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Brain Trauma


INTRODUCTION

Background

Trauma is the most common cause of death and a significant cause of morbidity in children. Both accidental and nonaccidental trauma are common in children.

Several anatomic differences in younger children should be highlighted to understand why younger children are more susceptible to certain types of injury. First, the skull of young children is thin and pliable and thickens during the first 2 years of life. Second, a skull with fused sutures transfers the force of an impact throughout the skull and is more prone to fracture compared to a skull with unfused sutures. Third, an infant’s head weighs about 10% to 15% of the total body weight compared to only 2% to 3% in an adult. Fourth, the infant brain has a softer consistency because of higher water content, immature glial cells, immature myelination, and smaller axons. Consequently, the unmyelinated brain has a lower threshold for injury than an adult. Last, the neck muscles of a child are less developed and provide less protection from acceleration-deceleration trauma.

Accidental head trauma includes injuries from birth trauma, motor vehicle accidents, drowning, crush injury, and falls. Short falls that occur in and around the home from a distance of less than 6 feet are associated with focal contact injuries such as scalp contusion or laceration. About 1% to 3% of short falls in young children cause a skull fracture. The majority of these skull fractures are simple linear fractures without associated intracranial hemorrhage or neurologic deficit.The minority of fractures are associated with an epidural hemorrhage or, less commonly, a subdural hemorrhage. With short falls there is no diffuse brain injury, however falls from heights greater than 10 feet, such as those from a building, lead to greater head injury and are similar to crush injuries. Crushing head injury is relatively common in children compared to adults. Examples of crush injuries include heavy objects, such as a television falling onto the head. Crush injuries cause parenchymal contusions, lacerations, and fractures.

Epidural hemorrhages require an impact to the head and are associated with skull fractures in 85% of cases. Epidural hemorrhages usually occur from falls in young children, rather than an inflicted blow to the head, which is more likely to cause acceleration of the head and more diffuse injury. Clinical significance of an epidural hemorrhage depends on the size and rate of enlargement.

Subdural hemorrhages can result from both impact injuries as well as from inertial forces. The most common cause of subdural hemorrhage in young children is abusive head injury.

Parenchymal contusions are commonly seen adjacent to a skull fracture. However, coup and countercoup contusions are rare in children less than 4 years of age because of the soft consistency of young brains. Because a young child is already near the ground, a fall does not accelerate the head sufficiently to cause a countercoup contusion.

Abusive head trauma (AHT) accounts for the majority of head injury in children less than 1 year, and head injury is the leading cause of death from child abuse. A multidisciplinary approach is necessary as the diagnosis involves clinical history, physical examination, laboratory results, radiological findings, and scene investigation and interviews with other family members by child protective services and police. AHT has a multitude of possible imaging findings, which are demonstrated in this chapter.

Imaging

Head trauma findings seen on imaging include soft tissue contusions, lacerations, fracture, epidural hemorrhage, subdural hemorrhage, subarachnoid hemorrhage, parenchymal contusion, parenchymal laceration, axonal injury, edema, and ischemia. Radiographs, ultrasound, CT, and MRI are imaging modalities commonly used to evaluate pediatric trauma patients. Radiographs are quick and useful for determination of fractures but have become less commonly used in the acute trauma patient. CT imaging is often the initial neuroimaging study performed for assessment of head trauma due to the fast acquisition, and excellent detection of fractures and intracranial hemorrhage. MRI is more sensitive than CT for extent of intracranial trauma, particularly diffuse axonal injury and ischemia but has longer acquisition time compared to CT and may require sedation so CT is currently the initial imaging study of choice. This section illustrates the imaging findings of head trauma and related diagnoses in children seen on radiographs, ultrasound, CT, and MRI.

REFERENCES

  • 1. Case M.E.: Accidental traumatic head injury in infants and very young children. Brain Pathol 2008 Oct; 18: pp. 583-589.
  • 2. Case M.E.: Inflicted traumatic brain injury in infants and young children. Brain Pathol 2008 Oct; 18: pp. 571-582.
  • 3. Orman G., Kralik S.F., Meoded A., et. al.: MRI findings in pediatric abusive head trauma: a review. J Neuroimaging 2019; pp. 1-13.

SCALP TRAUMA

Key Points

Caput Succedaneum

  • Serosanguinous, transudative fluid between the skin and galea aponeurosis typically located at the vertex that occurs during normal birth.

  • Crosses sutures.

  • Secondary to high pressure on the infant’s head during labor. Typically seen in primigravidas, prolonged deliveries, and premature rupture of membranes (due to reduced amniotic fluid).

  • Typically diffuses quickly and becomes stable or rapidly resolves within 24 to 48 hours. Consequently, treatment is rarely necessary.

  • Imaging may be performed to exclude subgaleal hematoma (SGH).

Subgaleal Hematoma

  • Many small emissary veins traverse the loose connective tissue of the subgaleal space. A tear or tears of these emissary veins is believed to be the cause of an SGH.

  • External force such as use of vacuum extraction (associated with SGH in 60% to 89% of cases) can result in rupture of veins in the subgaleal space and subsequent hemorrhage that crosses the sutures.

  • A SGH can result in significant blood loss. A 1-cm increase in depth of the subgaleal space can contain 40 to 260 mL of blood. The circulating blood volume in a neonate is approximately 90 mL/kg body weight such that in a 3-kg neonate, a blood loss of 54 mL is a 20% loss of circulating blood volume.

  • Signs and symptoms: Boggy head with pitting edema, increasing head circumference, jaundice, eye and ear swelling. A drop in hemoglobin is a late sign of severe hemorrhage because of insufficient time for fluid shift to cause the hemodilution.

  • Severity criteria: Approximately 6% are asymptomatic, 15% to 20% are mild (<1-cm increase in head circumference, no jaundice, no hypovolemia), 40% to 50% are moderate (1–3 cm increase in head circumference, jaundice, mild hypovolemia), and 25% to 33% are severe (>3 cm increase in head circumference, jaundice, severe hypovolemia).

  • Hypoxic ischemic injury occurs in 62% to 72% of subgaleal hematomas, and brain trauma (edema or hemorrhage) occurs in 33% to 40%.

Cephalohematoma (Also Known as a Subperiosteal Hematoma)

  • Localized hemorrhage between bone and periosteum

  • More common in primigravidas, fetal macrocephaly, instrument-assisted delivery, prolonged and/or difficult labor, premature rupture of membranes, and with oligohydramnios (can occur in utero)

  • Aspiration is not performed because typically the blood has clotted and there is risk for causing infection

  • Hemorrhage can take weeks to months to resorb and can calcify to result in skull asymmetry

  • Associated skull fracture in 5% to 18%

  • Does not cross sutures and not a risk for serious blood loss due to the containment

  • Unilateral or bilateral

  • May coexist with subgaleal hematoma and caput succedaneum

  • Calcification may occur in 3% to 5% of subperiosteal hematomas. Calcified subperiosteal hematomas have been subclassified as type 1 (nondepressed inner cortex) and type 2 (depressed inner cortex)

REFERENCES

  • 1. Huisman T.A.G.M., Phelps T., Bosemani T., et. al.: Parturitional injury of the head and neck. J Neuroimaging 2015 Mar–Apr; 25: pp. 151-166.
  • 2. Colditz M.J., Lai M.M., Cartwright D., et. al.: Subgaleal haemorrhage in the newborn. Journal of Pediatric and Child Health 2015; 51: pp. 14-146.
  • 3. Wong C.H., Foo C.L., Seow W.T.: Calcified cephalohematoma: classification, indications for surgery and techniques. J Craniofac Surg 2006 Sep; 17: pp. 970-979.

BIRTH-RELATED SUBDURAL HEMORRHAGE

Key Points

Background

  • Occurs in approximately 50% births

  • No intervention or follow-up imaging in vast majority

Imaging

  • Usually small (<4 mm in thickness)

  • T1W hyperintense signal on MRI and hyperdense on CT

  • No significant mass effect, and located posterior fossa, tentorium, posterior falx, posterior occipital (<4 mm in thickness)

  • Most resolve by 1 month. All resolve by approximately3 months

  • In addition to subdural hemorrhage (SDH), can also see small amounts of subarachnoid hemorrhage (SAH) and intraventricular hemorrhage (IVH) from birth trauma

REFERENCE

  • 1. Rooks V.J., Eaton J.P., Ruess L., et. al.: Prevalence and evolution of intracranial hemorrhage in asymptomatic term infants. AJNR Am J Neuroradiol 2008 Jun; 29: pp. 1082-1089.

VENOUS SINUS HEMOCONCENTRATION

Key Points

  • Hyperdense dural sinuses can be seen on head CTs of neonates and accentuated by the relative lower density of the immature brain. Differentiation from thrombus can be difficult and result in potential pitfall.

  • Mean Hounsfield units (HU) demonstrate a correlation with hemoglobin levels (correlation coefficient r = 0.411). The mean sinus density in normal pediatric population is 44 to 47 HU.

  • Thrombosed venous sinuses measured 66 HU; however, the neonatal population has not been adequately studied.

REFERENCE

  • 1. Yurtturan N., Kizildag B., Sarica M.A., et. al.: Effect of hemoconcentration on dural sinus computed tomography density in a pediatric population. Neuropediatrics 2016 Oct; 47: pp. 327-331.

SUBPIAL HEMORRHAGE

Fig. 10.8A-L

Fig. 10.1, Locations of Scalp Hemorrhage . Layers of the scalp are the skin, galea aponeurosis, and periosteum. Caput succedaneum is between the skin and galea aponeurosis and can cross sutures. Subgaleal hematoma is between galea aponeurosis and periosteum and can cross sutures. Cephalohematoma is between the periosteum and the bone and does not cross sutures.

Fig. 10.2, Scalp Hemorrhage . Coronal T2W images demonstrating a caput succedaneum, subgaleal hematoma, and cephalohematoma.

Fig. 10.3, Subgaleal Hematoma: Multiple Patients . (A) Coronal CT image demonstrating hyperdense scalp hematoma from a subgaleal hematoma that crosses the sagittal suture and left lambdoid suture. (B) Transverse ultrasound image across the sagittal suture demonstrates a mixed echogenic subgaleal collection crossing the sagittal suture. (C) Coronal 3D T2W image of the same patient in (B) demonstrates the subgaleal hematoma with areas of T2 hypointense and hyperintense signal.

Fig. 10.4, Cephalohematoma: Multiple Patients . (A) Coronal CT image demonstrating bilateral hyperdense cephalohematomas that do not cross the sagittal suture. (B) AP skull radiograph demonstrating peripheral calcification of a left parietal cephalohematoma. (C) Axial head CT image demonstrating ossification of a left parietal cephalohematoma. (D) 3D volumetric image demonstrating a bulge in the skull caused by a calcified cephalohematoma.

Fig. 10.5, Birth-Related Subdural Hemorrhage . (A) Axial head CT demonstrating hyperdense subdural hemorrhage along the right and left sides of the posterior falx ( arrows ). (B, C, D) Axial and sagittal T1W images demonstrating T1W hyperintense subdural hemorrhage along the tentorium, occipital lobes and posterior to the cerebellar hemispheres with associated susceptibility on (E and F) axial SWI images ( arrows ).

Fig. 10.6, Venous Hemoconcentration . (A and B) Axial and sagittal head CT images with mild hyperdensity along transverse sinuses, sagittal sinus, and straight sinus, which was indeterminate for thrombosis requiring a CT venogram (C and D), which confirmed patency and hyperdensity due to hemoconcentration.

Fig. 10.7, Subpial Hemorrhage . (A and B) Coronal and sagittal head ultrasound demonstrating ill-defined asymmetric right temporal lobe hyperechogenicity ( arrows ). (C to F) Axial, coronal, and sagittal T1W images with T1W hyperintense subpial ( thin arrow ) and parenchymal hemorrhage ( wide arrow ) in the right temporal and occipital lobes. (G and H) Coronal and axial T2W images show T2 hypointense signal in the hemorrhage and parenchymal edema. (I to L) Follow up axial T2 and multiplanar T1 weighted images demonstrate decreasing subpial and parenchymal hemorrhage with associated parenchymal volume loss.

Fig. 10.8, Subpial Hemorrhage . (A and B) Coronal T2W and (C) axial GRE demonstrating characteristic subpial hemorrhages in the temporal lobes as areas of T2 hypointense signal and GRE susceptibility in a triangular configuration as well as evidence of parenchymal edema.

Fig. 10.9, Accidental Trauma . A 1-year-old with fall from high chair. (A and B) Axial head CT, (C) coronal head CT reformat, and (D) 3D volumetric CT images demonstrate and right parietal scalp subgaleal hematoma, a nondisplaced right parietal skull fracture ( arrow , image B), and a hyperdense/acute epidural hemorrhage ( arrow , images A and C) along the lateral right parietal lobe adjacent to the fracture.

Fig. 10.10, Fracture-Related Dural Sinus Thrombus . A 13-year-old with backward fall onto concrete, subsequent vomiting, headache, and scalp swelling. (A) Axial head CT demonstrates a hyperdensity in the right sigmoid sinus. (B) Axial bone filter image demonstrates a subtle asymmetrically widened diastatic fracture of the right lambdoid suture ( arrow ). (C) Axial CT venogram demonstrates a filling defect with abrupt cutoff in the right sigmoid sinus due to thrombus.

Fig. 10.11, Fracture-Related Dural Sinus Compression . A 2-year-old hit by a car. (A) Coronal reformat head CT demonstrates acute extraaxial hemorrhage in the posterior fossa. (B) A 3D reformat head CT demonstrates bilateral diastatic fractures of the occipital bone. (C) Coronal reformat CT venogram image demonstrates compression and narrowing of the right and left sigmoid sinuses.

Fig. 10.12, Ping Pong Fracture . (A and B) 3D volumetric CT images, and (C and D) axial and coronal head CT images demonstrate a ping pong fracture of the right frontal bone with characteristic internal depression and angulation.

Fig. 10.13, Ping Pong Fracture . (A) axial head CT and (B and C) 3D volumetric CT images demonstrate a ping pong fracture of the right parietal bone with characteristic internal depression and angulation and noticeable contour deformity of the scalp.

Fig. 10.14, Leptomeningeal Cyst . (A to C) Axial CT and 3D volumetric CT images demonstrate an ovoid defect in the right parietal bone and adjacent linear fractures. The right frontal and parietal lobes herniate into the fracture site, and there is cystic encephalomalacia of the herniated parenchyma. (D) Axial 3D T2W image better demonstrates the encephalomalacia and gliosis of the right frontal and parietal lobe parenchyma.

Fig. 10.15, Leptomeningeal Cyst: Radiograph and Ultrasound Appearance . (A) Sagittal skull radiograph demonstrating a large ovoid lucency in the skull. (B) Focused ultrasound image demonstrating a scalp fluid collection extending and communicating with the intracranial extraaxial space through a skull defect (arrow).

Fig. 10.16, Accessory Suture . (A) 3D Volumetric CT image and (B) coronal reformat head CT image demonstrate an accessory suture in the occipital bone, differentiated from a fracture by the zigzag appearance. Axial images could mimic a fracture, which is why there is value in multiplanar and volumetric images.

Fig. 10.17, Accessory Suture . A 3D Volumetric CT image demonstrates an accessory suture in the lateral aspect of the parietal bone.

Fig. 10.18, Accessory Suture . (A and B) Axial CT images demonstrate large regions of parenchymal edema, hyperdensities in the subarachnoid spaces concerning for hemorrhage, and a lucency in the right side of the occipital bone concerning for a fracture ( arrow ). These findings were concerning for potential abusive head trauma. (C) 3D volumetric CT image, however, shows the sutures are widened and the right occipital lucency is a widened accessory suture. The infant was found to have bacterial meningitis. Autopsy confirmed an accessory suture.

Fig. 10.19, Parenchymal Contusion . (A) Axial head CT demonstrating foci of acute hemorrhage in the bilateral frontal lobes and left temporal lobe with surrounding edema. (B) Axial T2W image demonstrating areas of hemorrhage see as T2 hypointense signal and surrounding edema. (C) Axial SWI and (D) axial SWI phase image demonstrate multifocal susceptibility in the parenchyma consistent with hemorrhage as indicated on the phase map hyperintense signal similar to veins. (E) Follow-up axial head CT, demonstrating parenchymal volume loss and low density indicative of encephalomalacia and gliosis at sites of previous contusions.

Fig. 10.20, Diffuse Axonal Injury . (A) Axial head CT demonstrating foci of acute hemorrhage in the left putamen and thalamus. (B) Axial FLAIR image demonstrating areas of hyperintensity in the corpus callosum, bilateral thalami, and left putamen in addition to a right occipital subdural hemorrhage. A small subdural hematoma is also present posterior to the right occipital lobe. (C and D) Axial DWI images demonstrate hyperintense signal in the corpus callosum, left thalamus, left putamen, and right subinsular white matter. The right occipital subdural hemorrhage is also seen. (E to H) Axial SWI images demonstrate multifocal susceptibility in the parenchyma consistent with hemorrhage from diffuse axonal injury.

Fig. 10.21, Retroclival Hematoma . (A) Sagittal reformat head CT image demonstrating hyperdense hemorrhage posterior to the clivus. (B) Sagittal T1W image demonstrating isointense and mild hyperintense T1W signal posterior to the clivus due to hemorrhage ( arrow ). (C) Sagittal reformat CT image demonstrating hyperdense hemorrhage posterior to the clivus ( arrow ). (D) Sagittal T2W and (E) Sagittal T1W images demonstrate T2W hypointense and T1W isointense to mild hyperintense signal due to hemorrhage posterior to the clivus ( arrows ).

Fig. 10.22, Abusive Head Trauma . (A) Lateral skull radiograph demonstrates a linear parietal bone lucency due to a fracture ( arrow ). (B) AP chest radiograph demonstrates bilateral healing rib fractures ( arrows ). (C) AP foot radiograph demonstrates a healing first metatarsal fracture ( arrow ). (D) 3D volumetric CT demonstrates the parietal bone fracture. (E and F) Sagittal and coronal head CT reformat images demonstrate mixed density subdural hemorrhage along the right cerebral hemisphere and right temporal scalp edema.

Fig. 10.23, Abusive Head Trauma . (A) Axial head CT demonstrates enlarged bilateral frontoparietal low-density extraaxial spaces. No vessels traverse these spaces, which should raise concern for subdural fluid collections. (B and C) Axial and coronal ultrafast T2W images confirm bilateral subdural fluid collections and presence of internal septations. The dura is delineated by the arrows .

Fig. 10.24, Abusive Head Trauma: Ultrasound Appearance . (A) Coronal head ultrasound image demonstrates a mild hyperechoic subdural hematoma along the left vertex. (B) Coronal noncontrast reformat CT image correlate for image A demonstrates an isodense subdural hematoma along the left cerebral hemisphere. (C) Coronal head ultrasound image demonstrates a hypoechoic right vertex subdural fluid collection displacing the subarachnoid space and a left sided hyperechoic subdural hematoma along the left vertex. (D) Coronal reformat noncontrast CT image confirms bilateral subdural fluid collections of different densities.

Fig. 10.25, Abusive Head Trauma: Subdural Hemorrhage Patterns . (A) Axial head CT demonstrates bilateral frontoparietal low-density extraaxial spaces. No vessels traverse these spaces, which should raise concern for subdural fluid collections. (B) Axial T2W images demonstrate bilateral frontal subdural fluid collections with septations. (C) Axial SWI image shows susceptibility from hemorrhage in the bilateral subdural spaces. (D and E) Axial head CT demonstrating hyperdense subdural hemorrhage along the falx and left cerebral hemisphere in addition to large regions of parenchymal ischemia. (F) Axial head CT demonstrating a mixed density subdural hematoma along the lateral left frontal lobe with associated large region of loss of gray and white matter differentiation, midline to the right, and subfalcine herniation of the frontal lobe.

Fig. 10.26, The Structure of the Meninges . Layers of the dura are shown in shades of gray, the arachnoid in shades of pink, and the pia in green. (From Haines DE, Mihailoff GA. Fundamental Neuroscience for Basic and Clinical Applications. 5th ed. 2019; Elsevier.)

Fig. 10.27, Simplified Schematic Drawing of the Pathogenetic Pathways of the Origin and Fate of Subdural Hygromas (SDHys). ICP , Intracranial pressure; SDH , subdural hematoma. (From Wittschieber D, Karger B, Niederstadt T, Pfeiffer H, Hahnemann ML. Subdural hygromas in abusive head trauma: pathogenesis, diagnosis, and forensic implications. Am J Neuroradiol . 2014;36[3]:432–439. https://doi.org/10.3174/ajnr.a3989 )

Fig. 10.28, Abusive Head Trauma: Ischemia . (A and B) Axial head CT images demonstrate diffuse low density and loss of gray-white differentiation in bilateral cerebral hemispheres consistent with diffuse ischemia. (C) Axial T2W, (D) Axial DWI, (E) axial ADC, and (F) axial T1W images show diffuse parenchymal T2 hyperintensity and diffusion restriction from ischemia in addition to bilateral T2 hyperintense subdural fluid collections (with air anteriorly from recent surgical drainage) and a right temporo-occipital hemorrhage with T1W hyperintensity and T2W hypointensity with surrounding edema. Combination of subdural fluid collections, ischemia, and parenchymal hemorrhage is highly concerning for abusive head trauma. Diffuse ischemia can be challenging on MRI due to the symmetry.

Fig. 10.29, Abusive Head Trauma : Venous Injury. (A) Axial head CT image demonstrates linear hyperdensity from thrombosed bridging vein. (B) Axial T1W and (C) axial SWI images confirm vein thrombosis by the T1W hyperintense signal and susceptibility. (E) Coronal T2W image demonstrates a left occipital T2W hypointense subdural hemorrhage and adjacent parenchymal edema. (E) Coronal reformat CT venogram image demonstrates a tear of the left vein of Labbe and a “tadpole” sign from the retracted vein.

Fig. 10.30, Abusive Head Trauma: Parenchymal Laceration . (A) Axial CT head demonstrates a triangular low density in the right parietal lobe. (B) Axial FLAIR, (C) axial T2W, and (D) axial SWI images demonstrate a right parietal laceration with cleft-like fluid signal and hemorrhage.

Fig. 10.31, Abusive Head Trauma: Parenchymal Laceration . (A and B) Coronal ultrasound images demonstrate a triangular hyperechoic area in the left medial frontal lobe resulting from a laceration. Hyperechoic subdural hemorrhage along the left vertex, hypoechoic regions in the temporal lobes, and poor cortical differentiation are also present. (C) Coronal reformat CT head correlate demonstrates a triangular low density in the right parietal lobe related to the laceration. Hyperdense subdural hemorrhage is present along the falx and left vertex. Abnormal low densities in the temporal lobes and loss of cortical distinction are due to diffuse ischemia. This case shows how multiple parenchymal injuries are often present in abusive head trauma.

Fig. 10.32, Abusive Head Trauma: Spinal Trauma . (A) Axial T2W, (B) sagittal T1W, and (C) sagittal STIR images demonstrate abnormal T2W signal less than CSF and T1W signal greater than CSF along the periphery of the thecal sac in a configuration consistent with subdural hemorrhage. Large region of subcutaneous edema in the spine, edema along the nuchal ligament, and posterior fossa and falcine subdural hemorrhages are also seen.

Fig. 10.33, Abusive Head Trauma: Retinal Hemorrhage . (A) RetCam photograph of preretinal, intraretinal, and subretinal hemorrhages, extending to the periphery. (B and C) Axial T2W and (D) axial SWI images demonstrate hypointense foci in the posterior globes and right media globe consistent with retinal hemorrhage. MRI should not be the primary diagnostic tool to identify retinal hemorrhages. (A Courtesy Tineke Chan, MD, Children’s Hospital of Pittsburgh, University of Pittsburgh Medical Center, Pittsburgh, PA. In Zitelli B, McIntire S, Nowalk A. Zitelli and Davis’ Atlas of Pediatric Physical Diagnosis . 7th ed. Elsevier; 2018.)

SUBPIAL HEMORRHAGE

Key Points

Background

  • Etiology unknown; possibly birth-related trauma or venous compression, injury, or venous thrombosis

  • Potential explanation is that the pia mater is more easily separated from the brain in neonates than older children; therefore this may account for the relative low frequency of detection of this type of hemorrhage in older infants and children

  • Typical presentation is a term neonate with apnea or seizure following spontaneous vaginal delivery

  • Relatively uncommon but frequently occur in the temporal lobes

  • Limited data suggest good prognosis

Imaging

  • At time of imaging the hemorrhage is usually T2 hypointense and T1 hyperintense and demonstrates susceptibility. The hemorrhage has a characteristic triangular shape due to the extension into the sulcus and covering of the outer cortex.

  • Intraparenchymal and intraventricular hemorrhage can coexist in continuity with a subpial hemorrhage.

  • Follow-up imaging can demonstrate encephalomalacia, gliosis, and laminar necrosis.

REFERENCE

  • 1. Huang A.H., Robertson R.L.: Spontaneous superficial parenchymal and leptomeningeal hemorrhage in term neonates. AJNR Am J Neuroradiol 2004 Mar; 25: pp. 469-475.

ACCIDENTAL TRAUMA

Key Points

  • Head trauma findings in order of most common to least common are: scalp hematoma > scalp hematoma with skull fracture > scalp hematoma with skull fracture and epidural hemorrhage.

  • Skull fractures most commonly involve the parietal bone. Fractures can also be seen as suture diastasis rather than fracture lucency through the bone.

  • Most epidural hematomas are small but require consultation with neurosurgery for conservative versus surgical management.

  • Epidural hematomas are more likely from accidental rather than nonaccidental trauma.

  • Subdural hemorrhage can occur in accidental trauma but should raise suspicion of nonaccidental trauma in young children.

  • Fractures crossing a venous sinus are associated with sinus thrombosis in 20% to 40% of cases and external compression in approximately 30%.

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