In American Journal of Diseases of Children.
An understanding of the causation of intracranial birth hemorrhages, while admittedly important for diagnosis and treatment, is essential for the far more urgent problem of their prevention. Under prevailing conditions, the task of diagnosis and treatment in the main rests with pediatrician and surgeon. The question of prophylaxis, for evident reasons, concerns most of all the obstetrician.
This relative difference of interest in the problem of intracranial birth trauma on the part of the obstetrician, on the one hand, and the pediatrician on the other, finds its expression in the extensive literature of the past decade on this subject. Obstetricians, naturally, have the better opportunity of observing and studying the immediate and especially the mechanical causes of such injuries. They apparently have succeeded in revealing the exact mechanism in the origin of most of the more common types of cranial and intracranial lesions sustained by the child in the course of birth. Pediatricians, who with the rarest exceptions see these patients only later, have made valuable contributions, chiefly in regard to symptomatology. They have discovered the evident etiologic relation of intracephalic birth hemorrhages to a reduced coagulability of the blood, rather frequently ascertainable in the newborn.
But, in my belief, pediatricians and surgeons at present greatly overrate the role played by hemorrhagic diathesis in the etiology of these hemorrhages. There is danger, I fear, that a wider acceptance of this idea might impair the efforts of obstetricians in regard to the prevention of these lesions.
It is the purpose of this paper to present from the standpoint of the obstetrician the question of the causation of all types of intracranial birth injuries, which, it must be remembered, are not necessarily hemorrhages.
On a previous occasion1 I had an opportunity to describe in detail a certain confusion of ideas in literature concerning the actual factors responsible for injuries of intracranial structures during birth. Their frequent association with external traumatic lesions, their anatomic characteristics and their location, at first brought mechanical factors as the direct and immediate cause of their production into the foreground. The normal physiologic reduction of the intracranial space during molding, but especially forced and exaggerated compression in the cases of mechanical dystocia or of operative delivery (forceps and breech extraction), seemed most obviously to represent the mechanical factors responsible for the intracephalic traumatization. Further observations, however, and especially necropsy studies since the introduction of Beneke‘s method of opening the skull, revealed the fact, now generally accepted, that extensive destruction of structures frequently occurs also within the skulls of infants born spontaneously after easy and quick labors, and even in children delivered by cesarean section.
(1) Ehrenfest, Hugo : Birth Injuries of the Child, New York, D. Appleton & Co., 1922.
An explanation of the intracranial trauma on the basis of mechanical influences, at least for such cases, seemed unsatisfactory. Thus, writers began to add as causative factors prematurity, syphilis, asphyxiation, and more recently, hemorrhagic diathesis. It can be admitted that possibly all of these factors in some form may enter into the etiology of the various types of intracranial birth lesions, and especially of birth hemorrhages ; but more careful analysis leads to the inevitable conclusion that, in the individual case, they vary greatly among themselves in significance.
Various attempts have been made to group the cases of intracranial hemorrhage in the new-born in accordance with the supposed predominant etiologic factor. It was thought that such a division would prove of practical value for the purpose of diagnosis and treatment.
Warwick2 proposed the following classification :
- Traumatic cases, the result of the molding of the head in normal precipitate deliveries.
- Congestion of stasis, with rupture of veins, in protracted or complicated labors.
- A diseased condition of the child in intrauterine life, having no relationship to labor as such.
Warwick thought that the first division, theoretically at least, would represent the most common cause of injuries. In the second group, congestion and overdistension of veins lead directly to hemorrhage or indirectly to rapid degeneration and subsequent rupture. In the third group, the hemorrhagic disease of the new-born naturally would deserve first place.
Munro and Eustis3 accepted this division as essentially correct, but felt that asphyxia as a cause for congestion and stasis with rupture of the cerebral veins is sufficiently important to demand special consideration. They, therefore, modified Warwick‘s classification thus :
- Traumatic group : hemorrhage caused by excessive molding of the head and overriding of the sutures.
- Asphyxia group : hemorrhage caused by excessive cerebral venous congestion with rise of intracranial pressure.
- Fetal disease group : hemorrhage having no relation to the labor, but being most commonly caused by hemorrhagic disease and rarely by syphilis or other toxemias.
(2) Warwick, M. : Cerebral Hemorrhage of the New-Born, Am. J. M. Sc. 158:95 (July) 1919.
(3) Munro, Donald, and Eustis, R. S. : Diagnosis and Treatment of Intracranial Hemorrhage in the New-Born, Am. J. Dis. Child. 24:273 (Oct.) 1922.
Since grouping clinical asphyxia, “an easily diagnosed condition,” separately in their etiologic classification, Munro and Eustis have found that the number of cases of intracranial hemorrhage which might be properly classed as traumatic in origin has become relatively quite small. Almost as an apology for still maintaining the traumatic group in their classification, they add : “Nevertheless, as long as fracture of the skull occurs, and as long as there continues to be a tearing of the sinuses and meninges by excessive overlapping of the sutures, so long will it be necessary to classify certain of these cases as strictly traumatic in origin.”
Such a statement, if accepted as correct by pediatricians, will go far in obscuring what already has been revealed by the investigations of obstetricians concerning the traumatization of intracephalic structures incident to the process of birth.
At the outset, I wish to emphasize a striking difference in the points of view of pediatrician and obstetrician. The pediatrician tends to adhere to the erroneous belief that the terms intracranial birth hemorrhage and birth injury are synonyms. This evidently is due to the fact that he sees and, therefore, becomes interested only in injuries associated with hemorrhage, the latter alone causing symptoms evident immediately after birth. The obstetrician, from the standpoint of prophylaxis, is concerned with lesions without hemorrhage as well as with those associated with extravasation of blood.
There are a few facts concerning intracranial birth lesions which may be regarded as established beyond all reasonable doubt. Among them, as bearing more specifically on the problem under discussion, I shall mention the following : In necropsies properly performed on all stillborn infants and on new-born infants dying within the first few days of life, some lesion, clearly traumatic in origin, is discovered within the skull in approximately one half of the cases. Most common among them are tears of the tentorium. In a considerable number of the cases, estimated at from 20 to 25 per cent., the intracephalic injury is not directly responsible for the death but represents merely an incidental finding. In these instances, as a rule, the lesion is accompanied by only a negligible hemorrhage or none at all. Necropsies on somewhat older infants, dying from intercurrent diseases, often reveal the remnants or evident sequelae of hemorrhages which undeniably have occurred at the time of birth. In the larger number of instances in this latter group, the history fails to show any symptoms in the new-born which would have suggested an intracranial traumatization.
From these facts, we can draw at least two definite conclusions : (1) that not all intracranial birth lesions cause death or even marked symptoms in the new-born, and (2) that intracephalic injuries, sustained in birth, must occur with even greater frequency than is indicated by the post-mortem findings in new-born infants.
Observations and experimental studies, extensively recorded in the literature of obstetrics, have now determined the exact mechanical factors which effect the traumatization of the meninges, especially of the dura mater.
Compression of the fetal head, resulting in a relatively small reduction of the volume of the skull, but leading to a rather marked change in its configuration, represents an integral element of every labor.
Experience proves that, in general, this compression is free of any noteworthy harmful effect on the child. 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, 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 blood within the brain.
The process of molding effects a change in the relative position of adjoining skull bones which is most pronounced in the sagittal suture.
As the result of the overriding of the parietal bones, the subjacent dura is both folded and stretched. If this overlapping is excessive (mechanical dystocia) or is very suddenly accomplished (forceps extraction, large doses of pituitary extract), or if the dura is abnormally fragile (prematurity), the strained dura may break. The longitudinal sinus itself may be torn open or, as is more commonly the case, the tear may involve only the veins on one side, exactly at the site of their entrance into the sinus. If these vessels are engorged (asphyxiation, or passive congestion in the aftercoming head), they naturally will break under a relatively smaller strain. Under these conditions, obviously, the resulting hemorrhage will be more profuse.
If, coincidentally, there is an abnormal delay in the blood clotting (hemorrhagic diathesis), the hemorrhage will continue, and may attain dangerous proportions, even if the tear is small and involves but a few, and those small, vessels.
In a breech extraction not properly managed, exaggerated lapping of the parietals over the squama of the occipital bone in an identical manner may cause the rupture of veins emptying into the transverse sinus, or laceration of the sinus itself, or might push the cerebellum with sufficient force against the overlying tentorium to cause its laceration.
Far more significant, however, than this overlapping of adjoining skullbones is the changed configuration of the molded head in the direct mechanical causation of meningeal lacerations. The exact mechanism of the traumatization of the tentorium, the almost typical and indeed most common form of birth injury, has been definitely established by the pioneer work of Beneke4. It has been fully confirmed by many other investigators, among them Eardley Holland5 and Capon6. I refer readers interested in the details of the problem to my monograph, or to the papers of Holland and Capon, and I wish to emphasize in this connection that the mechanical conditions leading to tentorial laceration can easily be reproduced and demonstrated on the head of a new-born infant, opened at necropsy in accordance with Beneke‘s suggestion (Figs. 1,3,4).
Compression of the head in any one direction results in the shortening of the diameter lying in the direction of the pressure, and a simultaneous compensatory lengthening of the diameter perpendicular to the one reduced. Therefore, compression of the head, during the second stage of labor, along either the anteroposterior or the lateral diameters, always leads to an increase in the length of the vertical diameters of the infant’s head. The cranium becomes more convex and the falx is pulled upward. It is generally believed that certain histologic structural details of such tissues as bones or ligaments permit reliable deductions in regard to the functional purpose of these textures.
(4) Beneke : Ueber Tentoriumzerreissung bei der Geburt, etc., M\l=u”\nchen.med. Wchnschr. 57:2125, 1910.
(5) Holland : Cranial Stress of the Foetus During Labor, J. Obst. & Gynec. Brit. Emp. 29:551, 1922.
(6) Capon, N. B. : Intracranial Traumata in the New-Born, J. Obst. & Gynec. Brit. Emp. 29:572, 1922.
The longitudinal arrangement 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. But sudden or excessive compression in either a lateral or a longitudinal direction, by raising the falx, would exert a definite pull at the place where the fibers of the falx diverge to either side to form the upper blade of the tentorium.
This also represents the relatively weakest part of the falx and, as a matter of fact, it is the site of predilection for tentorial tears.
Three specimens, recently obtained in the service of the obstetric department of Washington University, clearly show various points of interest and importance.
In Figure 1, the head of a small fetus, the structure of the anterior part of the falx well expresses its vulnerability. The tentorial blades are so thin that the underlying cerebellum can be seen through them. Who will doubt that these thin dura folds might easily be torn, if this head by a strong uterine contraction (perhaps induced by pituitary extract) was quickly forced through a not fully dilated cervix or through the rigid vulvar ring of a primipara ? The softness and elasticity of the cranial bones of a premature fetus favor exaggerated change in configuration and thus increase the danger to the fragile dura.
Figure 1 : Head of small fetus showing the thinness and vulnerability of falx and tentoria. Through the latter the outline of the underlying cerebellum can be seen. The fibers of the falx diverge posteriorly on either side into the upper blade of the tentorium. The head was opened after the Beneke method.
This assumption is well supported by a comparison with the observations made in the next case. The specimen was obtained by the department from an outside physician. A futile attempt had been made to extract a very large, clearly overcarried infant, by means of a high forceps. The results can be seen in Figures 2 and 3.
Figure 2 : Head of a postmature fetus. The right parietal bone was fractured in an attempt at extraction by means of high forceps.
Figure 3 : Same head as in Figure 2, showing the interior. The dura is intact. Hemorrhages between the blades of the falx can be seen.
External force proved sufficient to cause deep fractures of both parietal bones (only the right parietal is shown in Fig. 2). The hard skull bones, however, proved too rigid to permit a marked change in the configuration. Falx and both tentoria remained intact, exhibiting the effect of the very severe trauma solely in the form of small hemorrhages confined between the dura blades (Fig. 3).
In the third skull (Fig. 4), that of a stillborn infant, spontaneously expelled, head first, the skull bones remained intact, but there was found a deep tear of the right tentorium, severing both blades, another tear through the left tentorium and an opening in the falx.
Figure 4 : Head of full-term infant, stillborn spontaneously in vertex presentation. Both tentoria are torn, the right more extensively. There is a hole in the falx, leaving the vessels crossing the opening intact. There are three distinct traumatic lesions, of which only two caused hemorrhage.
This last injury is particularly instructive. While the dura tissue itself was found split, the vessels running through this area remained intact, as can be seen in the illustration. Thus, this particular opening in the falx represents an intracranial traumatic birth injury causing no hemorrhage.
An appreciation of the direct mechanical causes of tentorial tears, as already described and convincingly demonstrated in the few specimens illustrated here, would seem to render entirely acceptable the assertion of some authors, that meningeal injuries may be the result of unskilful manipulations during resuscitation ; e. g., of too firm a fixation of the infant’s head between the wrists during swinging after Schultze‘s method ; or that they might be produced near the end of the second stage of a normal and spontaneous labor, when the attendant presses the occiput of the fully rotated head too forcibly toward the symphysis in an effort to protect the perineum against injury.
Serious intracranial hemorrhages have been recorded in infants delivered by cesarean sections. In some of these cases, the traumatization undeniably occurred before operation as the result of the effort of the uterus to force the relatively too large fetal head into the narrowed pelvic inlet.
In other instances, in which operation was actually performed before the onset of labor, the infant’s head evidently was severely traumatized solely by its forced extraction through a uterine incision of insufficient length.
The obstetrician, thoroughly familiar with such facts, must disagree with Monro and Eustis that intracranial birth hemorrhages are but rarely traumatic in origin.
These authors proclaim asphyxiation as the most common etiologic factor in such hemorrhages. They write : “At birth, clinically asphyxiated babies are cyanotic, do not start breathing well, or cry, and require treatment which is directed toward the artificial stimulation of respiration. It has also been repeatedly observed that these clinically asphyxiated babies, when they die, die from respiratory failure, the heart continuing to beat for some time after the respiratory center has definitely ceased to function, and after it will no longer react to artificial stimulation. Until this clinical evidence can be disproved by chemical studies of the blood of the new-born infant, therefore, we must consider the baby exhibiting the above symptoms as asphyxiated.”
One cannot resist the temptation to add : “If there is no necropsy in such a case, the diagnosis asphyxia will be given as the cause of death in the death certificate ; but if there is a necropsy, in the overwhelming majority of these cases an intracranial hemorrhage will be found ; and the cause of death should have been given as traumatic intracranial birth injury.”
In all cases of severe birth hemorrhage, the baby, if born alive, is asphyxiated. I maintain that every baby born seemingly asphyxiated should be considered as possibly suffering from an intracranial traumatization, and, therefore, should not be subjected to any violent efforts at resuscitation, because such manipulations might of the infant.
It is unfortunate that we are unable to differentiate in the new-born a true asphyxia, the result of mechanical interference with oxygen supply, from the clinical picture of asphyxiation, brought on by the traumatization of the breathing center.
The undisputed fact that the overwhelming majority of babies, found at post-mortem to have succumbed to an intracephalic hemorrhage, after birth were cyanotic and did not breathe properly, cannot be adduced as proof of the great importance of asphyxia as the direct cause of such hemorrhages. Of no more value in this respect is the often emphasized fact that small petechial hemorrhages, generally considered as characteristic of asphyxiation, are found in the various serosae of these infants. This is not surprising since these babies died in a state of asphyxiation resulting from the improper function of the breathing center. The one question under discussion is whether the asphyxia is responsible for the intracranial hemorrhage, or the intra¬ cranial hemorrhage for the asphyxia. I am not aware of the fact that asphyxiation in young children commonly, if ever, causes the rupture of meningeal veins or of a large sinus merely from overdistention. It then seems unreasonable to insist on this particular mechanism for the rupture of intracranial vessels in the course of birth simply on theoretical grounds, with the added necessity of disregarding deliberately the factor of the compression of the head, a factor unquestionably of a traumatic nature and present in the second stage of every labor. However, it can be readily admitted that a passively congested vein or sinus of a deeply asphyxiated infant is more liable to rupture under external pressure or strain.
The effect of a meningeal tear on the infant in the main is determined by the hemorrhage resulting from it. The occurrence of a hemorrhage and the size of the hematoma, therefore, actually depend on whether any vessels are torn and whether they are small or large, empty or full. Thus, asphyxiation enters into the problem of intracranial birth hemorrhages, but only as a predisposing and contributory cause, and not as the direct cause of the injury. Asphyxiation positively cannot have any bearing on the fact that so often in labor the tentorium is torn.
As a third etiologic factor. Warwick, Munro and Eustis and many others emphasize hemorrhagic diathesis. It is impossible to establish any immediate relation between this disease and lacerations of the dura mater per se. While this anomaly of the blood undeniably is responsible for certain fairly common types of hemorrhage from various mucosae of the new-born, I cannot see how it could he adduced as an acceptable explanation of hemorrhages evidently resulting from the rupture of a sinus or vein within the skull, again with utter dis regard of the mechanical factor of compression of the head during
the process of molding. Nevertheless, it must be admitted that hemorrhagic diathesis also plays some role in the etiology of intracranial birth hemorrhages, even more important than asphyxia, but again only as a contributory factor. If the blood coagulation time is greatly increased, the unduly prolonged extravasation of blood even from a very small vessel will finally prove as disastrous as the rupture of a large vessel in another infant with normal coagulation time. The very gradual formation of the hematoma under these conditions explains the not uncommon appearance of the first manifest symptoms of an intracranial injury only some time after birth.
I should like to call attention in this connection to the seemingly conclusive experiments and investigations of Evarts A. Graham7 concerning the pathogenesis of the hemorrhagic diseases. He established the fact that all those conditions of the new-born which are characterized by a hemorrhagic tendency most probably are the result of a deficiency in oxidation, and can be experimentally produced by chloroform as well as by direct asphyxiation. These, indeed, are findings of far-reaching importance in clearing up some of the obscurer points in the etiology of intracranial birth hemorrhages and their relation to asphyxiation and hemorrhagic diathesis.
Syphilis and the toxemias of pregnancy, which are cited as direct causes of birth hemorrhages, can be accepted only as predisposing factors. Any disease which tends to lead to the premature termination of pregnancy is of etiologic significance because all structures of the immature fetus, and especially those within the skull, admittedly are very fragile and vulnerable. As far as the toxemias are concerned, the fact furthermore must be borne in mind that they frequently call for the termination of labor by artificial and forcible means, which notoriously augment the direct mechanical dangers to the fetal head.
(7) Graham, E. A. : Pathogenesis of the Hemorrhagic Diseases of the New-Born, J. Exper. Med. 15:307, 1912.
In the light of our present information, it seems best to differentiate accurately between the direct mechanical and the predisposing and contributary factors in the causation of intracranial birth injuries in general, and of birth hemorrhages in particular. The etiology of intra¬ cranial injuries sustained in birth might be described briefly thus :
The meninges and the brain substance itself might be traumatized by severely injured skull bones (indentations, depressed fractures). More often, in the absence of any evidence of an external injury, a dura fold is torn as the result of a severe strain if molding is excessive or suddenly accomplished. Such mechanical traumatization of the meninges, therefore, most often is observed in difficult labors and those terminated artificially. But the physiologic trauma also, incident to a spontaneous and seemingly normal birth, might be sufficient to cause the laceration of parts of the dura mater and, with them, of a sinus or veins, in the presence of such predisposing factors as prematurity or marked congestion.
Contributory factors in the formation of the hematoma are congestion and hemorrhagic disease, more indirectly also certain reprehensible methods of resuscitation of the seemingly asphyxiated new-born infant.
A grouping of the various etiologic causes of intracranial birth injuries in this manner does not in the least detract from its value as an aid in diagnosis or treatment, but unquestionably is of greater advantage in the more important problem of their prevention.
Emphasis properly belongs on those primarily mechanical factors which cause intracranial structures to be crushed or torn, with more or less hemorrhage resulting from the injuries. The frequency with which such injuries involve more than one structure within the cranium (e. g, both tentoria and falx in the case shown in Fig. 4) well accounts for the perplexing symptomatology and the futility of surgical interference in many of the cases.