KEY POINTS
- 1.
Childbirth is a traumatic event; the head of the neonate is subject to multiple forces that, in turn, may result in clinically relevant neurologic injuries.
- 2.
Extracranial scalp traumatic injuries are the most common type of neonatal head trauma.
- 3.
Scalp lesions may hinder the diagnosis of more serious intracranial lesions, such as depressed skull fractures.
- 4.
Intracranial hematomas can be found in asymptomatic neonates, with a strong association with forceps-assisted deliveries. The management of neonates with intracranial hemorrhage depends on both clinical manifestations and radiologic findings.
- 5.
Head ultrasound can be a useful screening method for head injuries. MRI, the imaging modality of choice, avoids ionizing radiation and provides high-definition imaging of soft tissues, neurologic structures, and associated injuries such as hematomas.
- 6.
Timely medical stabilization and appropriate work-up of the injuries and possible associated conditions (coagulopathy, congenital malformations) is the main goal of the neonatologist. Surgical interventions are seldom needed; however, neurosurgical consultation should be considered in certain cases.
Introduction
Neonatal neurotrauma can be defined as disturbances of nervous (cerebrum, spinal cord, nerves) and adnexal tissues (meninges, spine, cranium, or scalp) due to mechanical forces exerted during birth (labor, delivery, cesarean section) or within the first 4 weeks of life.
Delivery (vaginally or cesarean section) can be a traumatic event with common injuries arising from it with varying degrees of clinical significance. The treatment of such injuries should be dictated by the clinical presentation and impact to the patient. Traumatic injuries from mechanical force can result in injury to any part of the neonatal nervous system. Even during uncomplicated deliveries, the neonate is exposed to several forces that can cause neurotrauma, which will be discussed further.
Epidemiology
Traumatic birth injuries of the central nervous system have become less common in the current era with the increased use of cesarean delivery in anticipated difficult vaginal delivery. The rate of birth trauma in the United States has been estimated at about 29 per 1000 births, with the most common birth related lesions being scalp injuries. Intracranial hemorrhage in full-term neonates has been found to be as prevalent as 26% of patients born via vaginal delivery. Skull fractures can also occur related to birth and delivery. Uncommonly, fractures can cause brain compression and significant neurologic and aesthetic damage if not treated effectively and promptly.
Neonatal Neurotrauma Anatomical Classification
- 1.
Head injuries
- a.
Scalp injuries and hematomas
- •
Cephalohematoma
- •
Caput succedaneum
- •
Subgaleal hematoma (SGH)
- •
- b.
Skull fractures
- a.
- 2.
Intracranial hematomas
- a.
Extraaxial hematomas
- •
Subdural hematoma
- •
Epidural hematoma
- •
- b.
Intraaxial hematomas
- a.
- 3.
Spine and spinal cord injuries
Head Injuries
Scalp Injuries
The most common birth-related neonatal traumatic injuries are scalp lesions. In order to discuss scalp lesions it is important to understand the basic scalp layered structure, which is often remembered by the mnemonic “SCALP”: S kin, dense C onnective tissue (where most of the vasculature lies), A poneurosis (Galea aponeurotica) , L oose areolar tissue, and P eriosteum ( Fig. 53.1) . Hematomas are termed according to the layer of the scalp in which they reside. Scalp lacerations, in turn, are graded based on the extent of layers they violate and the presence or absence of a skull fracture.
Scalp Hematomas
Caput Succedaneum
Caput succedaneum is the hemorrhagic edema of the scalp layers above the periosteum caused by head pressure against the birth canal or vacuum extractor. This pressure leads to obstruction of the venous return of the scalp and the consequent extravasation of fluid into the interstitial tissue. This edema of the scalp is usually soft and can cross suture lines of the cranium and the midline.
The management of caput succedaneum is expectant, requiring imaging only in cases of progression of the edema after 24 hours or failure of resolution after 48 to 72 hours. In cases of progression, the diagnosis of caput succedaneum should be questioned. Typical imaging can include a head ultrasound or a rapid sequence magnetic resonance image (MRI) of the head. In most cases, the correct diagnosis can be made by physical examination with determination that the edema (usually pitting) crosses suture lines and/or the midline. Pharmacologic treatment is usually not necessary and the condition usually resolves within a week of birth. Placement of scalp IVs are not contraindicated in cases of isolated caput succedaneum.
Cephalohematoma
A cephalohematoma is a collection of blood between the periosteum and the skull ( Fig. 53.2) . The hematoma is contained to a focal area of the cranium by the periosteal attachments to the sutures of the skull. Cephalohematoma occurs in about 1% to 2 % of all deliveries. The rate is higher with forceps-assisted (5%) and vacuum-assisted (4%) deliveries. Other significant risk factors for cephalohematoma include cephalo-pelvic disproportion, occipital-posterior and occipital-transverse presentations, large size, a primigravida mother, and placement of fetal scalp electrodes. Regardless of the cause, the hematoma is thought to develop from the disruption of emissary or diploic veins as the periosteum is lifted away from the skull when the head of the neonate moves with significant pressure against another surface (e.g., birth canal, forceps).
Management
- 1.
Diagnosis
- a.
Physical examination: The diagnosis should be suspected on physical examination of the head of the neonate. A finding of disproportionate head shape with a nonpedunculated subcutaneous mass that does not cross suture lines or leave pitting edema and is isolated to a region of the calvaria strongly suggests a diagnosis of cephalohematoma. Head circumference measurement and size of the hematoma must be documented and serially measured to establish stability or progression of the hemorrhage. A thorough neurologic examination should always be obtained, looking for associated deficits that can indicate a more serious lesion.
- b.
Imaging and laboratory workup: Head ultrasonography can be a practical bedside method to obtain objective measurements of the hematoma; it can also identify associated intracranial hemorrhage such as epidural hematoma. The use of higher-resolution techniques can further delineate the morphologic characteristics and the extent and location of the hematoma(s). The use of limited (rapid sequence T2-HASTE technique) MRI is of particular value in the sense that it provides more detailed images of the brain and scalp without exposing the neonate to ionizing radiation via computerized tomography (CT). In the setting of a cephalohematoma that is rapidly enlarging or larger than 5 cm, laboratory evaluation for coagulopathy, platelet dysfunctions, progressive anemia, or hyperbilirubinemia should be considered with abnormalities corrected accordingly.
- a.
- 2.
Treatment: By the end of the first week of life, the majority of neonates will show signs of dissolution (decreasing size or softening) of the hematoma, and complete resolution can be seen in most cases by the end of the second week without any intervention. Delayed increasing size or appearance of neurologic deficits should trigger neurologic consultation for evaluation.
- 3.
Complications: The main reported complications of cephalohematoma arise from nonabsorption of the hematoma.
- a.
Infection: Several cases of infection of the hematoma have been reported in the literature. In the setting of infection, treatment consists of washout and antibiotic therapy. Of note, in a neonate who meets criteria for sepsis without a known source and a history of cephalohematoma, drainage of the hematoma should be considered to obtain microbiological analysis.
- b.
Calcification: Calcification of the residual cephalohematoma (after 4–6 weeks from birth) is part of the expected natural history of these lesions. Significant head deformities can arise in large collections if left untreated, although they often remodel over time ( Fig. 53.3) . In this situation, patients can be referred to a craniofacial surgeon or neurosurgeon for drainage or evaluation for cranioplasty at a later age.
Fig. 53.3
Computed Tomography of the Head Without Contrast Demonstrating Right Parietal Calcified Cephalohematoma on a 3-Year-Old Female Patient .
- a.
Subgaleal Hematoma/Hemorrhage
SGH is an accumulation of blood between the galea aponeurotica (aponeurosis) of the scalp and the periosteum of the skull. SGHs are usually caused by the rupture of emissary veins or arterioles of the scalp during delivery or another traumatic event in a newborn. The peculiarity of this “virtual” space of the scalp is that there is no strong adhesion between the aponeurosis and the pericranium; therefore a significant amount of blood can accumulate (over 250 mL). , SGH can represent a significant threat for an actively bleeding neonate, given the small intravascular volume. The incidence of neonatal SGH increases significantly with the use of vacuum devices during delivery, from 0.4 in 1000 vaginal deliveries without the use of vacuum or forceps to 5.9 in 1000 in vacuum-assisted deliveries.
Management
- 1.
Diagnosis
- a.
Neonates diagnosed with SGH the day of admission appear to have better prognosis than those diagnosed the following day. SGH should be suspected on the grounds of examination and characteristics of delivery. Prolonged labor and vacuum extraction should trigger the neonatologist to look for signs of scalp lesions to establish the appropriate diagnosis. Differentiating SGH from cephalohematoma and caput succedaneum can usually be achieved by physical examination. Cephalohematoma, as discussed above, does not cross the midline or suture lines, whereas SGH usually does. In fact, SGH can involve the entire head circumference and it may displace the ear and the skin over the orbital rims. Cephalohematomas are usually tense to palpation and do not change with variations in head position, whereas SGHs palpate as a fluctuant (boggy) mass that can migrate to dependent areas when the position of the neonate is changed. SGH, in comparison to caput succedaneum, usually does not produce scalp pitting edema on palpation and takes longer to resolve than caput succedaneum, which tends to resolve as the swelling starts to dissipate within hours to days.
- b.
Head imaging such as head ultrasound and MRI of the brain can be obtained to rule out associated intracranial hemorrhage and pathology. Still, this imaging should not delay other diagnostic tests and measures in the setting of a potentially life-threatening hemorrhage or an unstable neonate. The use of head CT is discouraged given the exposure of the neonate to ionizing radiation and should be avoided if possible, depending on the urgency and medical center capabilities. Close monitoring for signs of hypovolemia, anemia, acidosis, and hyperbilirubinemia should be established, and related laboratory studies including coagulation studies should be obtained at baseline.
- a.
- 2.
Treatment
- a.
The mainstay of treatment for patients with SGH is avoidance of complications related to acute blood loss. Patients with suspected SGH or strong risk factors for SGH, such as prolonged vacuum-assisted deliveries, should be closely monitored. In the setting of proven SGH, hourly vital sings, neurologic checks, and recurring examination of the hematoma should be established. Blood transfusions, correction of acidosis, and other supportive measures should be promptly instituted. Surgical intervention is not typically indicated in the setting of isolated SGH. Some practitioners have advocated head wrapping to tamponade the hemorrhage and reduce the subgaleal space, but one must be careful because this can result in elevated intracranial pressure if the head wrap is too tight. Furthermore, the head wrap may make proper examination of the hematoma more difficult. Neurosurgical evaluation can be considered in the setting of an associated intracranial hemorrhage or skull fracture.
- a.
Skull Fractures
Skull fractures are usually classified as either linear or displaced. In linear fractures there is a separation of the skull bone without variation of the circumferential shape of the skull ( Fig. 53.4 ). They can be simple (single line of fracture) or complex (comminution of the bone or multiple ramifications of the line of fracture). In displaced fractures, the shape of the skull bone becomes irregular by depression or elevation of the fracture edges. Depressed fractures may cause pressure on the intracranial contents, whereas elevated fractures move away from the intracranial contents.
In the neonatal population and early infancy (6 months of age and younger), depressed fractures are usually “ping-pong” or “greenstick” fractures ( Fig. 53.5) . The name comes from the inversion of the cranial convexity to a concavity at the site of the fracture, reminiscent of an indentation on a ping-pong ball. This type of fracture occurs in the neonatal population due to the immaturity of the skull bones, because they have more elastic capabilities and resilience to physical separation. This type of fracture is the most common depressed skull fracture in the neonatal population, whereas linear skull fractures are the most common skull fracture in the neonatal age overall.
The incidence of congenital skull fracture has been estimated to be between 2% and 3% of every 100,000 deliveries. , It is unclear, however, the true incidence of skull fractures in this population; some fractures may have minimal symptoms and the diagnosis can be missed because patients are, appropriately, not routinely radiologically screened for such lesions.
Management
Diagnosis
Clinical Manifestations
It is important to differentiate between skull remodeling from labor and delivery and a skull fracture. Skull fractures are associated with a focal hematoma in more than 25% of cases, whereas skull remodeling occurs by overriding of the sutures of the skull and is a normal self-limited consequence of labor and delivery. Skull remodeling is often symmetric versus asymmetric with an isolated unilateral defect for skull fractures. An indentation defect can be palpated in most cases of depressed skull fractures. Associated clinical manifestations of skull fractures in the neonate can include seizures, focal motor deficits, and pupillary abnormalities.
Diagnostic Testing
The gold standard test for identification of a skull fracture is CT without contrast. CT is also helpful to identify associated hemorrhage intra- or extracranially. The drawback of CTs is the exposure of the neonate to radiation; thus CT should be reserved for patients with a high suspicion of skull fracture. Other imaging techniques, such as HASTE sequence MRI (also known as rapid sequence or ultrafast MRI), can be used as an initial test for a suspected traumatic injury, although the bone anatomy may not be as clear as with CT. Skull x-rays can be used if more advanced diagnostic studies are not available. Information about associated hemorrhage and intracranial tissue involvement is limited, and x-rays are not as sensitive as head CT for identification of linear skull fractures. Therefore, the use of skull x-rays is of limited utility in neonatal trauma.
Treatment
The identification of a skull fracture should prompt the neonatologist to consider a consultation with a neurosurgeon, although most identified skull fractures do not require a neurosurgical intervention. Criteria for surgical intervention of a neonatal skull fracture vary from case to case. Linear skull fractures without associated hematomas are managed nonoperatively. A depressed skull fracture may require surgical elevation if the depression is greater than 5 mm or significant brain compression is present. “Ping-pong” fractures can be successfully treated with suction devices by the neurosurgical team ; however, in more complex depressed skull fractures, surgical exploration and elevation should be considered.
Complications
Growing Skull Fracture: Skull fractures can disrupt the meninges covering the brain at the time of injury. In nonhealed meningeal defects, the growing brain and cerebrospinal fluid can herniate through the defect, creating a meningocele or meningoencephalocele. Patients with a neonatal skull fracture (formally diagnosed or not) can present with delayed neurologic deficits or skull deformity due to this phenomenon, often months after the injury. Therefore, any patient with an identified skull fracture should be followed to rule out development of a growing skull fracture.
Seizures: Seizures are of concern, particularly with depressed skull fractures and/or intracranial hematomas, due to potential cerebral cortical irritation.
Intracranial Hematomas
Hematomas related to trauma can occur in any of the different compartments of the intracranial space (both supra- or infratentorial): epidural, subdural, subarachnoid, intracerebral, or intraventricular. Intracranial hematoma in the setting of neonatal trauma has a different pathogenesis than intraventricular hemorrhage seen in premature neonates (germinal matrix hemorrhage) as well as other intracranial hematoma from nontraumatic medical conditions.
Risk factors for traumatic intracranial hematomas in neonates include assisted vaginal delivery, breech presentation, large fetal weight, and prolonged duration of labor. However, it has also been shown that intracranial hemorrhages can be commonly found in asymptomatic neonates after vaginal deliveries. There has likely been an increase in the identification of neonatal intracranial hemorrhages due to the availability of more advanced imaging techniques; however, the true incidence and repercussion of these hemorrhages is not fully known or understood. , Ultimately, given its close association with hypoxic-ischemic injury and other medical conditions, significant morbidity has been historically associated with hemorrhagic brain injuries.
As mentioned above, hematomas can occur in any compartment of the intracranial space. Table 53.1 depicts a summary of the anatomic location, radiologic characteristics, and pathogenesis of intracranial hemorrhage. In the neonate, hemorrhages can commonly be seen in multiple compartments.
| Intracranial Hemorrhage Type a | Definition | Cranial Computed Tomographic Scan Characteristics | Comments or Pathogenesis |
|---|---|---|---|
| Epidural | Blood between the skull and outside the dura | Lentiform hyperattenuation along inner side of calvarium | Rare, because the middle meningeal artery moves freely away from displacements of the skull |
| Subdural | Blood between the dura and arachnoid membrane | Crescent-shaped hyperattenuation conforming to the adjacent brain | Most common; vertical molding of skull causes tearing of blood vessels of tentorium |
| Subarachnoid | Blood between the arachnoid and the pia membrane | Hyperattenuating fluid in basal subarachnoid spaces or along cerebral sulci | Most common type; tearing of bridging blood vessels or dural sinuses during labor |
| Intraventricular b | Blood in lateral, third, or fourth ventricles | Hyperattenuating fluid typically seen as layering within the ventricles | Uncommon hemorrhage of choroid plexuses; extension of thalamic or subependymal matrix |
| Intraparenchymal | Blood within brain (intraaxial) parenchyma | Hyperattenuating focus within the cerebral or cerebellar hemispheres, with varying amount of surrounding vasogenic edema | Less frequent; primary hemorrhage must be distinguished from secondary intraparenchymal hemorrhage |
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