrospinal fluid into the spinal canal has been definitely proved by manometric measurement of the spinal fluid pressure in cases of breech labors. Spinal puncture for the purpose of reducing the size of the head and facilitating its passage in breech presentations has been advocated and successfully practiced by various obstetricians.
Temporary anemization of the brain during molding apparently does not cause any noticeable symptoms, at least not under normal conditions. It has been emphasized by various investigators that the bradycardia which could be expected as a sign of an intracephalic hypertension is uniformly absent ; however, it has been pointed out that bradycardia may fail to manifest itself only because in the newborn the vagus always is markedly hyposensitive.
Excessive ischemia of limited areas is assumed, as already pointed out, to cause in some cases a circumscribed necrosis with an occasional secondary hemorrhage into this area (Kruska). Some writers explain on the basis of this type of secondary hemorrhages the cases in which the child, apparently healthy and normal at birth, develops the unmistakable symptoms of a serious intracranial hemorrhage only several days later. This peculiar and not uncommon feature in the symptom-complex of intracranial hemorrhages for some of the cases, however, at present is more plausibly explained by the evident fact that a hemorrhagic tendency may cause a larger hematoma to form gradually and only a few days after the injury has been sustained.
Delay in the appearance of the symptoms of intracephalic hypertension and of hemorrhage may also be caused by a compensatory expansion of the skull cavity made possible by the stretching of sutures and the bulging of fontanels.
If hemorrhages are small, or an edema only limited in its extent and, therefore, quickly absorbed, physical and clinical signs may be so insignificant that they likely are overlooked or possibly cannot be ascertained even by careful observation. It is in this respect that the methods of examination at present available prove rather inefficient and are in urgent need of further refinement. In the present state of our information the possibility of an existing cerebral hemorrhage must be taken into consideration in every case in which melena or hemorrhages from other mucous membranes suggest a hemorrhagic diathesis, or the anomaly of coagulability is established by a test of the blood clotting time. It also seems quite evident that a more general, or preferably routine, use of ophthalmoscopic examination of the newborn will prove of decided value in the diagnosis of intracranial lesions which fail to cause the typical clinical manifestations.
The classic symptom of an increased intracranial pressure is the abnormal tension or actual bulging of the large fontanel. The latter indicates a comparatively large hemispheric or ventricular hemorrhage, or a pronounced cerebral edema which often develops as a direct sequela of a hemorrhage. It is important to remember that the large fontanel may remain normal if the hemorrhage is small or if it is primarily and entirely subtentorial. Tension or bulging of the fontanel may be noticed almost immediately or, more commonly, will become manifest only gradually. This latter phenomenon is a most valuable sign of a progressive process. In a similar, manner the observant obstetrician may be able to ascertain that only gradually also certain sutures become widened. These are extremely important points both in the diagnosis of continuation of the effusion of blood from a broken vessel, and in the localization of the primary focus.
In general, newborn infants with intracranial hemorrhages at first are very restless and cry almost incessantly, a phenomenon ascribed to the pain caused by the stretching of the dura mater. If the hemorrhage is not excessive, these infants refuse to nurse. This is due to the absence of the normal sucking reflex, easily established by gentle rubbing of the lips with a finger. In the normal newborn this irritation without exception prompts sucking attempts of the infant.
Various writers attribute the striking paleness of these children to an abnormal irritation of the vasomotor center rather than to the actual blood loss. They find a confirmation for this theory in the frequency of pronounced dermographism in these cases.
Respiratory symptoms, though hardly missing in any case, in themselves are not characteristic because in the main they are determined by the location of the effused blood. They are distinctly less pronounced in hemispheric hemorrhages than, e.g., in strictly infratentorial bleeding, when the resulting hematoma more directly affects the respiratory centers in the medulla.
With only slight intracranial hypertension respiration usually is slow and deep, at times irregular, but always interrupted by that rather persistent cry. The slow, stertorous breathing, so characteristic in the adult, as a rule is absent in the newborn. Therefore, in hemispheric hemorrhages with only slight hypertension, in the absence of convulsions, the infant rarely is cyanotic, which, on the other hand, is the common condition in infratentorial hemorrhages.
Convulsions. Convulsions represent the most obvious of all symptoms of an abnormal increase in intracranial tension. They are characteristically of the cortex type. Tonic and clonic, they involve chiefly the flexors of the extremities, but often include the muscles of the respiratory group, and usually are associated with rolling of the eyeballs, twitching of the face muscles, opisthotonos, with definite rigidity of the neck especially in infratentorial hemorrhages, occasionally with trismus, especially in ventricular hemorrhages.
The convulsions vary in frequency, duration, and interval, and are easily brought on by all manipulations of the infants, almost without fail by pressure against the bulging fontanel. A loud yelling cry during inspiration at the height of the spasm is followed by complete relaxation and a period of more normal breathing. If convulsions follow each other in close succession, the child, as a rule, becomes unconscious and remains in a comatose state.
On careful observation, a state of distinctly increased reflex irritability or spasticity can be noticed preceding the first convulsion. Touch or a slight scratch will cause sharp contraction of an extremity, or, indeed, may release the first convulsive seizure. Even between spasms the flexors persevere in a spastic and rigid state.
It is necessary in this connection to emphasize the well-known fact that all reflex phenomena are notoriously uncertain in the newborn. Though information available in this respect is somewhat contradictory, Reuss presents the following summary : the patellar reflex usually is very distinct within the first few days of life and may be found to differ in intensity on both sides. The achilles reflex has been found positive in 60 per cent of the cases by Furmann, in not quite 15 per cent by Bychowski. The cremaster reflex, according to some authorities, is present in the majority of infants within the first few weeks of life, which, however, is denied by others. The abdominal wall reflex, according to Farago, can be ascertained practically in every newborn infant by a slight scratch with a needle just above the mons veneris. This has not been found to be the case in the investigations of Furmann and Bychowski. Pediatricians for a long time have been acquainted with the fact that the Babinski reflex, as a rule, is positive in the newborn. But it has been claimed recently by some writers that instead of the typical Babinski in cases of intracranial hypertension one, not rarely, obtains a dorsal flexion of the foot associated with a plantar flexion of the toes.
It seems obvious that further progress in the problem of symptomatology and diagnosis of intracranial birth lesions to a large extent will depend upon better information concerning the actual status of the reflex irritability of the normal newborn.
Rather uniformly, writers emphasize some characteristics of the convulsions which occur in the cases of ventricular hemorrhages. These hemorrhages usually are profuse. All the symptoms of hypertension appear promptly. The convulsions often are of a decidedly tonic type. This is particularly pronounced in the extremities which seem rigid. Most characteristic is a trismus, a fact which accentuates the close resemblance of the symptomatology of ventricular hemorrhages in the adult and in the newborn, but also adds to the difficulties in the differential diagnosis from tetanus. Seitz emphasizes that in cases of ventricular hemorrhages careful observation might reveal that the upper extremities, at least at first, are more extensively involved than the lower, explained by him by the anatomic fact that a larger quantity of the blood escaping through the fourth ventricle is accumulated in the upper section of the spinal canal.
If a great deal of blood, either in infratentorial or in ventricular hemorrhages, enters the spinal canal, some of it may reach the lumbar cord and the cauda equina, and then give rise to such symptoms as erection of the penis or contraction of the scrotal skin.
Paralysis. As the intracranial hypertension increases, chiefly as the result of further extravasation of blood, the primary excitation and spastic condition gradually yields to a paralytic state, especially of the muscles of the extremities. Increased local pressure has finally paralyzed certain motor centers. Obviously in many cases death supervenes before this secondary paretic state is reached. In the infants who survive the primary excitation phase, the sequence in which one muscle group after another passes into flaccid paralysis offers a valuable aid in the localization of the primary source of the hemorrhage and in recognizing the direction of the gradual expansion of the hematoma. This point shall be discussed later in detail.
A paresis involving all extremities practically manifests the terminal stage. A most confusing clinical picture of a spastic condition in certain muscle groups with simultaneous paralysis of others, in some instances, is brought about by a combination of an irritative cortex hematoma with hemorrhages within the brain substance (chiefly ventricular) which paralyzes certain centers.
Localizing Symptoms. Definite localization of an intracranial hemorrhage in the newborn is of greatest importance for appropriate therapeutic, especially operative, interference. From this point of view, it is essential first to determine whether the hematoma lies above or underneath the tentorium. In the case of the supratentorial hematoma, an effort must be made to localize it either immediately above the tentorium at the base of the brain, or over the convexity of a hemisphere, with a final endeavor to determine its location either over the cortex surface or within the brain itself, on one or the other side.
At the outset it might be stated that in the newborn such an exact localization, however desirable, is extremely difficult and but rarely possible. Conditions in the newborn as compared with the adult patient differ in the following essential points : Hemorrhages in the newborn are likely to be profuse. Even a distinctly localized hematoma is less prone to exhibit definite local symptoms because the pressure is more readily diffused by the flexibility and expansibility of the skull. Perfectly normal newborn infants often show definite spasticity of certain muscle groups especially in the extremities. This spasticity frequently is followed by a striking flaccidity While the central nervous system at birth as a whole notoriously is in a state of imperfect development, the motor centers of the cortex are functionating fairly well. Therefore, the symptoms of cortical irritation will always tend to dominate the clinical picture, even if the cortex itself is not directly affected by the hemorrhage, and, e.g., only pressed upward by a hematoma lying beneath the hemisphere.
It will be shown in the following pages that the essential feature of more exact localization consists in the careful observation of the sequence of certain symptoms which, in many instances, precede the first convulsion. It is this indisputable fact which so clearly places the duty of painstaking observation on the physician who manages the labor and thus alone has the opportunity to see the child immediately after birth.
Supratentorial Hemorrhages. Hemispheric subdural hemorrhages, as a rule, are unilateral. The question as to which side is involved, is easily and reliably settled in the presence of definite unilaterality of symptoms. Every large hematoma, and usually also a secondary edema, however, unfortunately often will affect through compression the other hemisphere and thus the valuable symptom of unilaterality is quickly eliminated. In the opinion of some observers the typical bilateral convulsion always is preceded by a unilateral affection, which may be of very short duration, but is hardly ever absent. Seitz asserts that very careful observation during the first seizures often enables one to determine that the extremities of one side contract more violently than those of the other side. In this manner he succeeded in 5 out of 7 cases to diagnose correctly the seat of the hemorrhage before death.
Immediate and continued observation occasionally permits one to ascertain the gradual and successive involvement of cortex motor areas exactly corresponding to the natural course of expansion of a blood clot from its original source towards the lateral or posterior portions of the brain. Thus there might be recognized first the distinct affection of the motor center of a lower extremity in the upper third of the central convolutions of the opposite side. When the blood reaches the middle third of these convolutions, the upper extremity begins to be affected. With the escaping blood finally pressing against the lower third of the anterior central convolutions, symptoms of irritation and later of paresis will appear in the muscles innervated by the facialis and hypoglossus.
The final predominance of symptoms in the facial muscles and the striking rapidity with which the paretic stage as a rule follows the primary and short stage of irritation, according to Seitz, also is easily explained by certain mechanical factors. The extravasated blood gravitates downwards so that the upper portion of the coagulum will be comparatively thin and the lower portion thicker, thus pressing more firmly against the cortical centers of the facial nerve.
It is for this reason, according to Seitz, that an aggravation of the facials symptoms in form of paralysis often is accompanied by a coincident recession of the symptoms in the extremities if the hemorrhage has ceased. It will be well to remember in this connection that Seitz considered only hemispheric hemorrhages. This same prevalence of the facialis and hypoglossus symptoms over certain cortex symptoms in the early symptomatology of intracranial birth lesions is quite obvious for tentorial lacerations in which the escaping blood under the base of the brain directly affects the intracranial portions of these nerves. Thus the detailed symptomatology, so carefully worked out by Seitz, as it affects the various muscles innervated by facialis and hypoglossus is of eminent value in the diagnosis and more exact localization of all supratentorial hemorrhages, whether primarily hemispheric or basal.
Nervus Facialis. In contrast to the more common sequence in other muscle groups, especially of the extremities, of overstimulation followed later by paralysis, in the facialis group most frequently overstimulation is of very short duration, limited to some twitching, e.g., in the M. orbicularis oculi, or is entirely absent, so that in most instances the first noticed anomaly is a paralysis. In this intracranial type of facialis affection, as a rule, all branches are involved, and a circumscribed paralysis, such as a lagopthalmos alone, is the exception.
Unilateral spasticity or, as more frequently is seen, a unilateral paralysis of the entire facialis group definitely establishes the contralateral location of the hemorrhage, if it can be proved that the paretic condition is of central and not of peripheral origin. However, unilateral facial paralyse of intracranial origin is but rarely observed, because in a large hemispheric hematoma, indirectly through the increased pressure, the facialis of the other side, and, in cases of basal supratentorial hemorrhages directly, both faciales usually are affected.
By far the more common type is the extracranial peripheral facialis lesion, usually caused by the direct pressure of a forceps blade or of a protruding portion of the pelvic wall in a malformed pelvis. The peripheral nature of the trauma often is evidenced by a visible mark or depression. In these instances the paralysis always can be noticed immediately, and, as a rule, the symptoms disappear promptly within a few hours, or at least show definite improvement from day to day. In contradistinction the symptoms of an intracephalic injury of the facialis appear only from one to three days, and occasionally even later after birth, and are likely to become more marked from day to day.
All signs of anomaly in the muscles innervated by the facialis in the newborn demand most careful study and interpretation. Whenever the condition seems persistent or the symptoms are distinctly progressing, an intracranial origin should be considered. Almost conclusive for the intracephalic and truly central origin are tonic or clonic contractions in the affected muscle groups, especially if other muscles, e.g., those supplied by the oculomotorius also are involved, or if other definite signs of an intracranial hypertension are present.
Nervus Hypoglossus. This nerve usually is affected in the same sense as the facialis. In the paretic state the tip of the tongue is deviated toward the paralyzed side.
Nervus Accessorius. Affection of the eleventh nerve by a hemorrhage, most likely due to a tentorial laceration, will manifest itself chiefly in the condition of the sternomastoid muscle. The head will be turned toward the paralyzed side. Great care must be taken in the proper interpretation of this symptom ; first, because of the possibility of a congenital torticollis, and secondly, because during the convulsive state the head might be held fixed in this attitude, but then suddenly thrown into the opposite direction. Various observers emphasize the absence of all neck rigidity in the cases of hemorrhages in the upper cranium as compared with its frequency in infratentorial hemorrhages.
Nervus Oculomotorius. The condition of the M. levator palpebrarum superior proves most useful for the purpose of more exact localization. Since the larger portion of oculomotor fibers remain uncrossed, twitching or paresis of this muscle will occur on the same side on which the hematoma lies. This same rule also holds for the contracted pupil. However, in accord with the general experience of neurologists and surgeons in the adult, in the newborn as well the interpretation of a unilateral miosis or mydriasis for the purpose of localization is very unreliable. Extreme contraction of one pupil together with strabismus and nystagmus, can be seen in many cases of cranial hemorrhage in the newborn. Some of the effused blood, especially in hemispheric hemorrhages, is likely to reach and to irritate the cortical center of coordinate ocular movements in the gyrus angularis at the end of the temporal sulcus. For this reason a reactionless, widely dilated pupil renders the prognosis particularly bad, though the infant may continue to live for a few more days.
Infratentorial Hemorrhages. All severer hemorrhages of the infratentorial type are prone to impair the function of the important centers in the medulla oblongata to such extent that death will ensue quickly. On the other hand, it is generally conceded that slighter peribulbar hemorrhages, especially from minor injuries of the tentorium, may give rise to symptoms hardly distinct enough to permit their recognition.
In the foreground of all symptoms due to infratentorial hemorrhages stands impairment of respiration. The infant usually is cyanotic and very markedly so during a convulsion. However, in an infratentorial hemorrhage, like the signs of an abnormal intracranial tension, respiratory embarrassment may make only a delayed appearance.
If a considerable amount of the extravasated blood escapes down the spinal canal, at first convulsive contractions may be more marked in the arms than in the legs ; later the signs of an irritation of the lumbar cord might be noticed in the form of contraction of the scrotal skin or an erection of the penis.
Some of the most notable differences in the typical symptomatology of hemispheric and of infratentorial hemorrhages of the newborn can be tabulated as follows :
Hemispheric. Infant cries a great deal during first few days. Breathing center becomes affected comparatively late. Infant is pale. Death may be delayed. Fontanel becomes tense within comparatively short time. Prompt appearance of symptoms of intracranial hypertension. Rigidity of neck and opisthotonos hardly noticed. Symptoms from affection of facial and oculomotor nerves at first may be unilateral.
Infratentorial. Infant usually is very quiet, apparently is sleeping or is affected early. Infant is cyanotic, especially during convulsion. Death usually occurs early. Fontanel at birth is practically normal. Increased tension, if at all, becomes noticeable only later. Symptoms of hypertension appear late. Rigidity of neck and opisthonos usually marked. Symptoms from affection of facial and oculomotor nerves, as a rule, immediately are bilateral.
In spite of such clear differences in certain classical signs, the clinical picture in the individual case is likely to exhibit a mixture of symptoms for the very obvious reason that in the majority of instances, as now generally conceded, birth hemorrhages originate from tentorial lacerations. In them blood may diffuse both above and below the injured tentorium. Even in the more common basal supratentorial hemorrhages gravity often causes some of the blood to flow downwards and affect the cerebellum and medulla. Later, as already pointed out, the relatively more advanced development of the cortical motor centers usually will cause symptoms of indirect irritation of the cortex to predominate in the clinical picture of all forms of intracranial hemorrhage. It seems justifiable to emphasize in this connection once more the importance of a most careful observation of the early symptoms and of their gradual changes.
Ventricular Hemorrhages. Ventricular hemorrhages, in most cases, are profuse and lead quickly to the death of the infant. If this is not the case, convulsions are prone to be of markedly tonic type. Most writers mention a trismus as a very common and often misleading symptom.
Hemorrhages within the brain substance are comparatively rare. They are not likely to offer symptoms definite enough to permit their localization. This, in part, is due to the general underdevelopment of the central nervous system of the newborn infant.
The diagnosis of an existing intracranial birth lesion and its more definite localization necessarily depends upon the exact observation and correct interpretation of the various symptoms which have been described in detail in the foregoing pages. It would cause unnecessary repetition to outline here the different symptom-complexes which permit the diagnosis of each of the various types of lesions. It seems preferable rather to point out certain general facts which are of unquestionable importance in the recognition of an intracranial birth traumatism.
At the outset we shall emphasize that the history of the labor, whether it was spontaneous, delayed, or required artificial termination, is of decidedly less value than customarily accorded it.
In most of the severer cranial lesions, the child is stillborn or dies soon after birth. In the latter group the infant at birth seemingly is in a state of deep asphyxiation. Attempts at resuscitation obviously will fail, though regular contractions of the heart may continue for a short time. An intracranial traumatism as the cause of death can be suspected when a difficult forceps extraction has caused distinct external cranial injuries, or when after a very protracted labor marked overlapping in some sutures indicates long-continued and excessive compression, especially if the child is premature.
A cephalhematoma is a symptom of value only in the presence of other signs suggesting an intracranial injury. In the majority of cases of parturitional or neonatal death, the diagnosis of an intracranial birth trauma can be established only by an autopsy performed according to the method of Beneke. In this connection the fact should be borne in mind that serious and fatal injuries not infrequently occur in the course of spontaneous and quick labors.
On the other hand, no undue importance in the diagnosis of internal lesions must be placed on external evidence of traumatism, such as depression or laceration of the skin or even the indentation of a skull bone. It has been definitely established that those children who exhibit no noticeable symptoms in spite of definite external cranial lesions at birth, later in life, as a rule, remain physically and mentally normal.
Asphyxiation always should suggest the possibility of an intracephalic lesion, and especially if the child immediately after the expulsion seems fresh and normal, and only later exhibits the signs of impaired respiration.
A suspicion of an intracranial trauma should be aroused whenever the newborn is either crying almost incessantly or is strikingly quiet, especially when he does not respond with sucking motions to a slight irritation of his lips with a finger. The absence of these symptoms immediately at birth and their progressive appearance soon afterwards must be regarded strongly suggestive of a gradually developing intracranial hypertension. Particularly valuable for the purpose of diagnosis proves in this respect the observation of a gradual involvement of certain cranial nerves, chiefly facialis and oculomotorius, especially if the sequence in which new symptoms successively manifest themselves corresponds to the natural extension of a hematoma downwards and backwards as determined by gravitation.
Certain special methods of examination have proved particularly valuable in the diagnosis of existing and even of only impending intracephalic lesions.
Fetal Heart Sounds. Too recently to have permitted either confirmation or repudiation, at least two authors have offered interesting information concerning the possible value of variations in the pulse rate of the fetus in the diagnosis of imminent danger to his life.
From a large series of careful observations on parturient women combined with an autopsy study of all stillborn infants, Baumm concludes that a fetal tachycardia, appearing without a preliminary bradycardia in the course of a protracted labor of an afebrile woman, is pathognomonic for a threatened intracranial hemorrhage.
In a group of labors in which this phenomenon had been definitely ascertained by practically continuous observation of the fetal heart sounds, 11 babies died of brain hemorrhages, while 4 others who survived showed very definite symptoms of cerebral irritation of some sort. Baumm believes that the timely discovery of this symptom in some cases might enable the physician to save the child by quick delivery.
Baumm furthermore concludes from his observations that a tachycardia preceded by a bradycardia is rather suggestive of the fact that the hemorrhage already has occurred. No hope to save the child is held out by prompt delivery. The reversed sequence of a tachycardia followed by a bradycardia, in his opinion, probably is the expression of a beginning mechanical asphyxiation.
However, he found fetal death may occur suddenly during labor, recognized by the sudden cessation of all heart sounds without any preliminary changes in their rate. Of 7 stillborn babies, in whom the heart sounds had remained normal up to the moment of birth, 5 showed extensive intracranial, hemorrhages. Similar hemorrhages were found in 3 other infants in whom the heart had been observed to stop suddenly during labor.
Sachs, on the other hand, maintains that danger to the fetus is clearly denoted by a slowing of the fetal pulse below loo, or by repeated changes of the rate within wide limits even if it never slows below 100. He specifically asserts that this ominous bradycardia below 100 is characterized by the fact that it is not preceded by a tachycardia. He doubts that a retardation of the fetal pulse rate is an expression of abnormal intracranial tension, and in general is unwilling to accept all of Baumm’s deductions. Sachs emphatically states that a fetal pulse rate up to 160 must not be regarded as an indication for interference and positively does not justify a difficult forceps extraction which in itself implies great danger to the fetus.
The only acceptable indication for immediate interference can be found in a bradycardia below 100 persisting during the intervals between a few consecutive uterine contractions.
Delayed Coagulation Time. The etiologic relation of hemorrhagic diathesis as a contributory factor in the causation of serious intracranial hemorrhages has been adequately discussed in the foregoing pages.
The importance of establishing or excluding an anomaly of the coagulability of the blood of the newborn, in every case suggestive of a cerebral hemorrhage, seems self-evident. A comparatively simple and for all practical purposes sufficiently accurate method, found useful by Rodda, may be briefly described as follows :
The heel of the infant is cleansed with ether. A puncture is made with a sterile lance blade, deep enough to produce a free flow without requiring any squeezing of the skin. A clean watch glass containing a No. 6 shot receives the second drop of blood. Another watch glass is inverted over the first. The glasses, held together, are gently tilted every thirty seconds until the shot no longer rolls, but is fixed in the clot. In the end the shot is so firmly imbedded that the glass may be inverted without dislodgment of the shot. The greatest source of possible error lies with the blood flow. Blood obtained by pressure from too small a puncture will clot very quickly. For the sake of comparison it is preferable always to use the second drop ; it coagulates faster than later drops.
This method does not pretend to ascertain the absolute clotting time, but the result is a clear-cut relative time for comparative work. Its object is to discover merely gross variations from the normal range. The average coagulation time in the newborn, ascertained by this method, is seven minutes, with a normal range between five to nine and up to eleven minutes.
The newborn normally exhibits a tendency to prolongation of clotting time during the first days of life. Hemorrhagic conditions show a distinct exaggeration of this tendency or a markedly prolonged coagulation time up to thirty and forty and even ninety minutes. In Rodda’s belief routine determinations in the newborn will allow, the recognition of at least certain hemorrhagic conditions before the onset of symptoms, and thus will give the opportunity for prompt or even prophylactic administration of blood or serum. Markedly delayed clotting time or such evidences of a hemorrhagic diathesis as hematemesis, melena, hematuria, or petechial hemorrhages in visible mucous membranes, in the presence of other clinical signs will always strongly suggest or actually confirm the diagnosis of an intracranial hemorrhage.
Prolonged Bleeding Time. According to Rodda the bleeding time, ascertained by the method of Duke, in general shows the same type of curve as the clotting time. The bleeding time in normal newborn infants averages three and a half minutes, with a normal range between two and five minutes.
Hemorrhagic disease in most instances shows a corresponding marked prolongation of the bleeding time up to fifteen and twenty minutes.
External Traumatism. With the exception of evidently perforating injuries, fractures of skull bones and very deep indentations, other external traumatic birth injuries of the head do not “permit reliable conclusions concerning intracephalic conditions.
A very large caput succedaneum indicates a long-continued molding, but not that sudden and excessive compression of the head which is of such great importance in the causation of intracranial traumatization.
A cephalhematoma one finds frequently mentioned in the necropsy findings of infants with severe internal injuries. However, there is no direct relation of the true cephalhematoma to the serious and fatal cerebral damage. It has been mentioned in a preceding chapter, that anatomic conditions, the passing of blood vessels from the pericranium directly through the skull bones into the underlying dura, may cause small flat epidural hematomas to form close to the inner surface of the cranial bones. This epidural hematoma, however, represents only an accidental finding at autopsy, and, so far as is known, is of no particular clinical significance.
In cases of perforating cranial injuries some of the blood of a subdural hematoma may escape through the opening from the cranial cavity underneath the scalp. The resulting hematoma on superficial examination may resemble a typical cephalhematoma.
Its true origin and with it an intracephalic hemorrhage will be revealed by pulsation, and still more clearly, if pressure against this hematoma releases the typical symptoms of intracranial hypertension.
A very marked overriding of skull bones in certain sutures, observed immediately after birth, especially after a forced labor (quick forceps extraction, pituitrin, etc.), must be regarded as suggestive of a possible internal traumatism. On the other hand, this symptom may disappear very rapidly, indeed, possibly as the result of a rapid increase of intracranial tension from a hemorrhage.
Ophthalmic Examination. Though employed and advocated for many years as a most valuable aid in the diagnosis of cranial birth injuries, the ophthalmoscope still is but rarely used in obstetric clinics.
This lack of interest presumably is due to definite technical difficulties in its use on the newborn.
The first examinations of this kind date back to Jaeger in 1861.
An elaborate paper by Stumpf and Sicherer presents an interesting history of the various efforts made in this direction. These two investigators, from the study of a very large material, arrive, among others, at the following conclusions : The corpus vitreum was always found normal. The eyeground of the newborn in general resembles that of the adult, though, as a rule, all the colors are lighter. If the examination is made very soon after birth a distinct venous stasis is common. The papilla usually appears normal, but in some cases (as also emphasized by Jaeger and Koenigstein) is from a dark gray to a bluish gray. The usually coexisting reddish discoloration at the scleral edge with fine, red, radiary hemorrhagic lines, permits the interpretation of the darker and grayish hue of the papilla as due to a hemorrhage into the subvaginal space of the dural sheath. Within a few days the blood is resorbed and the color becomes normal.
Most striking in the ophthalmoscopic examination are the relatively common hemorrhages in various portions of the eye. The marked difference in the percentage figures of their frequency as given by the various authors, probably is due to the difference in the time when the examinations were made. Smaller hemorrhages are speedily resorbed and quickly become invisible. Sicherer’s figures are based on observations made within twenty-four hours after birth.
In 400 newborn infants he discovered 65 hemorrhages, of which 23 were bilateral, 14 in the right, and 5 in the left eye.
All investigators agree that these hemorrhages are fresh and could not possibly have developed during intrauterine life. Sicherer agrees with Schleich that the hemorrhages from the finer retinal vessels are the result of a congestion, and that, therefore, etiologically they stand in some relation to the minute tod larger cerebral hemorrhages.
The suggestion has been made that the congestion in the eye develops only secondarily to an intracranial hypertension. Compression of the sinus cavernosus interferes with the normal emptying of the ophthalmic vein in spite of the partial relief offered through the existing anastomoses with veins of the face. More unfavorable under such conditions, however, would prove the situation for the vena centralis retinae, which, as a rule, without any anastomosis with the vena ophthalmica, empties directly into the sinus cavernosus.
The more common occurrence of such hemorrhages in the eyes of premature infants is generally ascribed to the particular fragility of the retinal vessels as the result of underdevelopment.
A further support of Schleich’s theory that the congestion is the effect of the compression of the cavernous sinus is seen by Sicherer in the fact that in the more common left anterior occipital presentation the hemorrhage is more likely to occur in the right eye, or if bilateral, is more pronounced in the right eye, just the opposite ; findings being made in the right anterior presentation. This would seem to prove that the eye lesion is more frequently found on the side on which the sinus is exposed to greater pressure.
Most of the writers agree that small peripheral hemorrhages are of no importance for vision later in life, while large hemorrhages, especially when situated near the macula, may permanently affect central vision. Such hemorrhages may cause permanent structural changes or interfere with further normal structural development.
It seems interesting to note in this connection that in some of the reports concerning the eye findings mention is made of a complicating melena which is supposed to have been caused by the intracranial hypertension. There still are investigations wanting concerning a possible etiologic relation also of the ocular hemorrhages to a hemorrhagic diathesis.
Paul gives the following figures as expressing the relation of retinal hemorrhage to certain obstetrical anomalies : Narrow pelvis. 50 per cent ; prematurity, 40 per cent ; complicated and protracted labors, 40 per cent ; normal labors with child of normal size, 20 per cent. He lays particular stress on asphyxiation as the cause of the ocular hemorrhage.
In the opinion of Kearney the ophthalmoscopic study of the eyeground of the newborn offers one of the earliest and most reliable means of diagnosing intracranial hypertension. He described the characteristic ocular findings as follows: “There may be seen a mild edematous blurring of the upper and lower margins in the first few days of life, later an edematous blurring of the entire surface of the nerve head and all its margins. When the intracranial hemorrhage is severe and the tension greatly increased, gross edematous changes may appear quite early, the edema being confined to the nasal half of the disc, or affecting the entire disc, a typical papilledema.”
In Kearney’s belief such eyeground findings together with an increased pressure of the cerebrospinal fluid, as ascertained by lumbar puncture, in selected cases permit the definite diagnosis of a pathologic intracranial hypertension and justify a simple decompression operation even in the absence of convulsions.
Spinal Puncture. Cerebrospinal fluid is withdrawn by means of a spinal puncture in the main for two purposes : (1) to obtain fluid for morphological, cultural or chemical study, and (2) to relieve an abnormal tension. Spinal puncture serves the double purpose of diagnosis and therapy also in its employment on the newborn for which of late it has been recommended by serious workers and not mere enthusiasts “for every case of suspected intracranial hemorrhage.”
Obviously here we are concerned only with spinal puncture as an aid in diagnosis. Blood reaches the spinal canal directly in all infratentorial and peribulbar hemorrhages and indirectly, by gradual diffusion, from supratentorial basal, and even from hemispheric, hemorrhages if they are copious.
Most commonly the puncture is done in the lumbar section where an accidental injury of the cord by the needle is the least likely to occur. A fluid strongly mixed with red cells or representing almost clear blood will be obtained especially in the cases of free subtentorial hemorrhages but, as must be kept in mind, also in epidural spinal hemorrhages, i.e., in cases of traumatization of the spinal column during birth. If the fluid is only of a yellowish color, presum ably containing only a small amount of blood, it must be examined microscopically without delay. Morphologically altered, degenerated erythrocytes, detritus, hematin pigment, etc., prove an older hemorrhage, while perfectly normal red cells in small numbers do not exclude the possibility of an accidental contamination of the spinal fluid with blood from injuries of small vessels by the puncture needle. It is obvious that the absence of blood in the withdrawn spinal fluid does not necessarily exclude a supratentorial and especially hemispheric hematoma.
Statements concerning the diagnostic value of the pressure of the spinal fluid, estimated by the speed of the escaping fluid or actually measured with a manometer, are most contradictory. Most writers are inclined to deny any reliable diagnostic significance to a seemingly increased pressure.
A perusal of the numerous detailed case reports in literature, however, leaves the definite impression that withdrawal of spinal fluid or blood (quantities of 20 to 30 cubic centimeters are repeatedly mentioned) in a strikingly large number at least of the recorded cases, is followed by a prompt temporary or permanent cessation of those symptoms which commonly are ascribed to cerebral hypertension or localized cortical pressure.
Impressed by the great diagnostic value of spinal puncture, in spite of its evident short-comings and dangers, some authors, e.g., Henschen, have advocated making the puncture as near as possible to the primary source of the hemorrhage. A puncture between the second and third cervical vertebra thus will promptly establish the existence of a peribulbar extravasation of blood in its incipient stage.
The increased danger of a cervical puncture, in the belief of its various enthusiastic advocates, is more than outweighed by its beneficial effect in relieving the local pressure on the important centers in the medulla oblongata which necessarily will prove fatal if permitted to continue or to become excessive.
Henschen, Doazen, Frazier, Robt. M. Green, go a step further and practice in selected cases an “easy and harmless” cranial puncture which fails to yield the desired result only if the blood had time to clot firmly. However, most authorities agree that blood effused in intracranial hemorrhages as a rule clots very slowly and often is found still in a fluid state even at post mortem. In the special method of cranial puncture described by Henschen, a comparatively thick puncture needle is pushed, on one or if necessary on both sides, into the subdural space from the lateral corner of the large fontanel.
This puncture can also be made under the same precautions from the posterior fontanel. Some of the writers, e.g., Ball, Doazen, etc., from this point of view, consider it logical and practical to search for the blood clot through a small trephine opening whenever puncturing with the needle does not supply the desired information. Without sufficient personal experience one cannot undertake to pass judgment on such procedures as cervical or cranial puncture. It does not seem justifiable to recommend even the decidedly less dangerous lumbar puncture as a routine procedure to the practitioner for all suspected cases of hemorrhage. Nevertheless the fact deserves serious consideration and investigation, that diagnostic spinal punctures are employed and urgently recommended by such recognized authorities as Gushing, Frazier, Doazen, Henschen and many others.
Robt. M. Green, Foote, Brady, Sidbury, Hutinel and several other careful investigators feel no doubt that “in every case of suspected hemorrhage” (Sidbury), “in every newborn showing within twelve to twenty-four hours after birth respiratory distress and cyanosis, with or without muscular rigidity and twitching” (Foote), “in every baby that within a few days of birth becomes pale, refuses the breast and shows a peculiar though slight edema of the face” (R. M. Green), a lumbar puncture should be done promptly. According to Sidbury such a routine will help in three ways :
(1) letting off of the spinal fluid will relieve the intracranial pressure and stop the convulsions ; (2) it may cure the patient ; and (3) it will aid in the diagnosis.
However, it must be remembered that the relief of the intracephalic pressure may foster a continuation of the hemorrhage, especially in the cases of a decreased coagulability of the blood.
Therefore, it seems desirable, in my opinion, to combine a routine of spinal puncture in suspected cases with a routine of ascertaining the blood clotting time, and to precede the puncture with blood or serum injections, whenever there seems to be a delay in clotting.
The chief value of the puncture as a diagnostic aid undeniably lies in the readiness with which it can be applied, and in the promptness with which in some cases it will definitely establish an existing intracranial hemorrhage. Only little time, as a rule, is available for therapeutic and especially operative interference to prove useful or lifesaving.
We shall presently see that spinal puncture also is a procedure of no mean importance for the purpose of differential diagnosis from conditions closely resembling intracranial parturitional traumatisms.
The difficulties of early and accurate diagnosis of a traumatic intracranial hemorrhage at birth are augmented to a notable degree by the evident fact that the general clinical picture of such an accident or at least some of the outstanding symptoms of such lesions are closely simulated by certain other conditions not uncommonly affecting the newborn infant. This applies particularly to convulsions.
In an exhaustive study of this question, Esch clearly points out the essential differences of the convulsions of the first few days of life from those appearing later. Early convulsions are not rare.
D’Espine found in a total of slightly over 15,000 newborns in a large maternity service the incidence of early convulsions to be approximately two in a thousand, with a mortality of 62.5 per cent. A large part of these cases represents instances merely of a cortical or subcortical irritation as the immediate result of a birth trauma, while in many other cases definite cerebral lesions were discovered to account for the convulsions.
Esch, therefore, concludes that it is advisable to differentiate, as far as possible, the general convulsions or limited spasms of certain muscle groups of the newborn into a functional and an organic group.
Myotonia neonatorum (of Hochsinger). This condition manifests itself in a slight rigidity of the flexors of all extremities at birth and persists for a short time even in perfectly normal infants. This myotonia may increase the tendency to tonic spasms but never becomes their actual cause.
Reflex Irritability of the Brain.This is often increased at birth for a short time and may actually become responsible for convulsions. Despite the comparatively incomplete development and function of the central nervous system of the newborn, the reflex mechanism obviously is functionating. In no other manner could be explained the clearly reflectory manifestations of crying or sneezing.
Eclampsia Neonatorum. This is a term often rather loosely employed, especially by pediatricians, to denote a convulsion of a newborn infant. The obstetrician more commonly applies the term solely to the convulsions of infants born of eclamptic mothers. Presumably in these cases certain toxic substances, prone to cause convulsions, had been transmitted by way of placental circulation from the ma ternal into the fetal blood. Though this assumption is not based on any definitely known biologic facts, such a transition of soluble toxins, theoretically at least, seems possible. In the light of recent knowledge, however, it seems more plausible that in many of these cases the convulsions are due to a cranial trauma incident to a labor which, in view of the condition of the mother, often is terminated by means of a difficult forceps or a version with immediate extraction.
Tetany. In the opinion of Reuss, tetany should be specially grouped within the wider term of spasmophilic diathesis or tendency. He claims that typical tetany with its characteristic diagnostic symptomatology, including laryngospasm, has never been observed in the newborn. The precise diagnosis of true tetany within the first few weeks of life, however, really is impossible because the necessary proof of electric hypersusceptibility cannot be furnished. In the newborn the electric sensitiveness of all peripheral nerves is low. Typical tetanoid symptoms, closely resembling the classical trias of Erb’s, Trousseau’s and Chvostek’s phenomena, but never associated with laryngospasm, as pointed out by Reuss, have been observed by Kehrer (Arch. f. Gynakologie, 1913, 99:372). Reuss saw a very similar symptom-complex in a case of subdural hemorrhage.
How far such tetanoid symptoms in the newborn might be related to a traumatic birth injury of the parathyroid glands is a question I shall discuss later in its proper connection.
Organic Convulsions. In the majority of instances general convulsions or spasms limited to isolated muscle groups are due to organic lesions. Among them the traumatic intracranial lesions, considered in detail in the preceding pages, stand in the foreground.
For practical and especially therapeutic purposes it becomes indispensable to differentiate them diagnostically from certain other chiefly infectious processes which affect the child late in intra-uterine life or soon after birth and tend to cause spastic seizures.
Before entering into a detailed discussion of the differential diagnosis from this last group, it will prove advantageous to point out briefly a few essential facts. In marked contrast to the functional group, the cases in which convulsions or circumscribed spasms are caused by definite organic lesions are likely to exhibit one or more of the following symptoms : severe external injuries, slight stupor or coma between seizures, rigidity of neck, anomalies of fontanels or sutures, deformities of the head (hydrocephalus), a unilaterality of symptoms, or a progression of symptoms which in their sequence express the anatomic extension of an enlarging hematoma.
In the differentiation between the traumatic lesions, chiefly hemorrhages, and the other processes, chiefly infections, a consideration of the mother’s condition and of the history of labor is of a decidedly limited value. Fever in the newborn is practically always absent in the earlier stages of traumatic lesions. The most useful aid in the differential diagnosis is spinal and cranial puncture.
Tetanus. According to a report of Mirons (published in 1904) in Roumania out of a total of 23,000 infants dying within the first month of life 10,000, almost one-half, had succumbed to tetanus.
In some of the tropical countries the infant mortality from tetanus alone has been found to be between 10 and 25 per cent. It, therefore, cannot be surprising to meet in medical literature with the term “tetanus neonatorum,” but obviously it should be, and probably is not, strictly limited to denote the specific infection with tetanus.
This disease now is but rarely observed in the newborn in civilized countries, and hardly ever seen in a maternity since the modern technic of the aseptic management of the umbilical cord stump has been generally adopted. This very scarcity of tetanus renders the problem of a differential diagnosis proportionately more important.
The period of incubation in tetanus presumably varies from a day or two up to several weeks. The first symptoms, therefore, are not likely to manifest themselves within the first few days of life, and most commonly have been recorded as appearing at the end of the first or during the second week of life. However, Heubner claims to have seen a true case of tetanus develop on the day of birth.
The first symptom is a tonic contraction of the masseter muscles. The spasms then extend to other muscles of the face and neck, and later of extremities and trunk. They are of a markedly tonic type and cause an almost characteristic rigidity of the entire body. The temperature may remain normal but usually there is a high fever. Death may ensue quickly or is delayed for a day or two. Mortality figures vary widely, and are given by Fronz as 42 per cent, by Shukowski as 98 per cent (quoted from Reuss). In some rare cases the infection is of a chronic type and the child then is more likely to recover.
Convulsions of a pronouncedly tonic type are comparatively less frequent in intracephalic birth hemorrhage, though Waldstein, Abels, and others emphasize a trismus as rarely absent in ventricular hemorrhages. Seitz points out the fact, important in differential diagnosis, that, with the exception of the musculus orbicularis oculi, eye muscles do not participate in tetanic convulsions. But Abels observes that unfortunately the contractions of the orbicularis actually prevent a satisfactory examination of the behavior of the other eye muscles during the seizure.
A careful and critical analysis leaves no doubt that neither the presence nor the absence of the various clinical phenomena, enumerated above, either singly or in groups, will allow a definite differentiation of tetanus from a parturitional cerebral lesion in all cases.
There are only a very few cases on record in which the tetanus bacillus actually has been discovered in the newborn. If we consider the general uncertainty of the exact diagnosis of tetanus in the light of the fact that our more accurate information concerning the frequency and semeiology of cerebral birth lesions is of comparatively recent date, the deduction is permissible that even today probably in some cases the diagnosis of tetanus is made incorrectly and thus the infant deprived of proper therapeutic attention. Modern literature contains the records of several cases in which infantile death was ascribed to tetanus while the post-mortem examination revealed as its actual cause a cerebral hemorrhage.
Therefore, the demand can be made to attempt a differentiation in every suspected case of tetanus by means of a spinal puncture. If red blood cells in sufficient quantity or in characteristically altered forms are found in the spinal fluid, tetanus can be excluded promptly.
Encephalitis. Comparatively little is known concerning a septic encephalitis which occasionally is found in post-mortem examinations of newborn infants. In some instances the process evidently is of metastatic origin, in the majority of cases, however, the etiology remains obscure. Mention has been made of the possible connection of septic encephalitis and porencephaly to cerebral hemorrhages, and to the formation of ischemic foci as the direct result of birth traumatism. Kruska in 20 cases of ischemic brain lesions found that in three the resulting necrotic area had become infected and thus been transformed into a typical brain abscess.
Meningitis. Certain congenital deformities especially of the cortex and congenital hydrocephalus, in the belief of various writers, prove the possibility of an intra-uterine meningitis. Seitz (Arch. f. Gynakologie, 1907, 83:701) advanced suggestive reasons why there might exist a connection between severe traumatism of the abdominal wall during pregnancy and intracranial lesions with subsequent congenital encephalitis. In regard to hemorrhagic pachymeninigitis the opinion seems to prevail that it is rather of hereditosyphilitic origin.
A purulent meningitis not rarely is observed very early in life and even in the newborn. In most instances it is due to an otitis, which in the opinion of Aschoff, is caused by the entrance of infected amniotic fluid into the middle ear. A long-drawn-out labor, especially after the membranes have ruptured, and asphyxiation, favoring the aspiration of presumably infected amniotic fluid, thus possibly may play a role in the causation of purulent meningitis of the newborn.
In regard to the problem of differentiation of meningitis from meningeal hemorrhages, the following points are of importance : meningitis, as a rule, is accompanied by fever which, however, may be absent in fulminant cases ending fatally very quickly, or may not appear until the terminal stage. On the other hand, some cases of meningitis in the newborn exhibit such characteristic meningeal symptoms as convulsions, rigidity of neck, protrusion of the fontanel or distention of sutures, or almost typical tetanic symptoms (De Bruin).
Again the question suggests itself how often the diagnosis meningitis is made incorrectly. In the doubtful case a spinal puncture might solve the problem, as is well illustrated in a case mentioned by Bonhoff and Esch : A newborn baby exhibited the typical symptoms of a supratentorial hemorrhage. On the sixth day a spinal puncture was made. The spinal fluid was found turbid, containing many polynuclear leucocytes. On the ninth day convulsions, fever, with exitus five days later. Autopsy showed a purulent meningitis from a right otitis media.
However, as pointed out by Brady, blood in the spinal fluid in such instances does not necessarily prove an intracranial hemorrhage because the fluid will be bloody also in the rare instances of hemorrhagic spinal meningitis.
Acute Congenital Hydrocephalus. In Seitz’s opinion a serous ventricular meningitis may offer unsurmountable difficulties in the differential diagnosis from ventricular hemorrhage, though, in the case of a congenital hydrocephalus, the protrusion of the fontanels and distention of sutures is likely to be excessive. In such a case a spinal puncture may well settle the diagnosis.
Prognosis of Life. The immediate effect of a traumatic intracranial birth lesion is dependent upon the extent and the location of the resulting hemorrhage. Traumatic lesions not associated with hemorrhage, e.g., many of the tentorial lacerations, apparently leave the infant unharmed. The fact also is well established that small hemorrhages, like a cephalhematoma internum or especially the small subarachnoidal hematomas, as a rule, fail to cause any noticeable symptoms.
It is, on the other hand, known that a newborn may reveal signs strongly suggesting intracranial traumatization which, however, are so indefinite or disappear so quickly that it is impossible to determine whether they are due to small hemorrhages or, as suggested by Seitz, to a mere “concussion of the brain” or a fleeting edema. As a matter of fact they do not clearly indicate any immediate harm done to the infant. Whether such slight, and at first practically symptomless, intracranial lesions may be responsible for deficiencies in physical or mental development later in life, is a question discussed later in this chapter.
Whenever the effusion of blood is excessive and the clot interferes with the function of certain vital centers, especially those in the medulla oblongata, death ensues either immediately, during, or within a few days after birth. The pathology and etiology of these hemorrhages have been described sufficiently to make it obvious that in many of the cases the child may appear perfectly normal at birth and only a few days later begin to exhibit the signs of a hemorrhage which gradually or suddenly leads to a fatal issue. It is this group of cases in particular in which early diagnosis and prompt therapeutic interference will greatly enhance the prognosis both in regard to life and restitution of perfect health.
Smaller intracephalic hematomas are known to have indirectly caused a baby’s death through their infection or by favoring a pneumonia as a result of impeded respiratory function.
The prognosis always is decidedly unfavorable in cases in which intracranial hypertension has led to convulsions, especially if these follow each other in short intervals. The change from the convulsive to the paralytic state practically indicates the approaching end.
Of greater practical importance and interest in the problem of prognosis are the possible delayed consequences of a traumatization of the brain in parturition.
Prognosis of Health. Up to a comparatively recent date obstetricians have shown but little interest or belief in the claim of neurologists that traumatization and asphyxiation of the infant at birth are responsible for certain physical and mental anomalies which manifest themselves only in the later life of the child. These views of the neurologists of late, however, have prompted obstetricians to advocate operative termination of labors for the purpose of avoiding such untoward sequelae. There cannot be any doubt that in the light of more recent information concerning the causation of intracranial parturitional lesions the teachings both of the neurologist and the obstetrician call for thorough revision.
In 1843, Little, in his first paper dealing with cerebral spastic paralysis of children, asserted that the condition is due to a lack of development of cerebral tissues and also to meningitis. Only incidentally he mentioned in this connection that this abnormal condition seems to follow difficult and prolonged labor terminated with or without the use of instruments, and, in his opinion, under these circumstances probably was due to an intracranial hemorrhage. In a second paper, published in 1862, he expressed it as his belief that cerebral spastic paralysis of children in three-fourths of all instances was caused by an intracephalic birth hemorrhage.
Authors quoting Little are in the habit of adding that Sarah McNutt (1885) and Kundrat (1890) by certain findings at autopsies have definitely established this relation of palsies of central origin to such intracranial birth hemorrhages.
Congenital spastic paralysis in children quite frequently is found associated with mental defects. It is unnecessary for our purpose to show here by further quotations from literature how this fact gradually led writers to the deduction, now widely accepted, that asphyxiation, forceps extractions, or protracted labor play a most important role in the etiology of imbecility, idiocy and other mental deficiencies, of epilepsy, hydrocephalus, strabismus, deafness, speech defects, cortical aphasia (Ziehen) and so on.
What are the chief arguments commonly given in support of such an assumption ?
The still prevailing custom of writers to mention McNutt and Kundrat in connection with this particular aspect of the sequelae of parturitional injuries is not justified. That intracranial hemorrhages of the newborn may cause spastic conditions and convulsions and finally death, which represents the problem investigated by them, is an acknowledged fact. We are here, however, concerned only with those children who have survived the assumed brain injury. Anatomic findings to be acceptable as proofs for the contention that birth trauma bears a close etiologic relation to various deficiencies of the older child, therefore, necessarily would have to comply with the following essential requirements:
If discovered at the post-mortem examination of an older child, their character or location must leave no doubt that they are due to a trauma sustained at birth.
Of the known types of traumatic lesions of the newborn’s brain and meninges only those can be taken into consideration which do not cause death, i.e., those which in routine necropsies of all newborn babies represent solely accidental findings, not directly responsible for the infant’s death.
Pachymeningitis hemorrhagica has been ascribed especially by older writers (Doehle, Weyhe), to a birth trauma and has been looked upon as the anatomic lesion which accounts for nervous and mental defects in some cases.
Kowitz recently has published the results of his exhaustive studies concerning the relation of intracranial hemorrhages to pachymeningitis chronica interna. From the findings in 6000 autopsies, performed on children up to the age of two years, he concluded that subdural birth hemorrhages in a considerable number of cases give rise to a hemorrhagic pachymeningitis which is found in 3.9 per cent of all children dying between the age of eight days to two years. It seemed to him that all children thus affected gradually succumb in early childhood partly as the direct result of meningitis, partly from intercurrent diseases to which they apparently are rendered less resistant by the meningitis. He became convinced that a hemorrhagic pachymeningitis which manifests itself only later in life has no causal connection to this traumatic type seen in the newborn.
Finkelstein, Reuss, and various others of modern pediatricians apparently are of the opinion that the hemorrhagic type of meningitis is seen practically only in hereditosyphilitic infants. Anatomic findings have been recorded which are supposed to prove a direct connection between birth trauma and internal hydrocephalus. Two cases of Fischer may be briefly cited as illustrations :
(1) A child delivered by means of an abdominal cesarean section showed unmistakable signs of a brain injury within twenty-four hours. Gradually a hydrocephalus developed. Death at age of four months. At post-mortem evidence of an old hemorrhage was discovered in the middle and posterior fossa. Fischer thinks that pressure exerted by the hematoma interfered with the escape of the liquor and also caused a venous stasis which led to the development of the hydrocephalus.
(2) A child born under twilight sleep appeared perfectly normal at birth. Hydrocephalus became noticeable about three weeks later, followed in another week by exitus. A very large hematoma was found. Its size excluded any possibility that it could have existed at birth without causing any symptoms. The hemorrhage must have started later and progressed slowly. Also in this case Fischer felt quite certain that the hydrocephalus developed secondarily to the hemorrhage.
The ischemic foci described by Kruska may be regarded as suggestive, but not by any means conclusive, anatomic findings in support of the assumption that certain birth lesions stand in an etiologic relation to later physical and mental deficiency at least in some cases.
Plausible and entirely acceptable seems the assumption of Kahlden, Richter, Monakow and others, that porencephaly may be the sequela of a parturitional cerebral hematoma. The ischemic areas with subsequent necrosis, described by Kruska, may then be looked upon as the more definite anatomic findings in support of such a theory.
From a careful perusal of literature the definite deduction can be drawn that convincing anatomic evidence for an important or frequent causative connection of intracranial birth lesions to mental deficiency still is wanting.
History of difficult labor. The term “difficult labor,” especially in the writings of neurologists, is rather loosely applied to labors terminated artificially, to abnormal labors, especially if the child was born asphyxiated, and again to merely long labors. It is necessary to emphasize that the diagnosis “difficult labor” practically without exception in this particular literature is based solely on the assertion of the mother that her labor was difficult. This holds true for all the statistical investigations made in asylums for the insane or feebleminded which form the main basis for the view now rather prevalent that difficult labors are of considerable importance in the causation of mental deficiency. These statistics seem to prove also that a long labor is more prone to interfere with mental development later in life than a forceps extraction. It does not seem to have occurred either to these investigators, or the obstetricians who willingly accepted the deductions drawn from these statistical figures, that an investigation carried out in this manner implies at least two great errors which practically nullify its scientific value :
(1) It is claimed on theoretical grounds that the fetal brain suffers from the prolonged compression during a protracted second stage of labor. The mere claim of a mother that her labor was long may convince a neurologist, but should not prove to an obstetrician that the fetal head was exposed to undue compression. As a matter of fact, in primigravidae labor most often is abnormally prolonged only by a slow first stage.
(2) A study of this problem limited to children found in asylums obviously excludes all stillborn infants and those who died early in life. It is evident that this prevents the inclusion into calculation of a considerable number of children extracted by means of forceps. It seems fair to assume that these two great deficiencies of these statistical investigations account for the fact that they seemingly prove “difficult” labor more harmful than forceps for the later physical and mental development of the child.
The often-quoted paper of Arthur Stein and its discussion before the New York Academy of Medicine express well the present situation.
The obstetrician rather naively has accepted the verdict of the neurologist, based on superficial and truly unscientific statistical investigations, that a long-continued compression of the head must be avoided by prompt application of the forceps. The existing situation is well illustrated when we find in DeLee’s splendid book the following quotations : Beach found in 810 idiots a history of hard forceps in 4 per cent, and in 26.6 per cent of spontaneous but difficult labor. Porter states that 17 per cent of the epileptics in the Indiana School for the Feebleminded had a history of difficult labor.
A more promising route of approach for the possible solution of this important question from the standpoint of the obstetrician, will be discussed later in this chapter, but in this connection emphasis will be laid only on the fact that there is no acceptable proof extant for the assertion that forceps extractions are less dangerous to the infant than a long labor. Present information concerning the mechanical factors involved in the causation of intracranial birth lesions leaves no doubt that traumatic injuries are most prone to occur when the compression of the head is extreme, asymmetric, and most of all, if it is accomplished quickly. Any of these conditions is more likely to prevail if the passage of the head is hastened by means of oxytocics, manipulations or instruments.
Obstetricians who advocate a more liberal use of the forceps in the interest of the child also neglect to take into account the very important fact that the neurologic investigations, by which they are so greatly influenced, were made at a time when difficult and instrumental labors still rather generally were considered the most indispensable causative elements in all intracranial injuries at birth. It seems inconsistent to advocate hastening of the expulsion of the child in face of the established fact that in from 20 to 25 per cent of cases in which an intracephalic traumatic birth lesion of some kind is discovered at autopsy the exact obstetric history shows a spontaneous, often quick, but otherwise normal labor.
Primiparity. References to a striking frequency of firstborn among the inmates of institutions for the insane, epileptics, or feebleminded are commonly cited in literature, and incidentally it may be mentioned that some of these date back to the middle of the past century.
The high figure for primogenity among the inmates of these institutions was, and still is, considered a valid proof for the etiologic significance of a first, which means, of a difficult, labor for nervous and mental deficiency. If we once more recall the fact that complications of labor have lost much of their former dignity in our conception of the origin of intracranial lesions, primiparity obviously is deprived proportionately of its value as argument in this discussion. It, furthermore, is incorrect to draw any conclusions from the number of firstborn among defective children without including into the calculation of such a percentage figure also the percentage of firstborn among children ;of this particular age. So far as one can see this has not been done by any of the investigators though it seems essential for any statistical calculation worth serious consideration.
Clinical Observations. It would be futile to quote here various writers, chiefly neurologists, who simply express it as their personal belief that parturitional traumatization in many instances is the sole cause of retarded physical or mental development. Without any difficulty, as many authors could be cited who hold opposite views.
At times such opinions are based, at least partly, on certain clinical observations. M. Allen Starr states that post-mortem examinations of idiots reveal signs of an old hemorrhage in 20 per cent of the cases, and concludes that obstetricians are not to any noteworthy extent responsible for idiocies and palsies. In a study of epilepsy later in life in relation to convulsions of infancy Morse finds that epilepsy is far more likely to develop when the cause of the infantile spasms seemed to have been a brain injury than when they more probably were due to disturbances in the gastrointestinal tract. If the small infant has but one or even repeated convulsions, it is practically impossible to determine whether they are epileptic or not. Most authors agree that early epilepsy probable is extremely rare. Emmet Holt and also Koplik emphasize the fact that the overwhelming majority of children who have convulsions during infancy fail to develop epilepsy.
The connection of a certain anomaly of development with the normal or abnormal trauma of birth can be definitely established only in two ways : (1) by directly linking up the later defect with a definite intracranial lesion observed or accurately recorded at birth and (2) by following up the life histories of a large number of children whose birth histories are known in every detail. This latter method undeniably is the more reliable one and actually has been followed by several obstetricians on a large material. Investigations so far made along these two lines have furnished much valuable information.
Volland studied the histories of entire families and thus seemed to have been able to demonstrate a probable injurious influence of a birth trauma in some instances. In the same families normally born children remained well, whereas some of those born after abnormal labors became epileptic.
A possible relation of birth traumatism to the development of hydrocephalus is at least suggested by a recent observation of Oden. A mother of four children has a narrow pelvis. Both parents are free of all stigmata of disease. First child, born prematurely, is healthy ; the second, born at full term by instrumental delivery, developed a hydrocephalus ; third, born at full term after difficult labor, died with marked cephalic enlargement ; fourth, delivered at full-term with cesarean section, is well at age of four months.
Koenig acknowledges that in 25.7 per cent of the cerebral palsy cases seen by him, difficult labors or asphyxia at birth are recorded in the history, but that in all cases, with the exception of only 2, many other predisposing factors, such as syphilis, bad heredity, alcoholism of parent, etc., were discovered. Of these two exceptions one was a hydrocephalic, the other a microcephalic child.
Vogt in an analysis of the probably causative factors of epilepsy found that in the large majority of cases the history reveals a decidedly more plausible explanation than asphyxiation at birth. Out of a total of 471 cases of congenital or early cerebral defects only in 7 an injurious parturitional factor, by exclusion of all other so far known causes, remained as the only possible etiological factor to which the deficiency could be charged.
Zappert (in Pfaundler-Schlossmann’s Handbuch der Kinderheilkunde) states that but four conditions can be justifiably brought into any relation to intermeningeal hemorrhages :
- General rigidity with only slight or without dementia, usually also without convulsions (Little’s symptom-complex).
- Paraplegic rigidity without dementia and without convulsions.
- Simple hemiplegia with feeblemindedness and with convulsions.
- Bilateral hemiplegia with feeblemindedness and with convulsions developing into a pseudobulbar paralysis.
Group one and two presume bilateral lesions. One could think in connection with them of the more diffuse subarachnoidal hemorrhages which in the newborn may not cause any pronounced symptoms and still may later interfere with the normal development of the cortical motor and psychic centers. In the etiology of these two conditions also small hemorrhages within the cortex itself or severe contusions may be of importance.
In the etiology of groups three and four intermeningeal subdural hemorrhages undeniably play a definite role.
It must, however, be pointed out in this connection that tissue defects in the brain of the newborn may occur independent from any parturitional trauma. Thus Osier found a cavity in the brain of a fetus removed from the uterus of a mother who died fromtyphoid in the sixth month of pregnancy.
There are several cases on record in which an injury of the fetal brain apparently was solely due to a severe traumatism of the pregnant uterus. Cotard, e.g., recorded the following case : A pregnant woman sustained a severe blow against her abdomen. The child born three months later held all four extremities in forced flexion. Post-mortem examination revealed a necrotic defect in the brain. Reuss mentions similar observations of Seitz and Zappert.
Summarizing all this information we can say that in some, though rare, instances a physical or mental deficiency manifesting itself only later in life can be directly ascribed to a definite cerebral lesion noticed at birth. But even this fact does not offer us any clue concerning the assumed relation of slight and symptomless intracranial birth lesions to later defects. That such slight lesions do occur probably in many cases cannot be denied.
Do they exhibit delayed sequelae ?
It became apparent to Hannes among the first that an answer to this question could be supplied by the obstetrician who, in possession of a detailed record of all phases of the birth and of the immediate condition of the newborn, will study the physical and mental condition of a large series of these children in afterlife.
In consideration of the more general claim that asphyxiation and instrumental delivery are the prominent factors in the interference with normal development of the child, Hannes selected from his birth records two groups of 150 cases each, the one representing infants asphyxiated at birth, including a considerable number of deeply asphyxiated, resuscitated by swinging after the
Schultze method, the other group comprising children born by means of forceps, after versions, extractions, in breech presentation, etc. Both for the purpose of control, and also in view of the established fact that intracranial injuries occur also in the course of normal labors, Hannes added a third group of 150 perfectly normal, spontaneous labors. This study, most carefully carried out, revealed that each group showed almost the identical number of apparently abnormal, backward and actually defective children. In the total number there were only 2 manifestly idiotic children, i in the group of abnormal labors, i in the normal labors, and none among the asphyxiated. He discovered one child suffering from a spastic palsy, in the opinion of an expert neurologist, due to porencephaly, which might have been the result of a birth traumatism. This child was born after version and extraction.
Following the example of Hannes identical investigations were made by Kwozek, who concluded that his most careful examinations of the physical and mental condition of children born asphyxiated, or born either in instrumental labors, or spontaneously after difficult labors have failed to reveal any difference from the children born after perfectly normal labors. In the very few instances of manifest deficiency, in every case without any exception, other conditions, generally recognized as etiological factors for deficiency, were easily revealed. The same deductions were drawn by Rechtschaft from investigations made along the same lines. Hannes quite recently collected and analyzed all the material so far studied in the manner first suggested by him and presents the following instructive data : Group A, asphyxiated at birth, 157 children examined, 9 of them abnormal (57 per cent), in 3 distinct other hereditary factors, which leaves 6 (3.8 per cent) in whom asphyxiation might have to account for the later deficiency. Group B, artificially delivered but not asphyxiated, 242 children examined, 6 of them abnormal (including 1 case of brachial palsy but mentally normal) ; in 3 distinct hereditary factors, which leaves 3 (1.2 per cent) in whom the abnormal delivery may account for mental and physical defect.
Group C, normal labor, fresh at birth, 206 children examined, 10 of them (4.9 per cent) abnormal ; in 3 distinct hereditary factors, which leaves 7 (3.4 per cent) in whom the birth trauma of a perfectly normal labor in the absence of any symptoms might have to account for the deficiency. If Groups A and B are put together, which corresponds more closely to the classification of neurologists of “difficult labor,” we have 399 re-examined children with 3.7 percent deficiency, or with exclusion of those exhibiting recognized hereditary factors, 2.2 per cent in whom a birth trauma could be held responsible. In these combined groups were found 3 epileptics, 1 with marked heredity, that is, only 2 possibly injured during birth.
Hannes feels that all newer investigations only confirm the position he held ten years ago, that asphyxiation, abnormal labor or instrumental delivery do not differ from normal labor as a possible cause for abnormal mental development.
Researches have been made by obstetricians concerning the later effects, particularly of forceps extractions. Gans presents the following figures : out of a total of 180 forceps children, either examined by himself later in life or concerning whom reliable information had been obtained indirectly, there were discovered 2 backward children, and 9 with at least a history of convulsions of some sort.
In the 1 backward child (five years old) the forceps extraction was found recorded as very easy, not followed by any symptoms suggesting an intracranial injury. In the other backward child (nine years old) the forceps extraction was not difficult. Of the 9 children with convulsions, 5 had died in convulsions of not determined character. Of the 4 surviving children (ages between four and nine years) only i was a typical epileptic. All 9 were delivered by means of easy outlet forceps without any noticeable immediate injuries.
This last fact deserves strong emphasis in view of the common recommendation of the low forceps in the very interest of the child.
Out of a total of 448 forceps deliveries made between 1900 and 1914, Engelken was able in 1920 to obtain accurate information directly or indirectly concerning 232 children. Among them were 2 suffering from epilepsy, 2 from chorea, 1 idiot, 2 imbeciles, 4 feebleminded and 2 who died in convulsions of some kind. In this entire group other factors than a presumable parturitional injury were manifestly responsible for the mental anomalies, with the possible exception of i of the epileptics and i of the imbeciles.
A paper of Wulfif, published in 1892, still is often quoted by modern writers. He claimed that of children born asphyxiated, or after difficult labors only one-sixth begin to walk and only one-ninth begin to talk at the proper time. In order to test this striking claim,
Hannes in his investigations made specific inquiries in regard to these two points. He found that of such children 52.6 per cent walked at one year, that 42.6 per cent began to talk in the first year and 50 per cent in the second year. Thus no noteworthy deviation from normal conditions could be ascertained.
Analyzing critically this somewhat contradictory information furnished on the one hand chiefly by neurologists, on the other, by obstetricians, concerning an etiologic relation of birth trauma to physical, nervous, and mental defects of later childhood, the following facts become apparent :
(1) The deductions of neurologists rather uniformly are based on investigations which from the viewpoint of reliability and scientific value are decidedly objectionable.
(2) Neurologists have practically limited their researches to attempts of linking up the evident deficiency with some abnormality of labor.
(3) Obstetricians, in contradistinction, endeavored to reveal later sequelae of the trauma both of normal and of abnormal labor and delivery.
(4) Investigations more recently carried out by obstetricians tend to weaken to a considerable degree the older opinion of neurologists that asphyxiation and difficulties of labor subject the newborn to a great risk of later deficiency, so that they must be regarded etiological factors of great importance in the various forms of physical and mental defects, becoming apparent only later in life.
Klotz justly emphasizes that in the individual case a history both of difficult labor and of bad heredity does not a priori permit the deduction that heredity alone explains the deficiency. We can see the same appreciation of the difficulty of a decision, but from the opposite point of view, when Goddard in his exhaustive study of the causes of feeblemindedness, makes the following statement : “Since many normal children had been delivered by the use of instruments, with more or less temporary deformity of the head but without any effect on mentality, it is unreasonable to conclude in those cases where there is both hereditary feeblemindedness and a history of instrumental delivery, that the latter is the cause of the mental deficiency.”
Some clinical evidence has been cited in the foregoing pages which might be adduced in confirmation of still another opinion, expressed by Wulff almost thirty years ago, that cranial trauma might prove specifically risky for the child with a faulty heredity.
If writers, as, e.g., Tucker, believe that epilepsy in every case is due to definite cerebral cell lesions and that an idiopathic type of epilepsy does not exist, they necessarily are forced to the conclusion that very many cases of epilepsy must be due to birth traumatisms.
It is not quite clear how these writers can harmonize their views with the prevalent opinion of the importance of faulty heredity in the etiology of epilepsy, except by accepting Wulff’s hypothesis as an established fact.
The problem of prognosis concerning delayed sequelae has become more complex with the knowledge that undeniably also the physiological trauma of normal labor occasionally must account for them.
The following facts now seem irrefutably established :
(1) Intracranial traumatic lesions, light and severe, develop in the course both of normal and abnormal labors.
(2) Evidences of such injuries can be discovered at autopsy in approximately one-half of all infants, stillborn or dying within the first few days of life. But only in one half of these cases the injury caused the death. In the other half such traumatic lesions, chiefly tentorial lacerations without or with only slight hemorrhage (Vischer), represent but incidental findings.
(3) Post-mortem examinations of very young infants up to the age of two years reveal frequently the residuae of older hemorrhages which at least in part must have occurred at the time of birth. In some of these cases definite symptoms at birth had suggested or clearly indicated an intracranial traumatism, in many others even most careful observation had failed to reveal any sign of an anomaly.
(4) Changes in the eyeground of the newborn, presumably the expression of an intracranial parturitional trauma, can be discovered in a considerable number of cases (according to Paul, in 20 per cent of normal labors, and 50 per cent of contracted pelves).
(5) Reliable observations, in some instances extending far into adult life, have established the fact that a perfectly normal physical and mental development is certainly not precluded by marked cranial and intracranial injuries evidenced by such unmistakable symptoms of the newborn as convulsions (Seitz).
The present situation concerning the problem of possible delayed effects of parturitional brain injuries may be briefly stated as follows : meninges and brain are injured very frequently in the course both of abnormal and also of seemingly normal labors. Presumably in the large majority of instances in which the trauma leads to a free hemorrhage, death ensues within a short time. In those instances in, which the immediate symptoms of the intracranial lesion subside, later consequences might be expected though undoubtedly often they do not appear. Obviously no later consequences can be looked for if immediate symptoms either do not become manifest or are not recognized. Certain post-mortem findings prove that the lesions may be so slight that they can hardly cause noticeable symptoms.
Whether such slight lesions can be responsible for delayed manifestations, especially in form of mental defects, remains an unsettled problem though theoretically the possibility cannot be denied.
However, without fear of contradiction I make the assertion that in a large number of cases to-day definite symptoms of intracranial parturitional injuries are overlooked.
The obstetrician of to-day still fails to appreciate his responsibility in this matter. Obstetric routine will have to include a careful examination of the newborn and observation of his behavior during the first few days of life.
Such a routine, which some day may possibly include an ophthalmoscopic examination, a study of the coagulation time of the blood, and possibly a spinal puncture in all cases of suspected hemorrhage, will tend to reduce greatly the number of that still too large group of unrecognized cranial lesions. Such a routine may help clear up the question of the etiologic relation of birth trauma to later physical and mental defects, and incidentally may lessen the occurrence of such defects by affording an opportunity for prompt and effective therapeutic intervention.
In the preceding discussion of the etiology of intracephalic birth lesions, it has been shown that in the main they are the direct result of sudden or excessive compression of the head. It has furthermore been proved that in the presence of certain predisposing factors, especially of prematurity, the trauma of spontaneous normal labor may be sufficient to injure intracranial structures, and finally, that asphyxiation, brusque manipulation during resuscitation, and a hemorrhagic diathesis, as contributory causes, tend to exaggerate the effect even of minor lesions.
From this point of view it is entirely feasible to discuss an obstetrical prophylaxis of intracranial birth traumatization.
The newer knowledge, that severe traumatic lesions frequently occur also in spontaneous labors, has lessened but not eliminated that responsibility with which the obstetrician used to be charged for such injuries. Certain obstetric manipulations and procedures undeniably prove disastrous to the infant. Disregard of certain details in the proper execution of obstetrical operations renders these procedures needlessly dangerous.
Forceps. The immediate infantile mortality in 285 cases of high forceps has been calculated by Baisch as between 43 and 50 per cent. Almost without exception autopsy on these children reveals a serious cranial traumatism. The danger of the high forceps is notorious and every obstetrician of experience tries to evade this operation.
Great risk to the child is not limited to high forceps. Gans investigated the immediate and delayed effects on the infant. Of a total of 562 forceps extractions performed in Winter’s clinic, and this means a large series of operations performed only by more or less expert obstetricians, he found (excepting the macerated feti) an immediate mortality of 10.32 per cent, which is a rather low figure when compared with the statistical reports of other large maternity services which give a percentage of immediate mortality varying between 7 and 27.7 per cent.
Still more impressive are certain figures taken from a study made by E. Sachs. He took a special group of forceps extractions made soley in the interest of the child. In these 90 cases the infant was delivered in a normal and apparently unimpaired condition only 56 times. The child was asphyxiated slightly in 21, very deeply in 11, and stillborn in 2 cases. One of the deeply asphyxiated babies died immediately. Of the 3 that died, at autopsy i showed a parietal fracture, the two others tentorial lacerations.
A list of traumatic lesions seen in connection with forceps extractions will include, outside of minor external injuries, the following serious accidents : intracranial hemorrhages, injuries of skull bones varying from indentations to deep gutter fractures, fractures of the occipital squama, lacerations of sutures, tentorial tears, facial paralysis, Erb’s palsy, injuries to ears and eyes, fractures of the jaw, laceration of the sternomastoid muscle, accidental compression of the umbilical cord, and injuries of the vertebral column and spinal cord.
It will be well to remember that these represent injuries observed in obstetrical clinics where surely the majority of operations are in expert hands, and performed in general only under well-defined indications. A reduction in the number of these injuries, which in part are unavoidable, in the general practice of obstetrics, can be achieved only by limitation of the number of forceps applications.
Forceps must be applied only under definite indications. When the operation seems desirable in the interest of the mother, the possible mutilation of the infant should be taken into account more seriously than is the prevailing custom. This applies particularly to the obvious readinesss of many practitioners to apply the forceps on account of assumed exhaustion of the patient, which more critical analysis in many cases would reveal to be rather impatience of the parturient or weariness of the attendant. With the fetal head on the pelvic floor, the popular low forceps, often to the great disadvantage of the child, could be replaced by a small dose of pituitrin, an episiotomy, if necessary, being added to eliminate abnormal resistance on the part of the pelvic floor.
In considering a forceps extraction in the interest of the child, one must keep in mind the fact that prolonged compression of the head no doubt, is less harmful to the infant than a difficult extraction.
It is in this type of case that the liberal incision advocated by DeLee for his prophylactic forceps may prove particularly advantageous to the child. Authorities do not agree as to the exact significance of changes in the fetal pulse rate in the recognition of approaching danger. The observations of Baumm have already been mentioned. He concluded that a bradycardia by itself is of no prognostic value. A tachycardia following a marked retardation of the fetal pulse, in his opinion, indicates that a brain hemorrhage already has occurred. Even quick delivery cannot any longer save the child.
Only if in an afebrile woman a fetal tachycardia is not preceded by a bradycardia does he advocate prompt application of the forceps for the purpose of saving the infant. Benthin, on the other hand, summarizes his experience in the statement that an absolute indication for immediate delivery exists if either the fetal heartbeat remains below 100 at least during two consecutive uterine contractions, or the pulse rises above 180 with simultaneous passage of meconium, especially if the pulse rate fluctuates.
Careful observation of the fetal heart during labor in some cases will enable the attendant to recognize the imminent danger, but no hard and fast rules can be made concerning any typical changes in the pulse rate which would necessitate hurried delivery in the interest of the infant.
The decision of forceps application in the interest of the child, in the individual case, still is a matter of personal discrimination on the part of the operator. The one thoroughly familiar with the problem of birth injuries in the case in which the head is still higher up in the pelvis, will not fail to realize that any possible advantage to the child from a quick delivery is likely to be nullified by the greater risk of intracranial injury, and in such a situation will risk a forceps extraction only if the peril to the child is obvious and not merely suspected. Even in a low forceps he will eliminate any possible danger of sudden and severe compression of the head by an unprepared or abnormally rigid vulvar ring by making an episiotomy.
Serious traumatization of the head is proportionately reduced by greater skill of the attendant, not only by mere mechanical skill, but by his ability to recognize slighter degrees of disproportion between head and pelvis, minor and rarer anomalies of the pelvis, and all deviations from normal in the mechanism of the passage of the head through the pelvic canal. Both this diagnostic ability and the technical skill required for the correct performance of the operation, in the main, are the combined product of experience and judgment.
There cannot be any doubt that as a whole the practitioner underrates the difficulty of determining the necessity for a forceps extraction and of performing it properly with the least possible risk to the child.
In many instances serious or fatal injury can be ascribed to the following defects in the technic : the exact state of rotation of the head is not recognized and the forceps applied in the transverse diameter of the pelvis, but not, as it should be as closely as possible corresponding to the transverse diameter of the fetal head. During the progress of extraction the direction of traction is not changed so as to correspond exactly to the sequence of flexion, rotation, and extension required by the normal mechanism as the head passes from one pelvic plane into the next. A failure to adhere to these requirements always implies excessive and dangerous compression of the head in one or another direction.
The forceps should never be employed in an effort to overcome difficulties arising from a marked disproportion between head and pelvis. The traction should be made slowly and with interruptions sufficient to permit the head to mold gradually. If the head is larger than normal, or the forceps’ blades, on the incompletely or abnormally rotated head, cannot be applied along the shorter transverse diameters, the forceps’ handles necessarily will not lie in close apposition. They must be steadied in their relative position to avoid their compression during extraction.
Management of the Aftercoming Head. Statistics from large maternity services show an immediate infant mortality varying between 1.5 and 4 per cent for breech labors. It is conservatively estimated that the mortality under less skilled management in general practice probably averages 15 per cent. The clinical diagnosis of the cause of death still commonly is given as asphyxiation, presumably the result of the compression of the umbilical cord between the pelvic wall and the aftercoming head. Post-mortem studies, however, leave no doubt that in the majority of cases death is actually caused by spinal and intracephalic injuries, chiefly tentorial lacerations. If we take into consideration that outside of such fatal traumatisms also many slighter lesions, such as fractures of the upper extremities, or of the clavicle, damage to the sternomastoid muscle or brachial plexus are fairly common sequelae of labors in breech presentation, it becomes obvious that correction of the malpresentation by external version, before labor has started, represents a measure of distinct value in the prevention of birth injuries. Next in importance from the standpoint of prophylaxis is strict adherence to definite principles during the extraction of the aftercoming head.
It must be kept in perfect flexion, and at the proper moment the occiput must be rotated forward to avoid excessive compression by forcibly pulling too long a head diameter through comparatively too small a pelvic diameter. It has been shown in foregoing pages how, in the delivery of the aftercoming head, a tentorial tear may result if the cerebellum is brusquely pushed upwards against the tentorium.
This might be done if the occipital squama were forced against the pubic arch either by undue efforts to protect the perineum or by a very quick extraction of the head. It seems reasonable to assume that slow and deliberate extraction of the head through a vagina and vulvar ring, either dilated after the method of Potter or, if necessary, properly widened by means of an episiotomy, will greatly lessen the danger of intracephalic traumatization without unduly increasing the risk of asphyxiation. In some instances the application of the forceps to the aftercoming head may prove useful.
Premature Labor. There probably is no exaggeration in Vaglio’s statement that the notoriously high immediate mortality of premature infants may be due rather to the trauma of birth than, as is customarily assumed, to the immaturity of the newborn. Routine autopsies on all newborn infants bear evidence for the frequency of severe injuries after normal and quick labors in premature babies and even very small feti. The induction of premature labor, as a method of dealing with minor contractions of the pelvis, now is rather generally discouraged on account of the great loss of children in this procedure.
The evident vulnerability of the immature child renders it necessary also in spontaneous labors to avoid so far as possible any severe or abrupt compression of the skull. Even a small dose of pituitrin, if sufficient quickly to force the head through an incompletely dilated cervix or rigid vulvar opening, probably proves disastrous to many an infant.
Protection of the Perineum. The attempt to push the head through the vulvar ring between uterine contractions by means of strong pressure against the child’s forehead either over the distended perineum or with a finger introduced into the mother’s rectum, may cause an intracranial injury, most likely a tentorial tear. In this maneuver the occiput is too forcibly pressed against the subpubic arch. Injuries probably also prove an asymmetric pressure against the forehead, exerted more strongly over the one than over the other frontal or parietal bone. It is prone to strain the falx in an oblique direction. Passage of the head over an unyielding perineum is best retarded by symmetric pressure with the palm against the entire exposed surface of the occiput. One familiar with the etiology of cranial birth injuries will most readily resort to an episiotomy.
Resuscitation. All brusque manipulations must be shunned during the resuscitation of the asphyxiated newborn. In textbooks of obstetrics Schultze’s swingings should not be given the prominent place among the methods of artificial respiration still accorded to them. The method should never be described or recommended without proper warning against its various dangers, which can be avoided only by the experienced. If the asphyxiation of the newborn is not due to an intracephalic lesion, such simpler procedures as clearing of the pharynx of mucus, skin stimulation, including the hot and cold bath, tongue traction, or possibly careful compression of the thorax, etc., will prove sufficient to establish suspended respiration.
In every case of seemingly deep asphyxia the possibility of a cranial trauma as the cause of the asphyxiation must be kept in mind. All vigorous manipulations in such cases and all procedures in which the baby is held by its feet, head down, are prone to aggravate the condition.
Twilight Sleep. Even the most enthusiastic advocates of twilight sleep seem willing to concede the following facts : Twilight sleep lengthens labor, necessitates the application of forceps in many cases in spite of the administration of pituitrin and causes some degree of asphyxiation in a considerable number of newborn infants. Thus the procedure includes four distinct factors whose etiologic importance in the causation of intracranial injuries is generally recognized.
As a matter of fact, conclusive evidence for a direct relation of twilight sleep to physical or mental deficiency later in life is still wanting, but various writers express the opinion that such a relation will someday be established. In the reports of individual observations of later defects presumably the result of nonfatal lesions sustained at birth, one often meets with the assertion of the writers that twilight sleep was responsible for the injury.
Injection of Blood or Serum. Much clinical evidence has been adduced in preceding pages to prove that a hemorrhagic tendency necessarily represents a most serious complication of any, even the slightest, traumatic injury within the skull of the newborn. It must be conceded that Rodda’s simple method of ascertaining the clotting time, and Duke’s method of establishing the bleeding time are not scientifically accurate, and indeed may be misleading in some cases. On the other hand, it can be asserted that especially the subcutaneous injection of whole blood is void of any danger to the child. It, therefore, seems entirely logical that all authors who have investigated the relation of hemorrhagic diathesis to birth hemorrhages, without any exceptions, insist on the early and repeated injection of human whole blood, or of animal serum, thromboplastin, etc., whenever an anomaly of coagulability is reasonably suspected.
Most of these investigators strongly advocate, without any preliminary test, subcutaneous injection of from 10 to 30 cubic centimeters of the father’s blood, if necessary repeated in intervals of from four to eight hours, in every instance in which, immediately after birth or later, certain symptoms indicate an intracranial hemorrhage. This therapy is not only likely to check a further extravasation of blood but is also a very rational and useful prophylactic procedure in case further developments should make surgical interference inevitable. Seemingly excellent results are recorded in literature with blood injections. Foote obtained 6 permanent cures in 7 cases treated in this manner after the hemorrhage had been definitely established by spinal puncture.
The value of the prophylactic injection of blood before operation is well illustrated in 2 observations cited by Rodda :
Case IV. Spontaneous delivery after long labor. Cephalhematoma, petechial hemorrhages on arms, chest, and abdomen. Spasticity of right hand. Twelve hours post partum, 30 cubic centimeters of blood injected. Seven hours later another 20 cubic centimeters. Coagulation time, four minutes, bleeding time eleven minutes. On second day : First convulsions. Spinal fluid bloody. Coagulation time unchanged, bleeding time reduced to four and one-half minutes. Third day : Coagulation and bleeding time unchanged. Another 22 cubic centimeters of blood injected. Fourth day : Operation. By means of an osteoplastic flap a large blood clot is removed. Twenty-five cubic centimeters of blood injected. From then on gradual recovery. At the age of ten months child seems normal in every respect, though its head is rather large.
Case V. Baby born asphyxiated in breech presentation. Coagulation time twelve minutes, bleeding time nineteen minutes. Injection of 43 cubic centimeters of blood. Second day : Coagulation time six minutes, bleeding time six minutes. Injection of 15 cubic centimeters of blood. Third day: First convulsions. Twenty-five cubic centimeters of blood injected twice. Fourth day: Frequent convulsions. Coagulation time six minutes, bleeding time ten minutes. Twenty and twenty-five cubic centimeters of blood injected. Fifth day : Coagulation time eight minutes. After injection of 25 cubic centimeters of blood, operation. Brain bulges through a dura incision, hemorrhage presumably on the other side. Child recovers and at the age of four months seems perfectly well.
Spinal Puncture. Quite unlike the subcutaneous injection of blood, spinal puncture on the newborn is a procedure both comparatively difficult in execution and not entirely free of danger to the child. These two facts seem to be appreciated by all the writers who have extensively tested the method, and nevertheless they show no hesitation in recommending, some of them most extravagantly, spinal puncture as a routine procedure for all cases in which an intracephalic hemorrhage is suspected. A justification for this attitude can be found in the double advantage of spinal puncture both in the early diagnosis and in the treatment of these hemorrhages. The value of the method as a diagnostic aid already has been amply discussed in this chapter.
There is considerable evidence available to prove that the withdrawal of blood by means of the puncture in many instances is followed by an immediate, and not so rarely by a permanent, subsidence of all the symptoms of the intracranial hypertension, especially if the puncture is repeated. Even when no blood is found, the withdrawal of spinal fluid tends to relieve the pressure symptoms. Only favorable results are likely to appear in literature, but observations like those recorded, e.g., by Brady, convincingly prove the curative effect of spinal puncture at least in some of the cases, particularly if the hemorrhage is of the infratentorial type.
Brady saw 9 cases of meningeal hemorrhages in the newborn. Four of them died quickly. Two survived and now are typical examples of Little’s disease. In the 3 remaining cases, spinal puncture was tried, resulting in the recovery of two :
(1) First convulsions twenty-four hours after delivery. Twelve hours later 30 cubic centimeters of pure blood are removed from the spinal canal. All symptoms disappear promptly, the distended fontanel recedes. Rapid and permanent recovery.
(2) Child first seen six days after a difficult forceps delivery. Stupor. Large fontanel bulging, sutures widely separated. Embarrassed respiration. Infant apparently is in a hopeless condition. Lumbar puncture. Approximately 60 cubic centimeters of blood fairly gush from the needle. Fontanel recedes promptly, but gradually begins to bulge again. Next day another lumbar puncture. Blood escapes freely. On third and fourth days puncture repeated, on account of renewed bulging of fontanel. Each puncture followed by satisfactory immediate result. A total of 240 cubic centimeters of blood and spinal fluid had been withdrawn by the several punctures. Infant now begins to improve and shortly afterwards to thrive. At age of fourteen months the child is perfectly normal in every respect.
Many illustrative cases of this sort could be quoted, but I shall limit myself to mention only a most instructive observation of Lippman : Premature infant, weighing 5 ½ pounds. A lumbar puncture yields 25 cubic centimeters of blood. The bulging fontanel flattens immediately. Child recovers and remains well.
A single or repeated lumbar puncture in the hands of many writers (R. M. Green, Devraigne, Braillon, Cathala, etc.) has yielded satisfactory, and often surprising, results so frequently that it seems perfectly logical that other investigators went a step further. A spinal puncture between second and third cervical vertebrae would hold greater promise than a lumbar puncture to relieve the dangerous pressure of a peribulbar hematoma against the medulla oblongata.
Results so far recorded justify this procedure in selected cases. The same holds true for cranial punctures made through a fontanel or suture, which have been mentioned in preceding pages as aids in diagnosis. Such punctures are advocated by Frazier, Doazen, Green and others ; their technic is described in detail in the paper of Henschen.
Symptomatic Treatment. The following protective measures can be usefully applied in all cases of actual or suspected intracephalic trauma : the infant is manipulated as little as possible. He is kept in a warm and quiet room, and protected against all irritation including that of glaring. light. An icebag is placed on his head. Bromides and chloral hydrate are given as indicated by spasticity or convulsions. If the infant is unable to nurse, he is fed through a catheter used as a stomach tube.
Operative Treatment. In a volume like this, designed chiefly for the needs of the obstetricians and of all practitioners attending women in labor, it would be inconsistent to dwell in detail on the various operative methods which have been evolved for the treatment of intracranial birth hemorrhages. Their adequate description will be found in many modern treatises of surgery and in the writings of Brindeau, Carmichael, Gushing, Doazen, Frazier, Gilles, Sharpe, and Vignes, to mention but a few of the most important contributions. The operations recommended by these writers comprise small incisions, small and large trephine openings and large osteoplastic flaps.
It also seems superfluous, if not impossible, to quote here percentage figures of surgical cures. It can be readily admitted that the operative results so far obtained are far from satisfactory. This fault, however, in general should not be charged either against the operator or any specific operation. It is obviously due to the fact that most operations to-day are performed at a time when the condition of the child is practically hopeless. Every critical student of this more recent literature on cranial birth trauma is forced to the conclusion that better results of all operative interference, including spinal puncture, can be hoped for only when the obstetrician will have come to a full realization of his responsibility for a most careful observation of the newborn infant immediately after birth and during the first few days of life.
Such practice will necessarily lead to the early detection of signs of an intracephalic injury. It will also reveal all the symptoms which have preceded the first convulsion or the state of coma, the condition in which the surgeon at present usually finds his little patient when called for consultation. Only early therapeutic interference, surgical and nonsurgical, can be expected to lessen the immediate and delayed untoward effects of an intracranial birth trauma on the child’s life and future health.