Parturitional Injury of the Head and Neck

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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, MDFrom the Section of Pediatric Neuroradiology, Division of Pediatric Radiology, Russell H. Morgan Department of Radiology and Radiological Science, The Johns HopkinsUniversity School of Medicine, Baltimore, MD (TAGMH, TB, AT, AP); Department of Art as Applied to Medicine, The Johns Hopkins University, Baltimore, MD (TP)

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 correspon-dence to Thierry A.G.M. Huisman, MD,Director of Pediatric Radiology andPediatric Neuroradiology, The RussellH. Morgan Department of Radiologyand Radiological Science, The JohnsHopkins School of Medicine, Char-lotte R. Bloomberg Children’s Center,Sheikh Zayed Tower, Room 4174, 1800Orleans Street, Baltimore, MD 21287-0842, USA. E-mail: [email protected]

J Neuroimaging 2014;00:1-16.DOI: 10.1111/jon.12144

A B S T R A C TParturitional injuries refer to injuries sustained during and secondary to fetal delivery.The skull, brain, and head and neck regions are frequently involved. Accurate differen-tiation and classification of the various injuries is essential for treatment, prognosis,and parental counseling. In this review, we discuss the various “bumps and lumps” thatmaybe encountered along the neonatal skull as well as the most frequent calvarial andintracranial parturitional injuries. In addition, a short discussion of the most commonhead and neck, facial, and spinal lesions is included. Various mimickers and risk factorsare also presented.

IntroductionParturitional injury relates to any condition that affects the fe-tus adversely during labor and delivery.1 In the past decades,the improving pre-, peri-, and postnatal care has dramaticallydecreased the incidence of parturitional injuries. Currently,birth trauma is reported to occur in less than 3% of all livebirths in the United States. In addition, parturitional injury ac-counts for less than 2% of all neonatal deaths in the UnitedStates.

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, prim-iparity, and history of a macrosomic infant. Fetal risk factorsinclude macrosomia (birth weight >3,500 g), delayed and pro-longed delivery, abnormal fetal presentation (eg, breech presen-tation), instrumented delivery, perinatal depression, and shoul-der dystocia.1 Depending on the severity of parturitional injury,the impact on the short- and long-term quality of life of theneonate may be significant. In addition, even when the parturi-tional injuries are mild or benign, this may result in significantanxiety for the family.

Accurate diagnosis of parturitional injury is mandatory toguide treatment, prevent secondary complications, and to coun-sel the parents. Parturitional injury is typically classified in 2 ma-

jor categories; birth injury and birth trauma.2 Birth injuries re-sult from various combinations of hypoxia/hypoperfusion andinfection, while birth trauma results from the direct impact ofmechanical forces exerted to the fetus during labor and deliv-ery. In this manuscript, we will focus on the imaging findingsrelated to birth trauma involving the neonatal brain and skull.In addition, a short discussion will be included of injuries to theneonatal spinal cord and the head and neck region.

Parturitional Skull and Brain InjuriesIn the immediate postnatal time period, a wide spectrum ofextracranial, cranial (skull), and intracranial lesions may beencountered.3-7 Depending on the severity and type of the in-jury, location of the lesion, exerted mass effect on adjacentbrain structures, development of primary (eg, anemia and hy-povolemic shock in subgaleal hematomas), and/or secondary(eg, hyperbilirubinemia in subgaleal hematomas and secondaryischemic lesions in skull fractures with midline shift) complica-tions and presence of complicating factors outside of the centralnervous system (eg, systemic hypoxia, hypoperfusion, or sep-sis), various degrees of reversible or irreversible brain injurymay result. It is therefore essential to diagnose parturitionalinjury quickly as well as with high sensitivity, specificity, and

Copyright ◦C 2014 by the American Society of Neuroimaging 1

Fig 1. (A) Coronal section across the top of the skull with normal display of the various anatomical spaces and structures form outside toinside: 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 whitematter. (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 fluidcollection, red for a sanguineous fluid collection. (C) Coronal section across the top of the skull showing parturitional, intracranial injuriesincluding EDH, SDH, and SAH.

reliability in order to initiate appropriate treatment as soon aspossible.

Depending on the anatomical location, parturitional injuriesmay be classified in to various groups.3,4,6,7 Extracranial injuriesinclude: a) scalp abrasions/lacerations; b) caput succedaneum;c) subgaleal hematomas; and d) cephalohematomas. Cranial orskull injuries include: a) fractures (linear or depressed); b) lep-tomeningeal cysts; and c) sutural diastasis including occipitalosteodiastasis. Intracranial injuries include a) epidural hemor-rhage; b) subdural hemorrhage; c) subarachnoid and intraven-tricular hemorrhage (IVH); and d) intraparenchymal hemor-rhage. All these lesions may occur in isolation, but more fre-

quently combined injuries are noted. For the accurate clinicaland radiological diagnosis, familiarity with the various anatomi-cal spaces is a prerequisite (Fig 1).7 In the following paragraphs,we will review the neuroanatomy as well as the various kindsof parturitional injury.

Parturitional Extracranial Injuries

The various extracranial lesions may look very similar on initialclinical evaluation and typically present as “bumps or lumps.”Depending on their etiology, location, and composition, theclinical 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 amacrosomic 1-day-old female newborn (diabetic mother, shoulder dystocia) with a caput succedaneum (arrows). A large “bump” is noted alongthe parietal region of the skull. Matching T1-weighted MR images show a large T1-hypointense serous fluid collection in the space between skinand galea aponeurotica. The fluid collection extends over the midline across the sagittal suture. Follow-up MRI shows complete spontaneousresolution of the fluid collection.

Fig 3. Axial and coronal CT images of a 9-day-old female new-born with a large predominantly left-sided hyperdense subgalealhematoma (arrows). The hyperdense hematoma is located in thespace between the galea aponeurotica and calvarial periosteum.The hematoma crosses the lambdoid and sagittal sutures. In addi-tion, the hematoma extends deep into the neck region. An additionalsmaller and less dense serous-sanguineous fluid collection is notedbetween the skin and galea aponeurotica compatible with a coexist-ing caput succedaneum.

skull from the outside inward, the various fascial and tissueplanes can be identified. The outermost layer is the skin andsubcutaneous fat followed by the galea aponeurotica or epicra-nial aponeurosis which covers the periosteum of the calvarialbone. Serous, sanguineous, and serosanguineous fluid collec-tions can be seen in the various compartments between theselayers.

Scalp Abrasions and Lacerations

Scalp abrasions and lacerations are frequently noted after bothvaginal and instrumental deliveries. Lesions may be noted alongthe scalp, face, cheek, and in the region of the ears. After vaginaldelivery, the distribution of abrasions usually depends on thefetal presentation at delivery. After an instrumental delivery,distinct skin markings may be noted which match the appliedinstrument (vacuum cup or forceps blades). Additional iatro-genic scalp abrasions and lacerations include needle punctureof the fetal head as a result of blood sampling during deliv-

ery or scalp laceration secondary to the surgical opening of theamniotic sac during a Cesarean section. The last one occursparticularly when the Cesarean section is technically difficult.These lesions may be worrisome for the parents, but are rarelyof clinical significance. Most skin lesions resolve within a coupleof days without complications. A skin laceration may occasion-ally act as a port of entry for infection and should be treatedaccordingly.

Caput Succedaneum

A caput succedaneum refers to a predominantly serous or occa-sionally a serous-sanguineous fluid collection within the scalplocated in the compartment between skin and galea or epi-cranial aponeurosis (Fig 1). A caput succedaneum typically re-sults from high pressure exerted on the infant’s head duringlabor. These lesions are most often located along the present-ing portion of the scalp, usually within the region of the vertex.A caput succedaneum is typically present at delivery and de-creases spontaneously within the first 24-48 hours. The swellingis soft, has irregular margins, and may show small petechialhemorrhages, purpura, and/or ecchymosis. Pitting edema is of-ten seen. The subcutaneous fluid collection may shift from sideto side with varying head position and characteristically crossessutures, with frequent extension across the midline. The 20-40%of all vacuum extractions are complicated by a caput succeda-neum, which is as an “artificial caput,” also known as “chignon”named after the distinguished fashionable female French hairdress. A caput succedaneum is also seen after difficult, pro-longed deliveries, typically in primigravidas and in cases ofpremature rupture of the membranes (PROM). The lack of anadequate amount of amniotic fluid due to the PROM increasesthe risk for a caput succedaneum. A caput succedaneum mayalso be present intrauterine in the presence of oligohydram-nios and due to Braxton-Hicks contractions. Treatment is rarelynecessary and outcome is usually favorable. Neuroimaging isperformed to exclude a subgaleal hematoma. On imaging, thecaput succedaneum is seen as a focal subcutaneous fluid collec-tion, superficial to the galea aponeurotica and may cross cranialsutures or the midline (Fig 2).

Huisman et al: Parturitional Injury 3

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 a1-month-old girl. Multiple sutures are shown on this 3D CT reconstruction. The sagittal suture typically limits extension of a cephalohematomaacross the midline. Cephalohematomas may however cross the midline in the occipital region because the occipital bone is not divided bya midline suture. Familiarity with the location of the various sutures is mandatory for accurate diagnosis. (C) Plain radiography (5-week-old girl), axial CT (3-week-old boy) in soft tissue and bone window algorithm, and a 3D skull reconstruction (6-month-old boy) show 3examples of calcified cephalohematomas. On plain radiography, the calcified hematoma (arrows) typically follows the contour of the skullwith simultaneous elevation of the overlying soft tissues. On CT, ongoing calcification may result in a peripheral, shell-like calcification witha hypodense organizing central hematoma between the peripheral calcification and adjacent calvarium. If the calcification progresses, thecalcified hematoma can become incorporated within the skull with a resultant deformity. On CT, this may appear as a focal thickening of theskull 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 locatedbetween the calvarial periosteum and bony calvarium. The hematoma is limited by the sagittal and lambdoid sutures. Mild amount of subduralblood is noted intracranially along the falx cerebri and left tentorium cerebelli. (E) Sagittal, coronal, and axial CT images of a 10-day-old malenewborn with bilateral serous-sanguineous, mixed hypo-/hyperdense cephalohematomas (arrows). Both hematomas are limited by the sagittaland coronal sutures bilaterally.


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

Subgaleal Hematoma

A subgaleal hematoma is a predominantly sanguineous andoccasionally a serous-sanguineous fluid collection locatedbetween the galea aponeurotica and calvarial periosteum(Fig 1). It may be mistaken for a caput succedaneum because thehematoma and clinically appreciable swelling may also crosscranial sutures. A subgaleal hematoma is not always clinicallyapparent immediately postpartum but may develop or enlargeover the first few hours or days after delivery. A subgalealhematoma is believed to result from tearing of the emissaryveins which connect the intracranial dural sinuses with the scalpveins (Fig 1). Subgaleal hematomas are often encountered aftera vacuum-assisted delivery, but may also occur spontaneouslyor secondary to a skull fracture or rupture of a synchondro-sis. Most importantly, a subgaleal hematoma should be rec-ognized early and correctly differentiated from a caput suc-cedaneum. Most subgaleal hematomas show a benign courseand do not require treatment with complete resolution within2-3 weeks. However, large subgaleal hematomas may be a po-tentially life-threatening condition. The subgaleal space extendsin its anterior-posterior direction from the orbital ridges, wherethe galea aponeurotica or epicranial aponeurosis attaches to-ward the posterior neck along the superficial neck fascia. Thesubgaleal space if filled is estimated to potentially contain upto 260 ml of blood in term infants. Given the fact that terminfants have about 85 ml of blood per kg bodyweight, a largesubgaleal hematoma may result in hypovolemic shock and pos-sible neonatal death. Development of large-sized hematomas

is also facilitated by the fact that the galea aponeurotica hasno effective tamponading characteristics or mechanism. Var-ious coexisting inborn or acquired bleeding disorders (eg,vitamin K deficiency, thrombocytopenia, hemophilia, con-sumption coagulopathy secondary to septicemia) may furthercomplicate subgaleal hematomas. Occasionally, a packed redcell transfusion, infusion of blood products, or a surgical evac-uation is required. Finally, with a large hematoma, the neonatemay develop symptomatic hyperbilirubinemia or jaundice. Oncomputed tomography (CT) images, the subgaleal hematomais seen as an iso- or hyperdense fluid collection that may crosssutures, can extend into the neck region and is deep to the galeaaponeurotica (Fig 3).

Cephalohematoma

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


Fig 6. (A) Fetal T2-weighted MRI, lateral radiography, and 3D CT reconstruction of a fetus with an occipital meningocele (arrows) whichpresented as a focal “bump” on delivery located within the occipital region. On follow-up, the bony defect progressively enlarged requiringreconstructive 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 whichwas used for external cerebrospinal fluid drainage because of hydrocephalus as a complication of a IVH. A moderate-sized subgaleal fluidcollection (arrowheads) is noted as well as a focal herniation of infarcted/injured brain tissue through the burr hole (arrows). (D) Coronal andsagittal contrast-enhanced CT images in soft tissue and bone window algorithm of a 1-month-old male newborn with a focal “bump” due to avariant sinus pericranii (arrows). A conglomerate of veins is noted extending through a focal skull defect from the superior sagittal sinus towardthe adjacent subgaleal space.

a 2:1 predominance for the right side compared to the left.These hematomas may be unilateral and/or bilateral, and maycross the midline in the occipital region (Fig 4B). Because ofthe frequent coexistence of a caput succedaneum and/or asubgaleal hematoma, the sutural boundaries may be obscuredon palpation. Cephalohematomas are more common in prim-igravidas, fetal macrosomia, instrument-assisted delivery, pro-

longed and/or difficult labor, or if the fetus is in a deviant posi-tion. Cephalohematomas may also be present in utero in casesof oligohydramnios as well as in cases of premature and/orPROM. For unknown reasons, cephalohematomas are twice asoften encountered in boys compared to girls. On inspection, theoverlying skin is typically not discolored and the mass cannotbe transilluminated or shifted with palpation. Frequently, the


Fig 7. Axial bone and soft tissue CT image of a 10-day-old fe-male 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 in-tracranial hematoma is seen.

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

Fig 9. The 3D bone CT (2-month-old boy) reconstruction of the pos-terior skull base. The synchondrosis between the squamous and oc-cipital bony plates of the occipital bone (arrows) is at risk for disruptionwith resultant shift of the bony plates known as occipital osteodias-tasis. This may occur secondary to significant suboccipital pressureduring delivery.

Staphylococcus aureus superinfection. Cellulitis, osteomyelitis,or meningitis may occur, especially if scalp electrodes havebeen applied overlying the region of the hematoma, or afterneedle aspiration of the hematoma. Finally, during follow-up,the cephalohematomas may calcify, occasionally resulting in asignificant skull deformity (Fig 4C). In rare cases, a surgical aug-mentation of the bony prominence is indicated if conservativetreatment using a molding helmet has failed. On imaging, thesehematomas are iso- or hyperdense on CT, do not cross thesutures, and appear well-contained by the overlying elevatedperiosteum (Figs 4D,E).

Combined Extracranial Hematomas

In practical “daily life,” an accurate differentiation betweenthe various extracranial “bumps” may be difficult becausefrequently several hematomas affecting multiple compartmentsare 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.


Fig 10. Multiplanar 3D CT reconstruction of the bony calvarium of a 17-day-old male newborn with sutural diastasis secondary to significantlyincreased 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 aleptomeningeal cyst (arrows) after faulty positioning of a vacuum extractor. The dural defect is well seen on US, a large subgaleal fluid collectionis noted which communicates with a focal brain defect within the left superior frontal gyrus. Lateral skull radiography shows the progressivelyenlarging skull defect adjacent to the extracranial “bump.”

therefore be difficult (Fig 5). Familiarity with the imaging char-acteristics of the various extracranial “bumps” with high-qualityimaging, good clinical information including data about themode of delivery, gestational age at delivery, local physicalfindings, and temporal evolution of the “bump” usually allowsaccurate classification of the hematoma.

Differential Diagnosis

Several “other” pathologies may also present with a calvarial“bump or lump” at delivery. Differential diagnosis may includea meningoencephalocele, an epidermal inclusion cyst, a sinuspericranii, scalp arteriovenous malformations (AVM), or evena posttraumatic encephalocele, to mention a few. Hydrops fe-talis may result in a significant subcutaneous scalp edema andis usually easy to diagnose/differentiate because the fetus is typ-ically affected with subcutaneous edema extending along theentire fetus. If the birth history, clinical or physical examina-tion, or follow-up findings do not explain the presentation, analternative diagnosis should be considered. Based on clinicalhistory and examination, differentiation between extracranial

hematomas and other calvarial “bumps or lumps” is usuallystraightforward. If this is not the case, additional cross-sectionalimaging usually allows to make the accurate diagnosis (Figs6A–D).

Parturitional Calvarial Injuries

The neonatal skull is unique in its biomechanical proper-ties. The skull basically consists of a combination of mul-tiple mildly ossified bony and partially cartilaginous platesthat are separated from each other by multiple sutures, syn-chondroses, and fontanels. The various elements of the skullmay shift to a certain degree in relation to each other dur-ing delivery, but due to their inherent “softness,” they arealso at risk for dents, fractures, and dural tears. Conse-quently, a spectrum of calvarial injuries may be encoun-tered related to spontaneous or instrument-assisted traumaticdelivery.

Skull injuries or fractures must be suspected if a cephalo-hematoma or intracranial hemorrhage is present. Skull injuriesare caused by compression forces during labor while the skull


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 downfrom the couch while the mother was nursing the child. A linear mildly displaced right parietal fracture (arrows) is noted with an adjacentextracranial hematoma (arrowhead). (B) Axial CT images of a male newborn who fell out of the arms of the father who was walking down astaircase. A nondisplaced right parietal fracture is noted (arrow) with an adjacent extracranial hematoma. In addition, a moderate-sized SDHis noted anterior to the temporal lobe.

is being pushed against the maternal pelvis or may occurdue to the pressure exerted by forceps blades. The most fre-quent skull injuries that are encountered include linear or de-pressed fractures, sutural diastasis, occipital osteodiastasis, orleptomeningeal cysts.

Linear Calvarial Fractures

Linear fractures are frequently asymptomatic and heal with-out intervention (Fig 7). The parietal bone is most frequentlyaffected. Cephalohematomas may be associated with the frac-ture. Several studies have shown that there is no relation be-tween the size of a cephalohematoma and the presence of alinear fracture.4 Fractures are typically diagnosed by CT, butmay be difficult to recognize if the fracture is within the planeof image reconstruction. Multiplanar reconstructions and/or 3-dimensional (3D) reconstructions may be helpful. Alternatively,linear high-resolution ultrasound (US) can identify fractures.MRI should be considered if an intracranial lesion is noted orif the CT findings do not explain the neurological symptoms.

Depressed Calvarial Fractures

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

tures are often associated with additional extra- and intracranialhematomas. The borders of the fracture may be obscured by theassociated extracranial hematomas on palpation. The softnessof the skull makes the neonatal skull at risk for a characteristicneonatal fracture known as “ping pong ball” fracture (Fig 8).The skull is in this case indented like a “ping pong ball” andsurgical intervention may be necessary to achieve an adequateremodeling of the skull shape. Neurosurgical intervention isparticularly indicated in the setting of associated complicationssuch as increased intracranial pressure, cortical compression,or underlying hematoma.

Occipital Osteodiastasis

Occipital osteodiastasis is a unique postnatal finding charac-terized by a separation of the squamous and occipital bonyplates (Fig 9) due to an anterior displacement and upward ro-tation of the squamous portion of the occipital bone by sub-occipital pressure.6 Occipital osteodiastasis typically occurs af-ter breech delivery and is associated with an increased risk ofposterior fossa subdural hematomas (SDH) as well as injuryto the brain stem and cerebellum. Familiarity with the uniqueneonatal anatomy of the occipital bone increases the detectionrate. Sagittal images as well as a 3D reconstruction of the bony


Fig 13. (A) Multiplanar contrast-enhanced 3D CT images of a 3-week-old female newborn skull demonstrate the limited bony coverage ofthe 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 andadjacent veins that bridge the subdural and subarachnoid space. The dura appears mildly hyperechogenic.

skull facilitate diagnosis. If CT identifies occipital osteodiasta-sis, MRI should be considered because of its higher sensitivityfor soft tissue lesions in the posterior fossa. Alternative first-lineimaging may include linear high-resolution US, which can doc-ument the bony displacement easily. Additional images throughthe mastoid or posterior fontanel and suboccipital views canshow posterior fossa SDHs and cerebellar hemorrhages.

Sutural Diastasis

Any suture may be widened either due to direct injury (frac-ture extending toward the suture or intermittent shift of bonyplates due to shear forces) or secondary to adjacent intracranialhematomas or increased intracranial pressure (Fig 10). Typi-cally, the coronal, sagittal, or lambdoid sutures are involved.The 3D reconstructions of the skull typically show the widenedsutures. Alternatively, linear high-resolution US should be con-sidered as a valuable bedside imaging modality that can doc-ument widened sutures. The differential diagnosis of suturaldiastasis includes untreated hypothyroidism, which causes ageneral defect in skeletal ossification and delayed closure ofsutures and fontanels.

Leptomeningeal Cysts

Leptomeningeal cysts are unique complications of pediatricskull trauma, which may present as so-called “growing frac-tures.” In this rare entity, the sustained fracture does not heal buton the contrary gradually enlarges on follow-up. It is believedthat for this entity to occur, injured or torn leptomeninges be-come trapped within the fracture line preventing fracture heal-ing. In addition, the propagation of cerebrospinal fluid pulsewaves may result in progressive resorption of the bone alongthe fracture lines. On imaging, the fracture line is wide with her-niation of leptomeninges through the fracture line. Typically,the bony edges are smooth or scalloped. In rare instances, adural tear may also occur at the level of a fontanel secondaryto a faulty positioning of a vacuum extractor resulting in a“growing fontanel” (Fig 11).8 In most cases, the leptomeningealcysts present as a palpable scalp mass. However, occasionallythe child may present only with pain on palpation. First-lineimaging should include a high-resolution head US examina-tion followed by either a CT or MRI. In a small proportion ofcases, simultaneous intracranial lesions including parenchymaldefects may be present.


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

Nonaccidental Skull Fractures

The clinical history and reported trauma mechanism shouldalways be carefully correlated with the encountered imagingfindings (Figs 12A,B). Unfortunately, also in the immediatepostnatal time period, nonaccidental injury may occur. If thestory does not match the imaging findings or if the findingsare “unusual” with multiple simultaneous lesions at multiplelocations, nonaccidental injury should always be considered toprotect the child from further injury. A close collaboration be-tween the clinician and radiologist is essential in this scenario.Unexplained fractures may also be caused by a variety of bonediseases which have to be considered as differential diagnosesin suspected nonaccidental fractures. The best known of theseare the various forms of osteogenesis imperfecta. Others in-clude infantile hypophosphatasia, copper deficiency such as inMenkes disease and prematurity-related osteopenia.

Parturitional Intracranial Injuries

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

known posttraumatic lesions like epidural hematoma (EDH),SDH, subarachnoid hemorrhage (SAH), IVH, and parenchy-mal contusion or laceration. The intracranial lesions may occurisolated or more frequently in various combinations. Consid-ering the biomechanical properties of the neonatal skull andthe limited protection of major dural sinuses like the supe-rior sagittal sinus (Figs 13A,B), it is astonishing that intracranialhematomas are not seen more often after delivery.

Epidural Hematoma

In EDHs, the blood is located between the calvarial bone andthe periosteal or outer layer of the dura mater (Fig 1). EDHsare believed to result from shear forces and vertical overrid-ing/molding motion of the calvarial bones with concomitantinjury to the dura. EDHs are frequently arterial in origin butmay also be venous. EDHs are more often seen after instru-mented deliveries. Surgical evacuation may be necessary incases of significant brain compression or midline shift. EDHsare frequently associated with a cephalohematoma or a skullfracture with secondary injury to the middle meningeal artery.Prognosis is favorable for neonates with isolated EDHs, whileoutcome is poorer for newborns with associated injuries includ-ing SDH, IVH, or SAH. Overall, EDHs are rare in neonates(2% of all intracranial hemorrhages) and may be related to thefact that the middle meningeal artery is not yet embedded orimmobilized within the skull. In neonates, the groove for themiddle meningeal artery is either nonexistent or very shallow(Fig 14A). In neonates, EDHs are usually close to the sutures butrarely cross the sutures. If the EDH results from an injury to themajor dural sinuses like the superior sagittal sinus or transversesinus, 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 andimaging. On CT, a high- or wide window-level setting may benecessary to differentiate the hematoma from the adjacent skull(Fig 14B). The EDHs are usually well demarcated by the ele-vated dura, appear lenticular (biconvex) in shape, rarely crossthe sutures, and may exert mass effect on the adjacent brain tis-sue. Due to their peripheral location, EDH may go undetectedby head US, because they are obscured by the bony edges ofthe fontanels.

Subdural Hematoma

In SDHs, blood collects in the virtual space between the duraand arachnoid membrane (Fig 1). The hemorrhage is usuallyvenous and is believed to result from shear forces that tear thebridging veins or dural sinuses. Skull molding and sutural di-astasis are more frequently linked to dural sinus injury. SDHsare the most frequently encountered intracranial hemorrhagesaccounting for about 70% of neonatal intracranial hemorrhagesand may extend over an entire hemisphere, cross sutures, ex-tend from the supra- into the infratentorial space, and mayextend along the falx cerebri or tentorium cerebelli.9 In addi-tion, they may extend into the spinal canal (Fig 15A). While asignificant subdural hemorrhage is most often related to birthtrauma, a small subdural may be commonly noted when MRI isperformed in asymptomatic full-term neonates. Clinical symp-toms include irritability, poor feeding, apnea, seizures, or


Fig 15. (A) Axial and sagittal T1- and axial diffusion-weighted MR images of a 1-week-old female newborn with bilateral T1-hyperintenseoccipital SDHs (arrows). The hematoma is seen above and below the tentorium cerebelli. In addition, an SDH is seen within the upper dorsalcervical spinal canal. Incidental note is made of a focal hemorrhagic thromboembolic infarct in the left paracentral region which appearsbright in diffusion-weighted image (arrowhead). (B) Axial CT and sagittal T1-weighted MRI of a 2-day-old female newborn with a subtle mildlyCT-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 relativelyhypointense dural sinus.

bradycardia. On CT and MRI, the density and signal character-istics, respectively, again depend on the time interval betweenhemorrhage and imaging. Typically, SDHs are less well definedcompared to EDHs, follow the contour of the brain surface, andefface the sulci. In addition, SDHs may be difficult to differen-tiate from the adjacent physiological dense dural sinuses onCT. Dural sinuses frequently appear more dense in neonateson CT compared to older children due to the high hematocrit,higher density of fetal hemoglobin, and the low attenuation ofthe neonatal brain due to the high water content and imma-ture myelination. High- and wide window-level settings withmultiplanar CT reconstructions and the use of fluid-attenuatedinversion recovery (FLAIR) sequences on MR may enhanceits differentiation (Fig 15B). US including color-coded duplex

sonography performed at the asterion usually allows to differen-tiate between an SDH close to the dural sinuses, a normal duralsinus, and dural sinus thrombosis reliably. Transfontanellar USmay however be limited if the SDH is small and/or locateddistant to the acoustic window/fontanel.

Neuroimaging may assist in dating intracranialhemorrhages.10 Depending on the encountered densitieson CT and signal intensities on the various MRI sequences, theage of the hematomas can be estimated. On CT, it is acceptedthat an SDH is hyperdense during a period of about 8 days.After then it becomes isodense and 2-3 weeks after hemorrhagethe density of the hematoma will be lower than that of thebrain and closer to that of CSF. Hyperacute extraaxial hemor-rhages are typically hypointense on T1- and hyperintense on


Fig 16. Axial CT in soft tissue and bone window algorithm and susceptibility-weighted (SWI) MR images of a 1-day-old male neonate witha comminuted left parietal skull fracture (arrowhead) and a combination of a multicompartment extracranial hematoma, SDH, and SAH. TheSAH 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 malenewborn with a left temporal skull fracture (arrowhead) and adjacent intraparenchymal temporal lobe hemorrhage (arrows). The hematoma isseen along the periphery of the field of view of the coronal US image. CT and MRI show the combination of the intraparenchymal hemorrhageas well as the overlying subdural and subarachnoid blood in direct proximity to the skull fracture. The hemorrhage is prominently hypointenseon the SWI image.

T2-weighted images, while acute extraaxial hemorrhages arehyperintense on T1- and hypointense on T2-weighted images.In the early subacute stage, extraaxial hemorrhages remainhyperintense on T1- and become isointense on T2-weightedimages. The exact timing of intracranial hematomas may how-ever be challenging. There is, however, a considerable overlapbetween the different phases and various additional factorsmay delay or accelerate the signal evolution over time. Thehematocrit level is known to play a role, as well as the temporaloccurrence of the hematoma (one time acute hemorrhagevs. multiphase recurrent hemorrhage), mixture with CSF,arterial versus venous hemorrhage, and primary location of thehemorrhage (epidural, subdural, subarachnoid, etc) to mentiona few. It is consequently difficult to exactly time a hemorrhagesolely based upon the imaging characteristics. This may havesignificant implications for medicolegal questions in which

an exact timing of a hemorrhage based upon the imaging isfrequently pursued.

Subarachnoid Hemorrhage and Intraventricular Hemorrhage

SAH relates to blood products within the space between arach-noid membrane and pia mater (Fig 1). Parturitional SAH typ-ically result from a rupture of the small veins bridging theleptomeninges or may be secondary to a subarachnoid rup-ture and extension of intracerebral or intraparenchymal hem-orrhage. SAHs are the second most common intracranial hem-orrhages and are often associated with IVH. Intraventricularblood may reach the basilar subarachnoid space secondarythrough the foramina of Luschkae and Magendie.6 Neonatesmay present with seizures, hypotonia, irritability, apnea,somnolence, or focal neurological symptoms. Isolated SAHwith or without IVH usually has a good prognosis. However,


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

Fig 19. Axial and coronal high-resolution T2-weighted MRI of thespinal canal using a myelography technique of a 5-week-old boyshows a right-sided pseudomeningocele (arrows) with avulsion ofseveral nerve roots after shoulder dystocia. On the left, the in-tact nerve roots appear hypointense outlined by hyperintense cere-brospinal fluid.

secondary hydrocephalus may develop because of obstructionof the fourth ventricle by clot formation or by subarachnoidadhesions over the convexities. SAH and IVH are usually wellseen on CT and MRI; FLAIR sequences are especially help-ful to identify the blood products within the sulci as hyperin-tense signal. IVHs frequently show sedimentation of corpuscu-lar blood elements within the dependent parts of the ventriclesoutlined by cerebrospinal fluid. Transfontanellar US examina-tion can easily depict the blood products within the dependentparts of the ventricles in IVH. In addition, hyperechogenicitywithin the sulci suggests SAH. Serial US may also be helpfulin following the changes in the echogenicity of the subarach-noid blood products as the hemorrhage ages. Images throughthe mastoid fontanel are especially helpful to identify subarach-noid blood products within the basal and perimesencephalic

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

Parenchymal Hemorrhages

Isolated parenchymal hemorrhages (IPH) are rarely seen sec-ondary to parturitional injury. Typically, parenchymal hem-orrhages are seen in combination with a skull fracture, oftensecondary to or aggravated by direct traumas (eg, instrumenteddelivery), coagulation disorders (deficient coagulation factorsor neonatal alloimmune thrombocytopenia),11 or a preexistingAVM. Parenchymal hemorrhages may occur even prenatallysuch as in fetuses with a mutation in the COL4A1 and COL4A2genes.12 Seizures are the most common presenting symptomsin newborns with parenchymal hemorrhages, but symptomsdepend on the extent and location of the hemorrhage. IPHsare typically well seen on transfontanellar US as a focal hy-perechogenic mass lesion. CT and MRI can identify the hem-orrhage 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

Posttraumatic arterial ischemic stroke is rare in newborns.13 Itmay be caused by: 1) direct trauma to an intracranial vessel (eg,rupture of the middle meningeal artery due to skull facture dur-ing forceps delivery), 2) arterial compression and vasospasmdue to basal convexity SDH, 3) vasospasm due to SAH, 4)stretch injuries of the arterial vessels due to extraction forceson the skull base arteries, and 5) arterial dissection of cervic-ocephalic arteries due to minor parturitional head trauma, eg,due to precipitate delivery. Similar to older children, the inter-nal carotid artery is the most commonly affected vessel and themost common site of dissection is at the level of the skull base.14

The clinical presentation may include Horner’s syndrome, cra-nial nerve palsy, and symptoms related to secondary cerebralischemia (eg, hemiparesis, seizures). Conventional angiographywas considered the diagnostic gold standard for intracranialartery dissection. Noninvasive neuroimaging techniques suchas MRI and magnetic resonance angiography have been shownto be as sensitive and specific as conventional angiography andare now considered the neuroimaging tool of choice in intracra-nial artery dissection. In addition, color-coded duplex US mayshow the dissection as well as the hemodynamic sequelae bed-side.

Parturitional Head, Neck, and Spine InjuriesAn extensive range of additional parturitional injuries may beencountered affecting the head, neck, and spine regions.1,2,15

Head and neck injuries include clavicular fractures, as well asinjuries to the brachial plexus, phrenic nerve, facial nerve, la-ryngeal nerve, and nasal skeleton. Despite the fact that theseinjuries are overall rare, they may present with various degreesof stridor, respiratory distress, feeding difficulties, and cosmeticdeformities.


Fig 20. Panel of plain radiographs, CT, and MR images of various newborns (0-10-day-old) with multiple congenital conditions which increasethe risk for parturitional injuries. The top row images show a newborn with cleidocranial dysostosis with partial absence of the skull andabsent clavicles. SWI images showed moderate amount of subarachnoid blood (arrows). The lower row images show children with confirmedosteogenesis 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 malforma-tion/deformity related to atelosteogenesis type III. This newborn is at increased risk for injuries to the spinal cord and lower brainstem duringdelivery.

Clavicular Fracture

Clavicular fractures are seen in 2.7–5.7/1,000 live births. Riskfactors include macrosomia and shoulder dystocia. Clavicu-lar fractures may be a lead sign for additional injuries to thebrachial plexus, phrenic nerve, or right recurrent laryngealnerve (Fig 18).

Brachial Plexus Injury

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

palsy, the lower motor neurons (C7/T1) are affected result-ing in the lack of the Moro and grasp reflexes. In addition,Horner syndrome may be present due to a simultaneous in-jury to the sympathetic fibers of T1. Isolated Klumpke’s palsyis extremely rare and Klumpke’s palsy is almost always asso-ciated with Erb’s palsy as a complete plexus injury resultingin atonic “flail limb” and Horner’s sign. In most cases, a spon-taneous recovery is the rule. US and CT have little value inthe diagnostic work-up of these patients. High-resolution heav-ily T2-weighted MRI and diffusion tensor imaging (DTI) mayshow a traumatic pseudomeningocele as well as a disruptednerve root (Fig 19). DTI is evolving as a new technique thatallows studying the integrity and course of the brachial plexusfibers.


Facial Nerve Palsy

Facial nerve palsy is seen in 0.8% of birth trauma and is linkedto forceps deliveries. An inadequate positioning of the posteriorblades may compress the facial nerve in the region of the parotidgland and cheek. In addition, facial nerve palsies are seen in33% of spontaneous deliveries. Boys are affected twice as oftenas girls. Spontaneous recovery usually occurs within hours toweeks. There is no value for imaging other than to rule outdevelopmental nerve palsy (eg, Moebius syndrome).

Spine Injury

Parturitional spine injuries are rare, but may be seen in difficultdeliveries with deviant fetal position. Craniocervical ligamen-tous injuries may result from forceful hyperextension of theneck. Direct spinal cord injuries are seldom seen but should besuspected if the neonate is hypotonic with flaccid quadriplegiaor paraplegia. CT or preferably MRI should be performed toevaluate the extent and quality of injury. US examinations havevery little value.

Preexisting Fetal and Maternal ConditionsMany prenatal conditions may increase the risk for parturi-tional injuries. Congenital heart disease, neonatal coagulationdisorders, brain malformations, skeletal dysplasias (eg, clei-docranial dysostosis), osteogenesis imperfecta, or spinal anoma-lies (eg, atelosteogenesis) can result in a complicated deliv-ery (Figs 20 and 21). Prenatal injuries to the central nervoussystem (eg, intrauterine stroke; Fig 19) may delay or com-plicate delivery and possibly result in additional parturitionalinjuries. A complete and expert prenatal screening is essen-tial to determine and guide the mode of delivery in order toprevent or limit degree and extent of parturitional injury. Fi-nally, fetomaternal pelvic disproportion should be recognizedbefore an emergent instrumented delivery becomes necessary.Nowadays, MR pelvimetry allows determining if a sponta-neous delivery is possible or a Cesarean section should bepursued.

SummaryParturitional injuries involving the skull, central nervous sys-tem, head and neck region, and spine may be seen. Neonates

may present with various “bumps and lumps,” and accurate dif-ferentiation is essential for management and prognosis. In ad-dition, multiple simultaneous intracranial lesions may be seen.These parturitional injuries can easily be classified based upontheir anatomical location. Familiarity with the anatomy is a sinequa non for accurate identification. Lesions should be differen-tiated from preexisting pathologies and additional risk factorsare to be recognized.

References1. Hughes CA, Harley EH, Milmoe G, et al. Birth trauma in the head

and neck. Arch Otolaryngol Head Neck Surg 1999;125:193-199.2. Parker LA. Part 1: early recognition and treatment of birth trauma:

injuries to the head and face. Adv Neonatal Care 2005;5:288-297;quiz 298-300.

3. Doumouchtsis SK, Arulkumaran S. Head injuries after instrumentalvaginal deliveries. Curr Opin Obstet Gynecol 2006;18:129-134.

4. Nicholson L. Caput succedaneum and cephalohematoma: the Csthat leave bumps on the head. Neonatal Netw 2007;26:277-281.

5. Pressler JL. Classification of major newborn birth injuries. J PerinatNeonatal Nurs 2008;22:60-67.

6. Reichard R. Birth injury of the cranium and central nervous system.Brain Pathol 2008;18:565-570.

7. Sharman AM, Kirmi O, Anslow P. Imaging of the skin, subcutis,and galea aponeurotica. Semin Ultrasound CT MR 2009;30:452-464.

8. Huisman TA, Fischer J, Willi UV, et al. “Growing fontanelle”: aserious complication of difficult vacuum extraction. Neuroradiology1999;41:381-383.

9. Pollina J, Dias MS, Li V, et al. Cranial birth injuries in term newborninfants. Pediatr Neurosurg 2001;35:113-119.

10. Demaerel P. MR imaging in inflicted brain injury. Magn Reson Imag-ing Clin N Am 2012;20:35-44.

11. Kamphuis MM, Paridaans NP, Porcellin L, et al. Incidence andconsequences of neonatal alloimmune thrombocytopenia: a sys-tematic review. Pediatrics 2014;epub Mar 3.

12. Vermeulen RJ, Peeters-Scholte C, Van Vugt JJ, et al. Fetal originof brain damage in 2 infants with a COL4A1 mutation: fetal andneonatal MRI. Neuropediatrics 2011;42:1-3.

13. Lequin MH, Peeters EA, Holscher HC, et al. Arterial infarctioncaused by carotid artery dissection in the neonate. Eur J PaediatrNeurol 2004;8:155-160.

14. Orman G, Tekes A, Poretti A, et al. Posttraumatic carotid arterydissection in children: not to be missed! J Neuroimaging 2013;epubNov 19.

15. Vialle R, Pietin-Vialle C, Ilharreborde B, et al. Spinal cord injuriesat birth: a multicenter review of nine cases. J Matern Fetal NeonatalMed 2007;20:435-440.


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Parturitional Injury of the Head and Neck