Review Article Parturitional Injury of the Head and Neck Thierry A.G.M. Huisman, MD, Timothy Phelps, MS, FAMI, Thangamadhan Bosemani, MD, Aylin Tekes, MD, Andrea Poretti, MD From the Section of Pediatric Neuroradiology, Division of Pediatric Radiology, Russell H. Morgan Department of Radiology and Radiological Science, The Johns Hopkins University School of Medicine, Baltimore, MD (TAGMH, TB, AT, AP); and Department of Art as Applied to Medicine, The Johns Hopkins University, Baltimore, MD (TP).

ABSTRACT Parturitional injuries refer to injuries sustained during and secondary to fetal delivery. The skull, brain, and head and neck regions are frequently involved. Accurate differentiation and classification of the various injuries is essential for treatment, prognosis, and parental counseling. In this review, we discuss the various “bumps and lumps” that maybe encountered along the neonatal skull as well as the most frequent calvarial and intracranial parturitional injuries. In addition, a short discussion of the most common head and neck, facial, and spinal lesions is included. Various mimickers and risk factors are also presented.

Keywords: Neonatal, trauma, head, neck. Acceptance: Received December 13, 2013, and in revised form March 23, 2014. Accepted for publication March 30, 2014. Correspondence: Address correspondence to Thierry A.G.M. Huisman, MD, Director of Pediatric Radiology and Pediatric Neuroradiology, The Russell H. Morgan Department of Radiology and Radiological Science, The Johns Hopkins School of Medicine, Charlotte R. Bloomberg Children’s Center, Sheikh Zayed Tower, Room 4174, 1800 Orleans Street, Baltimore, MD 212870842, USA. E-mail: [email protected] J Neuroimaging 2015;25:151-166. DOI: 10.1111/jon.12144

Introduction Parturitional injury relates to any condition that affects the fetus adversely during labor and delivery.1 In the past decades, the improving pre-, peri-, and postnatal care has dramatically decreased the incidence of parturitional injuries. Currently, birth trauma is reported to occur in less than 3% of all live births in the United States. In addition, parturitional injury accounts for less than 2% of all neonatal deaths in the United States. Many maternal and fetal risk factors have been identified.1 Maternal risk factors include diabetes, obesity, a small pelvis, large weight gain, induction of labor, epidural analgesia, primiparity, and history of a macrosomic infant. Fetal risk factors include macrosomia (birth weight >3,500 g), delayed and prolonged delivery, abnormal fetal presentation (eg, breech presentation), instrumented delivery, perinatal depression, and shoulder dystocia.1 Depending on the severity of parturitional injury, the impact on the short- and long-term quality of life of the neonate may be significant. In addition, even when the parturitional injuries are mild or benign, this may result in significant anxiety for the family. Accurate diagnosis of parturitional injury is mandatory to guide treatment, prevent secondary complications, and to counsel the parents. Parturitional injury is typically classified in 2 ma-

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jor categories; birth injury and birth trauma.2 Birth injuries result from various combinations of hypoxia/hypoperfusion and infection, while birth trauma results from the direct impact of mechanical forces exerted to the fetus during labor and delivery. In this manuscript, we will focus on the imaging findings related to birth trauma involving the neonatal brain and skull. In addition, a short discussion will be included of injuries to the neonatal spinal cord and the head and neck region.

Parturitional Skull and Brain Injuries In the immediate postnatal time period, a wide spectrum of extracranial, cranial (skull), and intracranial lesions may be encountered.3-7 Depending on the severity and type of the injury, location of the lesion, exerted mass effect on adjacent brain structures, development of primary (eg, anemia and hypovolemic shock in subgaleal hematomas), and/or secondary (eg, hyperbilirubinemia in subgaleal hematomas and secondary ischemic lesions in skull fractures with midline shift) complications and presence of complicating factors outside of the central nervous system (eg, systemic hypoxia, hypoperfusion, or sepsis), various degrees of reversible or irreversible brain injury may result. It is therefore essential to diagnose parturitional injury quickly as well as with high sensitivity, specificity, and

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Fig 1. (A) Coronal section across the top of the skull with normal display of the various anatomical spaces and structures form outside to inside: skin and subcutaneous fat, galea aponeurotica, periosteum, skull, emissary veins, dura mater, superior sagittal sinus, subdural space, arachnoid mater, subarachnoid space, cerebral arteries and veins, pia mater, Pacchioni’s granulations, cerebral cortex, and hemispheric white matter. (B) Coronal section across the top of the skull showing parturitional, extracranial “lumps and bumps” including caput succedaneum, subgaleal hematoma, and cephalohematoma. The color of the hematomas represents their composition: violet for a serous-sanguineous fluid collection, red for a sanguineous fluid collection. (C) Coronal section across the top of the skull showing parturitional, intracranial injuries including EDH, SDH, and SAH.

reliability in order to initiate appropriate treatment as soon as possible. Depending on the anatomical location, parturitional injuries may be classified in to various groups.3,4,6,7 Extracranial injuries include: a) scalp abrasions/lacerations; b) caput succedaneum; c) subgaleal hematomas; and d) cephalohematomas. Cranial or skull injuries include: a) fractures (linear or depressed); b) leptomeningeal cysts; and c) sutural diastasis including occipital osteodiastasis. Intracranial injuries include a) epidural hemorrhage; b) subdural hemorrhage; c) subarachnoid and intraventricular hemorrhage (IVH); and d) intraparenchymal hemorrhage. All these lesions may occur in isolation, but more fre-

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quently combined injuries are noted. For the accurate clinical and radiological diagnosis, familiarity with the various anatomical spaces is a prerequisite (Fig 1).7 In the following paragraphs, we will review the neuroanatomy as well as the various kinds of parturitional injury.

Parturitional Extracranial Injuries The various extracranial lesions may look very similar on initial clinical evaluation and typically present as “bumps or lumps.” Depending on their etiology, location, and composition, the clinical consequences may vary significantly. Approaching the

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Fig 2. Three-dimensional (3D) surface shade reconstructed, sagittal, and coronal T1-weighted and follow-up T2-weighted MR images of a macrosomic 1-day-old female newborn (diabetic mother, shoulder dystocia) with a caput succedaneum (arrows). A large “bump” is noted along the parietal region of the skull. Matching T1-weighted MR images show a large T1-hypointense serous fluid collection in the space between skin and galea aponeurotica. The fluid collection extends over the midline across the sagittal suture. Follow-up MRI shows complete spontaneous resolution of the fluid collection.

ery or scalp laceration secondary to the surgical opening of the amniotic sac during a Cesarean section. The last one occurs particularly when the Cesarean section is technically difficult. These lesions may be worrisome for the parents, but are rarely of clinical significance. Most skin lesions resolve within a couple of days without complications. A skin laceration may occasionally act as a port of entry for infection and should be treated accordingly. Caput Succedaneum

Fig 3. Axial and coronal CT images of a 9-day-old female newborn with a large predominantly left-sided hyperdense subgaleal hematoma (arrows). The hyperdense hematoma is located in the space between the galea aponeurotica and calvarial periosteum. The hematoma crosses the lambdoid and sagittal sutures. In addition, the hematoma extends deep into the neck region. An additional smaller and less dense serous-sanguineous fluid collection is noted between the skin and galea aponeurotica compatible with a coexisting caput succedaneum.

skull from the outside inward, the various fascial and tissue planes can be identified. The outermost layer is the skin and subcutaneous fat followed by the galea aponeurotica or epicranial aponeurosis which covers the periosteum of the calvarial bone. Serous, sanguineous, and serosanguineous fluid collections can be seen in the various compartments between these layers. Scalp Abrasions and Lacerations

Scalp abrasions and lacerations are frequently noted after both vaginal and instrumental deliveries. Lesions may be noted along the scalp, face, cheek, and in the region of the ears. After vaginal delivery, the distribution of abrasions usually depends on the fetal presentation at delivery. After an instrumental delivery, distinct skin markings may be noted which match the applied instrument (vacuum cup or forceps blades). Additional iatrogenic scalp abrasions and lacerations include needle puncture of the fetal head as a result of blood sampling during deliv-

A caput succedaneum refers to a predominantly serous or occasionally a serous-sanguineous fluid collection within the scalp located in the compartment between skin and galea or epicranial aponeurosis (Fig 1). A caput succedaneum typically results from high pressure exerted on the infant’s head during labor. These lesions are most often located along the presenting portion of the scalp, usually within the region of the vertex. A caput succedaneum is typically present at delivery and decreases spontaneously within the first 24-48 hours. The swelling is soft, has irregular margins, and may show small petechial hemorrhages, purpura, and/or ecchymosis. Pitting edema is often seen. The subcutaneous fluid collection may shift from side to side with varying head position and characteristically crosses sutures, with frequent extension across the midline. The 20-40% of all vacuum extractions are complicated by a caput succedaneum, which is as an “artificial caput,” also known as “chignon” named after the distinguished fashionable female French hair dress. A caput succedaneum is also seen after difficult, prolonged deliveries, typically in primigravidas and in cases of premature rupture of the membranes (PROM). The lack of an adequate amount of amniotic fluid due to the PROM increases the risk for a caput succedaneum. A caput succedaneum may also be present intrauterine in the presence of oligohydramnios and due to Braxton-Hicks contractions. Treatment is rarely necessary and outcome is usually favorable. Neuroimaging is performed to exclude a subgaleal hematoma. On imaging, the caput succedaneum is seen as a focal subcutaneous fluid collection, superficial to the galea aponeurotica and may cross cranial sutures or the midline (Fig 2).

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Fig 4. (A) Coronal MR-venography image of a male child displays the extensive vascular network of emissary and diploic veins (arrows) connecting the intracranial and extracranial subcutaneous venous system. (B) Multiplanar 3D CT reconstructions of the bony calvarium in a 1-month-old girl. Multiple sutures are shown on this 3D CT reconstruction. The sagittal suture typically limits extension of a cephalohematoma across the midline. Cephalohematomas may however cross the midline in the occipital region because the occipital bone is not divided by a midline suture. Familiarity with the location of the various sutures is mandatory for accurate diagnosis. (C) Plain radiography (5-weekold girl), axial CT (3-week-old boy) in soft tissue and bone window algorithm, and a 3D skull reconstruction (6-month-old boy) show 3 examples of calcified cephalohematomas. On plain radiography, the calcified hematoma (arrows) typically follows the contour of the skull with simultaneous elevation of the overlying soft tissues. On CT, ongoing calcification may result in a peripheral, shell-like calcification with a hypodense organizing central hematoma between the peripheral calcification and adjacent calvarium. If the calcification progresses, the calcified hematoma can become incorporated within the skull with a resultant deformity. On CT, this may appear as a focal thickening of the skull which is limited by the sutures. (D) Axial, coronal, and sagittal CT images of 5-day-old female newborn with a cephalohematoma (arrows). A mildly hyperdense well-circumscribed sanguineous fluid collection, predominantly hypodense is noted within the subperiosteal space located between the calvarial periosteum and bony calvarium. The hematoma is limited by the sagittal and lambdoid sutures. Mild amount of subdural blood is noted intracranially along the falx cerebri and left tentorium cerebelli. (E) Sagittal, coronal, and axial CT images of a 10-day-old male newborn with bilateral serous-sanguineous, mixed hypo-/hyperdense cephalohematomas (arrows). Both hematomas are limited by the sagittal and coronal sutures bilaterally.

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Fig 5. Coronal, axial (top row), and sagittal (lower row) CT images of 10-day-old male newborn with a combination of various extracranial hematomas occupying multiple anatomical spaces. A subgaleal hematoma (arrows) is seen in combination with a cephalohematoma (arrowheads) as well as adjacent subcutaneous edema. The combination of hematomas obscures the distinct identification of the borders of the hematomas on palpation.

Subgaleal Hematoma

A subgaleal hematoma is a predominantly sanguineous and occasionally a serous-sanguineous fluid collection located between the galea aponeurotica and calvarial periosteum (Fig 1). It may be mistaken for a caput succedaneum because the hematoma and clinically appreciable swelling may also cross cranial sutures. A subgaleal hematoma is not always clinically apparent immediately postpartum but may develop or enlarge over the first few hours or days after delivery. A subgaleal hematoma is believed to result from tearing of the emissary veins which connect the intracranial dural sinuses with the scalp veins (Fig 1). Subgaleal hematomas are often encountered after a vacuum-assisted delivery, but may also occur spontaneously or secondary to a skull fracture or rupture of a synchondrosis. Most importantly, a subgaleal hematoma should be recognized early and correctly differentiated from a caput succedaneum. Most subgaleal hematomas show a benign course and do not require treatment with complete resolution within 2-3 weeks. However, large subgaleal hematomas may be a potentially life-threatening condition. The subgaleal space extends in its anterior-posterior direction from the orbital ridges, where the galea aponeurotica or epicranial aponeurosis attaches toward the posterior neck along the superficial neck fascia. The subgaleal space if filled is estimated to potentially contain up to 260 ml of blood in term infants. Given the fact that term infants have about 85 ml of blood per kg bodyweight, a large subgaleal hematoma may result in hypovolemic shock and possible neonatal death. Development of large-sized hematomas

is also facilitated by the fact that the galea aponeurotica has no effective tamponading characteristics or mechanism. Various coexisting inborn or acquired bleeding disorders (eg, vitamin K deficiency, thrombocytopenia, hemophilia, consumption coagulopathy secondary to septicemia) may further complicate subgaleal hematomas. Occasionally, a packed red cell transfusion, infusion of blood products, or a surgical evacuation is required. Finally, with a large hematoma, the neonate may develop symptomatic hyperbilirubinemia or jaundice. On computed tomography (CT) images, the subgaleal hematoma is seen as an iso- or hyperdense fluid collection that may cross sutures, can extend into the neck region and is deep to the galea aponeurotica (Fig 3). Cephalohematoma

A cephalohematoma refers to a sanguineous fluid collection in the subperiosteal space between the calvarial periosteum and bony calvarium (Fig 1). Cephalohematomas are usually not present at birth unless the neonate has been exposed to prolonged labor. Typically, cephalohematomas develop within the first 24 hours after delivery. Clinically they present as firm, tense mass lesions that do not cross sutures because they are limited by the periosteum. Cephalohematomas result from shear forces during birth that tear emissary veins and diploic veins (Fig 4A). The resultant hematomas typically slowly lift the periosteum from the adjacent calvarium. The dense and firm periosteum usually tamponades the hemorrhage effectively. Cephalohematomas are frequently in a parietal location with

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Fig 6. (A) Fetal T2-weighted MRI, lateral radiography, and 3D CT reconstruction of a fetus with an occipital meningocele (arrows) which presented as a focal “bump” on delivery located within the occipital region. On follow-up, the bony defect progressively enlarged requiring reconstructive surgery. (B) Sagittal and coronal CT images of a 1-month-old girl with a focal “bump” in the region of the anterior fontanel. CT showed a hypodense, well-circumscribed midline epidermal inclusion cyst overlying the anterior fontanel without intracranial extension (arrows). (C) Sagittal and coronal T2-weighted MR images of a 2-month-old boy with a large “bump” in close proximity to a burr hole which was used for external cerebrospinal fluid drainage because of hydrocephalus as a complication of a IVH. A moderate-sized subgaleal fluid collection (arrowheads) is noted as well as a focal herniation of infarcted/injured brain tissue through the burr hole (arrows). (D) Coronal and sagittal contrast-enhanced CT images in soft tissue and bone window algorithm of a 1-month-old male newborn with a focal “bump” due to a variant sinus pericranii (arrows). A conglomerate of veins is noted extending through a focal skull defect from the superior sagittal sinus toward the adjacent subgaleal space. a 2:1 predominance for the right side compared to the left. These hematomas may be unilateral and/or bilateral, and may cross the midline in the occipital region (Fig 4B). Because of the frequent coexistence of a caput succedaneum and/or a subgaleal hematoma, the sutural boundaries may be obscured on palpation. Cephalohematomas are more common in primigravidas, fetal macrosomia, instrument-assisted delivery, pro-

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longed and/or difficult labor, or if the fetus is in a deviant position. Cephalohematomas may also be present in utero in cases of oligohydramnios as well as in cases of premature and/or PROM. For unknown reasons, cephalohematomas are twice as often encountered in boys compared to girls. On inspection, the overlying skin is typically not discolored and the mass cannot be transilluminated or shifted with palpation. Frequently, the

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Fig 9. The 3D bone CT (2-month-old boy) reconstruction of the posterior skull base. The synchondrosis between the squamous and occipital bony plates of the occipital bone (arrows) is at risk for disruption with resultant shift of the bony plates known as occipital osteodiastasis. This may occur secondary to significant suboccipital pressure during delivery.

Fig 7. Axial bone and soft tissue CT image of a 10-day-old female newborn with a minimally displaced linear fracture (arrows) of the right temporal bone. A small adjacent extracranial “bump” hematoma (arrowhead) is noted overlying the fracture and no intracranial hematoma is seen.

hematoma is painful on palpation. The prognosis is excellent and cephalohematomas typically resolve spontaneously within weeks or months. Rarely complications occur, which may be related to an underlying skull fracture (seen in 5-18% of cases), anemia, hyperbilirubinemia, or infection. Infection should be suspected if the neonate presents with a local erythema, or in cases of unexplained fever or sepsis. Cephalohematomas may be the source of infection, typically due to Escherichia Coli or

Staphylococcus aureus superinfection. Cellulitis, osteomyelitis, or meningitis may occur, especially if scalp electrodes have been applied overlying the region of the hematoma, or after needle aspiration of the hematoma. Finally, during follow-up, the cephalohematomas may calcify, occasionally resulting in a significant skull deformity (Fig 4C). In rare cases, a surgical augmentation of the bony prominence is indicated if conservative treatment using a molding helmet has failed. On imaging, these hematomas are iso- or hyperdense on CT, do not cross the sutures, and appear well-contained by the overlying elevated periosteum (Figs 4D,E). Combined Extracranial Hematomas

In practical “daily life,” an accurate differentiation between the various extracranial “bumps” may be difficult because frequently several hematomas affecting multiple compartments are simultaneously present. A clear distinct differentiation may

Fig 8. The 3D soft issue/bone reconstruction and axial/coronal CT images of a 1-day-old female newborn with a depressed “ping pong ball” fracture of the right frontal bone (arrows). A significant deformity of the skull is noted.

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Fig 10. Multiplanar 3D CT reconstruction of the bony calvarium of a 17-day-old male newborn with sutural diastasis secondary to significantly increased intracranial pressure after perinatal brain injury. The sutures are widened and the fontanels are enlarged.

Fig 11. Sagittal high-resolution US, coronal T2-weighted MR, and lateral radiography of the skull show an enlarging fontanel secondary to a leptomeningeal cyst (arrows) after faulty positioning of a vacuum extractor. The dural defect is well seen on US, a large subgaleal fluid collection is noted which communicates with a focal brain defect within the left superior frontal gyrus. Lateral skull radiography shows the progressively enlarging skull defect adjacent to the extracranial “bump.” therefore be difficult (Fig 5). Familiarity with the imaging characteristics of the various extracranial “bumps” with high-quality imaging, good clinical information including data about the mode of delivery, gestational age at delivery, local physical findings, and temporal evolution of the “bump” usually allows accurate classification of the hematoma. Differential Diagnosis

Several “other” pathologies may also present with a calvarial “bump or lump” at delivery. Differential diagnosis may include a meningoencephalocele, an epidermal inclusion cyst, a sinus pericranii, scalp arteriovenous malformations (AVM), or even a posttraumatic encephalocele, to mention a few. Hydrops fetalis may result in a significant subcutaneous scalp edema and is usually easy to diagnose/differentiate because the fetus is typically affected with subcutaneous edema extending along the entire fetus. If the birth history, clinical or physical examination, or follow-up findings do not explain the presentation, an alternative diagnosis should be considered. Based on clinical history and examination, differentiation between extracranial

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hematomas and other calvarial “bumps or lumps” is usually straightforward. If this is not the case, additional cross-sectional imaging usually allows to make the accurate diagnosis (Figs 6A–D).

Parturitional Calvarial Injuries The neonatal skull is unique in its biomechanical properties. The skull basically consists of a combination of multiple mildly ossified bony and partially cartilaginous plates that are separated from each other by multiple sutures, synchondroses, and fontanels. The various elements of the skull may shift to a certain degree in relation to each other during delivery, but due to their inherent “softness,” they are also at risk for dents, fractures, and dural tears. Consequently, a spectrum of calvarial injuries may be encountered related to spontaneous or instrument-assisted traumatic delivery. Skull injuries or fractures must be suspected if a cephalohematoma or intracranial hemorrhage is present. Skull injuries are caused by compression forces during labor while the skull

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Fig 12. (A) Lateral skull radiography and axial CT soft tissue and bone window algorithm images of a 5-day-old male newborn who fell down from the couch while the mother was nursing the child. A linear mildly displaced right parietal fracture (arrows) is noted with an adjacent extracranial hematoma (arrowhead). (B) Axial CT images of a male newborn who fell out of the arms of the father who was walking down a staircase. A nondisplaced right parietal fracture is noted (arrow) with an adjacent extracranial hematoma. In addition, a moderate-sized SDH is noted anterior to the temporal lobe. is being pushed against the maternal pelvis or may occur due to the pressure exerted by forceps blades. The most frequent skull injuries that are encountered include linear or depressed fractures, sutural diastasis, occipital osteodiastasis, or leptomeningeal cysts. Linear Calvarial Fractures

Linear fractures are frequently asymptomatic and heal without intervention (Fig 7). The parietal bone is most frequently affected. Cephalohematomas may be associated with the fracture. Several studies have shown that there is no relation between the size of a cephalohematoma and the presence of a linear fracture.4 Fractures are typically diagnosed by CT, but may be difficult to recognize if the fracture is within the plane of image reconstruction. Multiplanar reconstructions and/or 3dimensional (3D) reconstructions may be helpful. Alternatively, linear high-resolution ultrasound (US) can identify fractures. MRI should be considered if an intracranial lesion is noted or if the CT findings do not explain the neurological symptoms. Depressed Calvarial Fractures

Depressed fractures are typically recognized by a deformity of the skull shape on inspection or palpation. Depressed skull frac-

tures are often associated with additional extra- and intracranial hematomas. The borders of the fracture may be obscured by the associated extracranial hematomas on palpation. The softness of the skull makes the neonatal skull at risk for a characteristic neonatal fracture known as “ping pong ball” fracture (Fig 8). The skull is in this case indented like a “ping pong ball” and surgical intervention may be necessary to achieve an adequate remodeling of the skull shape. Neurosurgical intervention is particularly indicated in the setting of associated complications such as increased intracranial pressure, cortical compression, or underlying hematoma. Occipital Osteodiastasis

Occipital osteodiastasis is a unique postnatal finding characterized by a separation of the squamous and occipital bony plates (Fig 9) due to an anterior displacement and upward rotation of the squamous portion of the occipital bone by suboccipital pressure.6 Occipital osteodiastasis typically occurs after breech delivery and is associated with an increased risk of posterior fossa subdural hematomas (SDH) as well as injury to the brain stem and cerebellum. Familiarity with the unique neonatal anatomy of the occipital bone increases the detection rate. Sagittal images as well as a 3D reconstruction of the bony

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Fig 13. (A) Multiplanar contrast-enhanced 3D CT images of a 3-week-old female newborn skull demonstrate the limited bony coverage of the superior sagittal sinus and adjacent bridging veins at the level of the anterior fontanel and along the course of the open sagittal suture. (B) Sagittal and coronal color-coded Doppler US images through the anterior fontanel demonstrate the course of the superior sagittal sinus and adjacent veins that bridge the subdural and subarachnoid space. The dura appears mildly hyperechogenic. skull facilitate diagnosis. If CT identifies occipital osteodiastasis, MRI should be considered because of its higher sensitivity for soft tissue lesions in the posterior fossa. Alternative first-line imaging may include linear high-resolution US, which can document the bony displacement easily. Additional images through the mastoid or posterior fontanel and suboccipital views can show posterior fossa SDHs and cerebellar hemorrhages. Sutural Diastasis

Any suture may be widened either due to direct injury (fracture extending toward the suture or intermittent shift of bony plates due to shear forces) or secondary to adjacent intracranial hematomas or increased intracranial pressure (Fig 10). Typically, the coronal, sagittal, or lambdoid sutures are involved. The 3D reconstructions of the skull typically show the widened sutures. Alternatively, linear high-resolution US should be considered as a valuable bedside imaging modality that can document widened sutures. The differential diagnosis of sutural diastasis includes untreated hypothyroidism, which causes a general defect in skeletal ossification and delayed closure of sutures and fontanels.

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Leptomeningeal Cysts

Leptomeningeal cysts are unique complications of pediatric skull trauma, which may present as so-called “growing fractures.” In this rare entity, the sustained fracture does not heal but on the contrary gradually enlarges on follow-up. It is believed that for this entity to occur, injured or torn leptomeninges become trapped within the fracture line preventing fracture healing. In addition, the propagation of cerebrospinal fluid pulse waves may result in progressive resorption of the bone along the fracture lines. On imaging, the fracture line is wide with herniation of leptomeninges through the fracture line. Typically, the bony edges are smooth or scalloped. In rare instances, a dural tear may also occur at the level of a fontanel secondary to a faulty positioning of a vacuum extractor resulting in a “growing fontanel” (Fig 11).8 In most cases, the leptomeningeal cysts present as a palpable scalp mass. However, occasionally the child may present only with pain on palpation. First-line imaging should include a high-resolution head US examination followed by either a CT or MRI. In a small proportion of cases, simultaneous intracranial lesions including parenchymal defects may be present.

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known posttraumatic lesions like epidural hematoma (EDH), SDH, subarachnoid hemorrhage (SAH), IVH, and parenchymal contusion or laceration. The intracranial lesions may occur isolated or more frequently in various combinations. Considering the biomechanical properties of the neonatal skull and the limited protection of major dural sinuses like the superior sagittal sinus (Figs 13A,B), it is astonishing that intracranial hematomas are not seen more often after delivery. Epidural Hematoma

Fig 14. (A) The 3D CT reconstruction of the inner surface of the skull in a 1-month-old male newborn and an adolescent subject. In the newborn time period, the inner contour of the skull is smooth, compared to the adolescent skull and no apparent groove is noted for the middle meningeal artery and its branches in the neonate. (B) Coronal, axial, sagittal, and 3D CT images of a 1-day-old female newborn with a moderate-sized hyperdense right parietal EDH (arrows). The hematoma appears biconvex and is limited by the adjacent sutures. A mild vertical displacement of the parietal bone is noted. In addition, a small focal cephalohematoma (arrowheads) is present.

Nonaccidental Skull Fractures

The clinical history and reported trauma mechanism should always be carefully correlated with the encountered imaging findings (Figs 12A,B). Unfortunately, also in the immediate postnatal time period, nonaccidental injury may occur. If the story does not match the imaging findings or if the findings are “unusual” with multiple simultaneous lesions at multiple locations, nonaccidental injury should always be considered to protect the child from further injury. A close collaboration between the clinician and radiologist is essential in this scenario. Unexplained fractures may also be caused by a variety of bone diseases which have to be considered as differential diagnoses in suspected nonaccidental fractures. The best known of these are the various forms of osteogenesis imperfecta. Others include infantile hypophosphatasia, copper deficiency such as in Menkes disease and prematurity-related osteopenia. Parturitional Intracranial Injuries

Intracranial injuries occur in 5–6/10,000 live births in the United States. Risk factors include forceps delivery (x6), vacuum extraction, prolonged delivery, and macrosomia.3-7 A variety of lesions may be encountered, which include all well-

In EDHs, the blood is located between the calvarial bone and the periosteal or outer layer of the dura mater (Fig 1). EDHs are believed to result from shear forces and vertical overriding/molding motion of the calvarial bones with concomitant injury to the dura. EDHs are frequently arterial in origin but may also be venous. EDHs are more often seen after instrumented deliveries. Surgical evacuation may be necessary in cases of significant brain compression or midline shift. EDHs are frequently associated with a cephalohematoma or a skull fracture with secondary injury to the middle meningeal artery. Prognosis is favorable for neonates with isolated EDHs, while outcome is poorer for newborns with associated injuries including SDH, IVH, or SAH. Overall, EDHs are rare in neonates (2% of all intracranial hemorrhages) and may be related to the fact that the middle meningeal artery is not yet embedded or immobilized within the skull. In neonates, the groove for the middle meningeal artery is either nonexistent or very shallow (Fig 14A). In neonates, EDHs are usually close to the sutures but rarely cross the sutures. If the EDH results from an injury to the major dural sinuses like the superior sagittal sinus or transverse sinus, the adjacent sutures may be crossed. On CT and MRI, the density or signal characteristics of the EDH, respectively, varies depending on the time interval between the injury and imaging. On CT, a high- or wide window-level setting may be necessary to differentiate the hematoma from the adjacent skull (Fig 14B). The EDHs are usually well demarcated by the elevated dura, appear lenticular (biconvex) in shape, rarely cross the sutures, and may exert mass effect on the adjacent brain tissue. Due to their peripheral location, EDH may go undetected by head US, because they are obscured by the bony edges of the fontanels. Subdural Hematoma

In SDHs, blood collects in the virtual space between the dura and arachnoid membrane (Fig 1). The hemorrhage is usually venous and is believed to result from shear forces that tear the bridging veins or dural sinuses. Skull molding and sutural diastasis are more frequently linked to dural sinus injury. SDHs are the most frequently encountered intracranial hemorrhages accounting for about 70% of neonatal intracranial hemorrhages and may extend over an entire hemisphere, cross sutures, extend from the supra- into the infratentorial space, and may extend along the falx cerebri or tentorium cerebelli.9 In addition, they may extend into the spinal canal (Fig 15A). While a significant subdural hemorrhage is most often related to birth trauma, a small subdural may be commonly noted when MRI is performed in asymptomatic full-term neonates. Clinical symptoms include irritability, poor feeding, apnea, seizures, or

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Fig 15. (A) Axial and sagittal T1- and axial diffusion-weighted MR images of a 1-week-old female newborn with bilateral T1-hyperintense occipital SDHs (arrows). The hematoma is seen above and below the tentorium cerebelli. In addition, an SDH is seen within the upper dorsal cervical spinal canal. Incidental note is made of a focal hemorrhagic thromboembolic infarct in the left paracentral region which appears bright in diffusion-weighted image (arrowhead). (B) Axial CT and sagittal T1-weighted MRI of a 2-day-old female newborn with a subtle mildly CT-hyperdense and T1-hyperintense occipital SDH. On CT, the dural sinuses appear physiologically mildly hyperdense. The hematoma (arrow) is slightly denser than the dural sinus allowing differentiation. On MRI, acute blood appears prominently T1-hyperintense next to the relatively hypointense dural sinus.

bradycardia. On CT and MRI, the density and signal characteristics, respectively, again depend on the time interval between hemorrhage and imaging. Typically, SDHs are less well defined compared to EDHs, follow the contour of the brain surface, and efface the sulci. In addition, SDHs may be difficult to differentiate from the adjacent physiological dense dural sinuses on CT. Dural sinuses frequently appear more dense in neonates on CT compared to older children due to the high hematocrit, higher density of fetal hemoglobin, and the low attenuation of the neonatal brain due to the high water content and immature myelination. High- and wide window-level settings with multiplanar CT reconstructions and the use of fluid-attenuated inversion recovery (FLAIR) sequences on MR may enhance its differentiation (Fig 15B). US including color-coded duplex

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sonography performed at the asterion usually allows to differentiate between an SDH close to the dural sinuses, a normal dural sinus, and dural sinus thrombosis reliably. Transfontanellar US may however be limited if the SDH is small and/or located distant to the acoustic window/fontanel. Neuroimaging may assist in dating intracranial hemorrhages.10 Depending on the encountered densities on CT and signal intensities on the various MRI sequences, the age of the hematomas can be estimated. On CT, it is accepted that an SDH is hyperdense during a period of about 8 days. After then it becomes isodense and 2-3 weeks after hemorrhage the density of the hematoma will be lower than that of the brain and closer to that of CSF. Hyperacute extraaxial hemorrhages are typically hypointense on T1- and hyperintense on

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Fig 16. Axial CT in soft tissue and bone window algorithm and susceptibility-weighted (SWI) MR images of a 1-day-old male neonate with a comminuted left parietal skull fracture (arrowhead) and a combination of a multicompartment extracranial hematoma, SDH, and SAH. The SAH is especially well seen on the SWI image (arrows), characterized by a SWI-hypointense signal following the course of the brain sulci.

Fig 17. Coronal US, coronal and axial CT in soft tissue and bone window algorithm and axial T2-weighted and SWI images of a 1-day-old male newborn with a left temporal skull fracture (arrowhead) and adjacent intraparenchymal temporal lobe hemorrhage (arrows). The hematoma is seen along the periphery of the field of view of the coronal US image. CT and MRI show the combination of the intraparenchymal hemorrhage as well as the overlying subdural and subarachnoid blood in direct proximity to the skull fracture. The hemorrhage is prominently hypointense on the SWI image. T2-weighted images, while acute extraaxial hemorrhages are hyperintense on T1- and hypointense on T2-weighted images. In the early subacute stage, extraaxial hemorrhages remain hyperintense on T1- and become isointense on T2-weighted images. The exact timing of intracranial hematomas may however be challenging. There is, however, a considerable overlap between the different phases and various additional factors may delay or accelerate the signal evolution over time. The hematocrit level is known to play a role, as well as the temporal occurrence of the hematoma (one time acute hemorrhage vs. multiphase recurrent hemorrhage), mixture with CSF, arterial versus venous hemorrhage, and primary location of the hemorrhage (epidural, subdural, subarachnoid, etc) to mention a few. It is consequently difficult to exactly time a hemorrhage solely based upon the imaging characteristics. This may have significant implications for medicolegal questions in which

an exact timing of a hemorrhage based upon the imaging is frequently pursued. Subarachnoid Hemorrhage and Intraventricular Hemorrhage

SAH relates to blood products within the space between arachnoid membrane and pia mater (Fig 1). Parturitional SAH typically result from a rupture of the small veins bridging the leptomeninges or may be secondary to a subarachnoid rupture and extension of intracerebral or intraparenchymal hemorrhage. SAHs are the second most common intracranial hemorrhages and are often associated with IVH. Intraventricular blood may reach the basilar subarachnoid space secondary through the foramina of Luschkae and Magendie.6 Neonates may present with seizures, hypotonia, irritability, apnea, somnolence, or focal neurological symptoms. Isolated SAH with or without IVH usually has a good prognosis. However,

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cisterns. Frequently, SAH/IVH is present together with other intracranial hemorrhages like EDH or SDH (Fig 16).

Parenchymal Hemorrhages

Fig 18. Radiography of the right clavicle of a 1-month-old boy shows a mildly displaced mid clavicular fracture (arrow) secondary to shoulder dystocia.

Isolated parenchymal hemorrhages (IPH) are rarely seen secondary to parturitional injury. Typically, parenchymal hemorrhages are seen in combination with a skull fracture, often secondary to or aggravated by direct traumas (eg, instrumented delivery), coagulation disorders (deficient coagulation factors or neonatal alloimmune thrombocytopenia),11 or a preexisting AVM. Parenchymal hemorrhages may occur even prenatally such as in fetuses with a mutation in the COL4A1 and COL4A2 genes.12 Seizures are the most common presenting symptoms in newborns with parenchymal hemorrhages, but symptoms depend on the extent and location of the hemorrhage. IPHs are typically well seen on transfontanellar US as a focal hyperechogenic mass lesion. CT and MRI can identify the hemorrhage in better detail and the density/signal characteristics, respectively, frequently allow in dating the hematoma (Fig 17). Moreover, early complications may be identified.

Arterial Ischemic Stroke

Fig 19. Axial and coronal high-resolution T2-weighted MRI of the spinal canal using a myelography technique of a 5-week-old boy shows a right-sided pseudomeningocele (arrows) with avulsion of several nerve roots after shoulder dystocia. On the left, the intact nerve roots appear hypointense outlined by hyperintense cerebrospinal fluid.

secondary hydrocephalus may develop because of obstruction of the fourth ventricle by clot formation or by subarachnoid adhesions over the convexities. SAH and IVH are usually well seen on CT and MRI; FLAIR sequences are especially helpful to identify the blood products within the sulci as hyperintense signal. IVHs frequently show sedimentation of corpuscular blood elements within the dependent parts of the ventricles outlined by cerebrospinal fluid. Transfontanellar US examination can easily depict the blood products within the dependent parts of the ventricles in IVH. In addition, hyperechogenicity within the sulci suggests SAH. Serial US may also be helpful in following the changes in the echogenicity of the subarachnoid blood products as the hemorrhage ages. Images through the mastoid fontanel are especially helpful to identify subarachnoid blood products within the basal and perimesencephalic

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Posttraumatic arterial ischemic stroke is rare in newborns.13 It may be caused by: 1) direct trauma to an intracranial vessel (eg, rupture of the middle meningeal artery due to skull facture during forceps delivery), 2) arterial compression and vasospasm due to basal convexity SDH, 3) vasospasm due to SAH, 4) stretch injuries of the arterial vessels due to extraction forces on the skull base arteries, and 5) arterial dissection of cervicocephalic arteries due to minor parturitional head trauma, eg, due to precipitate delivery. Similar to older children, the internal carotid artery is the most commonly affected vessel and the most common site of dissection is at the level of the skull base.14 The clinical presentation may include Horner’s syndrome, cranial nerve palsy, and symptoms related to secondary cerebral ischemia (eg, hemiparesis, seizures). Conventional angiography was considered the diagnostic gold standard for intracranial artery dissection. Noninvasive neuroimaging techniques such as MRI and magnetic resonance angiography have been shown to be as sensitive and specific as conventional angiography and are now considered the neuroimaging tool of choice in intracranial artery dissection. In addition, color-coded duplex US may show the dissection as well as the hemodynamic sequelae bedside.

Parturitional Head, Neck, and Spine Injuries An extensive range of additional parturitional injuries may be encountered affecting the head, neck, and spine regions.1,2,15 Head and neck injuries include clavicular fractures, as well as injuries to the brachial plexus, phrenic nerve, facial nerve, laryngeal nerve, and nasal skeleton. Despite the fact that these injuries are overall rare, they may present with various degrees of stridor, respiratory distress, feeding difficulties, and cosmetic deformities.

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Fig 20. Panel of plain radiographs, CT, and MR images of various newborns (0-10-day-old) with multiple congenital conditions which increase the risk for parturitional injuries. The top row images show a newborn with cleidocranial dysostosis with partial absence of the skull and absent clavicles. SWI images showed moderate amount of subarachnoid blood (arrows). The lower row images show children with confirmed osteogenesis imperfecta and the typical skeletal deformities with multiple fractures that may already have occurred during intrauterine life.

Fig 21. The 3D and sagittal CT and sagittal T2-weighted MR images of a 2-day-old male newborn with a bony cervical spine malformation/deformity related to atelosteogenesis type III. This newborn is at increased risk for injuries to the spinal cord and lower brainstem during delivery.

Clavicular Fracture Clavicular fractures are seen in 2.7–5.7/1,000 live births. Risk factors include macrosomia and shoulder dystocia. Clavicular fractures may be a lead sign for additional injuries to the brachial plexus, phrenic nerve, or right recurrent laryngeal nerve (Fig 18).

Brachial Plexus Injury Brachial plexus injury is seen in 1/1,000 live births. Historically, brachial plexus injuries were described as Erb or Klumpke palsy depending on which nerves of the brachial plexus were injured. In Erb’s palsy, the upper motor neurons (C5/6) are involved resulting in a lack of the Moro reflex while in Klumpke’s

palsy, the lower motor neurons (C7/T1) are affected resulting in the lack of the Moro and grasp reflexes. In addition, Horner syndrome may be present due to a simultaneous injury to the sympathetic fibers of T1. Isolated Klumpke’s palsy is extremely rare and Klumpke’s palsy is almost always associated with Erb’s palsy as a complete plexus injury resulting in atonic “flail limb” and Horner’s sign. In most cases, a spontaneous recovery is the rule. US and CT have little value in the diagnostic work-up of these patients. High-resolution heavily T2-weighted MRI and diffusion tensor imaging (DTI) may show a traumatic pseudomeningocele as well as a disrupted nerve root (Fig 19). DTI is evolving as a new technique that allows studying the integrity and course of the brachial plexus fibers.

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Facial Nerve Palsy Facial nerve palsy is seen in 0.8% of birth trauma and is linked to forceps deliveries. An inadequate positioning of the posterior blades may compress the facial nerve in the region of the parotid gland and cheek. In addition, facial nerve palsies are seen in 33% of spontaneous deliveries. Boys are affected twice as often as girls. Spontaneous recovery usually occurs within hours to weeks. There is no value for imaging other than to rule out developmental nerve palsy (eg, Moebius syndrome).

Spine Injury Parturitional spine injuries are rare, but may be seen in difficult deliveries with deviant fetal position. Craniocervical ligamentous injuries may result from forceful hyperextension of the neck. Direct spinal cord injuries are seldom seen but should be suspected if the neonate is hypotonic with flaccid quadriplegia or paraplegia. CT or preferably MRI should be performed to evaluate the extent and quality of injury. US examinations have very little value.

Preexisting Fetal and Maternal Conditions Many prenatal conditions may increase the risk for parturitional injuries. Congenital heart disease, neonatal coagulation disorders, brain malformations, skeletal dysplasias (eg, cleidocranial dysostosis), osteogenesis imperfecta, or spinal anomalies (eg, atelosteogenesis) can result in a complicated delivery (Figs 20 and 21). Prenatal injuries to the central nervous system (eg, intrauterine stroke; Fig 19) may delay or complicate delivery and possibly result in additional parturitional injuries. A complete and expert prenatal screening is essential to determine and guide the mode of delivery in order to prevent or limit degree and extent of parturitional injury. Finally, fetomaternal pelvic disproportion should be recognized before an emergent instrumented delivery becomes necessary. Nowadays, MR pelvimetry allows determining if a spontaneous delivery is possible or a Cesarean section should be pursued.

Summary Parturitional injuries involving the skull, central nervous system, head and neck region, and spine may be seen. Neonates

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may present with various “bumps and lumps,” and accurate differentiation is essential for management and prognosis. In addition, multiple simultaneous intracranial lesions may be seen. These parturitional injuries can easily be classified based upon their anatomical location. Familiarity with the anatomy is a sine qua non for accurate identification. Lesions should be differentiated from preexisting pathologies and additional risk factors are to be recognized.

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