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Non-accidental CNS trauma

Traumatic central nervous system (CNS) injury is reportedly the leading cause of morbidity and mortality in childhood, accounting for nearly 100,000 emergencies per year in the United States and half the deaths from infancy through puberty 1 2. The major causes are accidental and include falls, car accidents, and recreational mishaps. However, nonaccidental, inflicted, or intentional, trauma is said to be an increasingly frequent cause of CNS injury, being responsible for about 80% of the deaths (estimated 3,000 per year) from brain injury in children less than two years of age 3 4. Nonaccidental injury (NAI), or nonaccidental trauma (NAT), is the terminology more recently applied to the original and traditional labels "child abuse", "battered child syndrome", and "shaken baby syndrome". A more recent restatement of the definition of the "shaken baby syndrome (SBS)" has been offered: "The shaken baby syndrome is a form of physical non-accidental injury to infants, characterized by acute encephalopathy with subdural and retinal hemorrhages, occurring in the context of inappropriate or inconsistent history, and commonly accompanied by other apparently inflicted injuries" 4 5 The peak incidence of child abuse resulting in CNS injury is about 6 months of age. The acute life threatening consequences of CNS injury as well as the long term effects on the development of the child have been a focus of major interest since Caffey's landmark article of 1946 and Silverman's Rigler lecture in 1972 6 7. CT, and more recently, MRI have reportedly provided data that allow more accurate estimates of the incidence of CNS trauma in alleged NAI with a reported range of 7 to 19 percent 2 8-36. The reported spectrum of CNS injury associated with trauma, accidental or nonaccidental, may be classified into 9 11 15: Primary vs. secondary Focal vs. diffuse Acute vs. chronic Primary injury is immediate, irreversible, and the direct result of the initial traumatic force (e.g., contusion, shear injury). Secondary injury refers to those reactive phenomena which occur as a result of the primary injury (e.g., swelling, hypoxia-ischemia, herniation). Direct contact, or impact, phenomena are said to result in a localized cranial distortion, or deformation, and thus produce focal injury. Examples are fracture, contusion, and epidural hemorrhage. Accidental injury, particularly as a single event, is said to be typically associated with direct contact as the primary mechanism for injury 11 24 37-39. Although common in NAI, it has been reported that impact injury, with the exception of epidural hematoma, is usually not life threatening. In SBS, it is indirect trauma (independent of skull deformation) that is considered responsible for the most severe CNS injury 11 24 37-39. Inertial loading accompanying sudden angular acceleration or deceleration of the head on the neck (as with shaking) results in shear strain deformation, disruption at tissue interfaces, and therefore diffuse injury. Such a mechanism may seem logical in the susceptible young infant predisposed by weak neck muscles, a relatively large head, and the vulnerability of an immature brain. It is this shaking mechanism that has been traditionally postulated to produce the primary traumatic injury pattern (subdural hematoma, retinal hemorrhages, and diffuse axonal injury), with or without the secondary injury pattern (edema, swelling, hypoxia-ischemia, herniation) that is stated to be characteristic, if not pathonomonic, of SBS 11 24 37-52. Reportedly, such patterns of damage are often associated with the most severe and fatal CNS injuries, and are often readily demonstrated by neuroimaging, surgical neuropathology, and postmortem neuropathology 8-58. More recently this mechanism has been extended to include impact in the "shaken-impact theory". It has further been declared that: Retinal hemorrhages of a particular pattern are diagnostic of NAI Such CNS injury on an accidental basis can only be associated with a massive force equivalent to a motor vehicle accident or a fall from a two-story building Such injury is immediately symptomatic and cannot be followed by a lucid interval, and Changing symptoms in a child with prior head injury is due to newly inflicted injury and not just a rebleed 23-24 46-47 52-53 59-66 Therefore, from this reasoning, the last caretaker with the injured child is automatically guilty of abusive injury, especially if unwitnessed 43 60 64 65. The range of acute primary and secondary CNS injury reported to occur with abuse (e.g., as a single event) includes: Multiple or complex cranial fractures Acute interhemispheric SDH Acute/hyperacute convexity SDH Multiple contusion Shear injury (diffuse axonal injury, white matter tears) Brain swelling, edema, and hypoxia-ischemia The range of chronic CNS injury in abuse includes: Chronic SDH Communicating hydrocephalus Atrophy, or encephalomalacia The combination of acute and chronic findings suggests multiple events. Imaging evidence of CNS injury may occur with, or without, other clinical findings of trauma (e.g., bruising) or other "higher specificity" imaging findings associated with violent shaking (e.g., metaphyseal, rib, or other typical skeletal injuries) 11 24. Therefore, clinical and imaging findings of injury out of proportion to the history of trauma, and injuries of different ages have become two of the key diagnostic criteria indicating the "probability" of NAI or child abuse, particularly when encountered in the premobile, young infant11 24 38. Such clinical and imaging findings have traditionally formed the basis from which health professionals, including radiologists, have provided a medical diagnosis and offered expert testimony that such findings are "proof" of NAI. It has further been declared that: Retinal hemorrhages of a particular pattern are diagnostic of NAI Such CNS injury on an accidental basis can only be associated with a massive force equivalent to a motor vehicle accident or a fall from a two-story building Such injury is immediately symptomatic and cannot be followed by a lucid interval, and Changing symptoms in a child with prior head injury is due to newly inflicted injury and not just a rebleed 23-24 46-47 52-53 59-66 Therefore, from this reasoning, the last caretaker with the injured child is automatically guilty of abusive injury, especially if unwitnessed 43 60 64 65. The range of acute primary and secondary CNS injury reported to occur with abuse (e.g., as a single event) includes: Multiple or complex cranial fractures Acute interhemispheric SDH Acute/hyperacute convexity SDH Multiple contusion Shear injury (diffuse axonal injury, white matter tears) Brain swelling, edema, and hypoxia-ischemia The range of chronic CNS injury in abuse includes: Chronic SDH Communicating hydrocephalus Atrophy, or encephalomalacia The combination of acute and chronic findings suggests multiple events. Imaging evidence of CNS injury may occur with, or without, other clinical findings of trauma (e.g., bruising) or other "higher specificity" imaging findings associated with violent shaking (e.g., metaphyseal, rib, or other typical skeletal injuries) 11 24. Therefore, clinical and imaging findings of injury out of proportion to the history of trauma, and injuries of different ages have become two of the key diagnostic criteria indicating the "probability" of NAI or child abuse, particularly when encountered in the premobile, young infant11 24 38. Such clinical and imaging findings have traditionally formed the basis from which health professionals, including radiologists, have provided a medical diagnosis and offered expert testimony that such findings are "proof" of NAI. Despite imaging advances, fundamental difficulties persist in extracting a definitive diagnosis of NAI based on a causative event (for example, shaking) that is inferred, in a number of cases, from clinical, radiologic, and pathologic findings in the absence of witnessed or admitted violent shaking 23-24 43 51 61 63-64. This problem is further magnified by the lack of consistent and reliable criteria for the diagnosis of NAI, and that the vast body of literature on child abuse is comprised of anecdotal case series, case reports, reviews, opinions, and position papers 22-23 43 56 61 63-64. Furthermore, many reports include cases having impact injury (a hallmark of "accidental" trauma) which not only raises doubt regarding the "shaking only" mechanism but also questions that this injury is always "nonaccidental". From an evidence-based medicine perspective, quality of evidence ratings for diagnostic criteria regarding the literature on SBS reveal that few published reports merit a rating above class IV (any design where test not applied in blinded evaluation or, evidence provided by expert opinion alone or in descriptive case series without controls) 67. Such quality of evidence ratings do not meet criteria to establish any clear diagnostic standards. This is particularly true, traditionally, of the neuroimaging literature on NAI, the clinical NAI literature that utilizes neuroimaging, and the forensic pathology literature 8-36 45-46 53-57 64 67. The inclusion criteria for many of these series often encompass arbitrary diagnostic categories beyond "definite or confirmed abuse" such as "suspected abuse", "presumed abuse", "likely abuse", and "indeterminate". Furthermore, circular logic often provides the basis for the diagnosis of SBS, for example, SBS = subdural plus retinal hemorrhages (inclusion criteria), therefore subdural plus retinal hemorrhages = SBS (conclusion). The only widely reported attempt (at the time of this review) of a scientific study to test NAI used a biomechanical approach and measured stresses from shaking versus impact in a doll model and correlated those stresses with injury thresholds in subhuman primate experiments established in another study 39. Only stresses associated with impact exceeded the injury thresholds that correlated with the pathological spectrum of concussion, subdural hematoma, and diffuse axonal injury. The authors concluded that CNS injury in NAI in its most severe form is usually not caused by shaking alone. These authors also concluded that fatal cases of NAI, unless in children with predisposing factors (subdural hygroma, atrophy, etc.), are not likely to result from shaking during play, feeding, swinging, or from more vigorous shaking by a caretaker for discipline. Although subsequent reports have indicated that CNS injury in NAI from shaking may be associated with impact, those and other publications have also provided "evidence" that shaking alone can produce serious intracranial injury NAI revisited Some past and more recent reports have brought forward information based upon clinical, surgical, imaging, pathological, biomechanical, social, and legal observations that raise serious doubt regarding NAI as the cause in all cases of infant CNS injury otherwise attributed to abuse using traditional diagnostic criteria for NAI 11 38-39 43 65-66 68-78. This includes reports of skull fracture and/or acute subdural hematoma from accidental simple falls in young infants, such as those associated with wide extracerebral spaces (e.g., benign external hydrocephalus, benign macrocrania of infancy, subdural hygromas, etc.) 49 73 74 75; and, fatal pediatric head injuries caused by witnessed, accidental short-distance falls, including those with a lucid interval and retinal hemorrhages 76. Updated neuropathological studies indicate: Cerebral swelling in young infants (< 1 year of age) with "SBS", as compared with older infants, is more often due to diffuse axonal injury of hypoxic-ischemic origin rather than traumatic origin (the latter more appropriately termed multifocal traumatic axonal, or shear, injury) Although fractures, interhemispheric subdural hemorrhage, and retinal hemorrhages are commonly present, the usual cause of death was increased intracranial pressure from brain swelling associated with hypoxia-ischemia Cervical epidural hemorrhage and focal axonal brain stem, cervical cord, and spinal nerve root injuries are characteristically seen in these infants (presumably due to shaking, although most had impact findings) which may be associated with apnea and responsible for the hypoxic-ischemic brain injury 54 55 56 Furthermore, additional neuropathologic series have shown that dural hemorrhages are also seen in non-traumatic fetal, neonatal, and infant cases and that the common denominator is cerebral venous hypertension and congestion, arterial hypertension, brain swelling, and immaturity plus hypoxia-ischemia and/or infection related vascular fragility 57. Reports of neurosurgical, neuroradiological, and neuropathological findings in head trauma as correlated with biomechanical analyses indicate that subdural hematoma and retinal hemorrhages occur with rotational deceleration injuries whether "accidental" (where the axis or center of rotation internal to the skull, including those due to short-distance falls), or "non-accidental" (where the axis of rotation external to the skull, such as at the craniocervical junction or cervical spinal level in SBS) There is no scientific basis to date to indicate how much, or how little, force is necessary to produce traumatic injury to the developing CNS. Furthermore, the specificity of retinal hemorrhages for child abuse and their dating has also been questioned. Such hemorrhages reportedly may be seen with a variety of conditions including accidental trauma, resuscitation, increased intracranial pressure, increased venous pressure, subarachnoid hemorrhage, sepsis, coagulopathy, certain metabolic disorders, systemic hypertension, and other conditions The child with trauma, including suspected NAI, whether primarily neurologic, skeletal, or involving other systems, must not only receive protective evaluation, but also deserves a timely and complete clinical and imaging workup to evaluate pattern of injury and timing issues, as well as to exclude the mimics of abuse. For CNS injury, this includes not only CT and skeletal survey, but also MRI, and in some cases US. Serial imaging, particularly with MRI, may also be necessary. Imaging protocols, utilization guidelines, and interpretative principles are presented in greater detail in a number of recent publications. Scalp ans Skull injury The range of CNS injury in childhood trauma, whether accidental or nonaccidental, that is often demonstrated by imaging may be categorized according to primary vs. secondary (as previously described) and by specific anatomical involvement including scalp, cranial, intracranial, spinal, and head and neck 11 24 84. Regarding SCALP injury, edema or swelling may be localized to any layer: S=skin C=subcutaneous A=galea aponeurotica L=loose or subgaleal space P=periosteum) Subperiosteal collections (e.g., cephalohematoma) tend to be more confined (by periosteal attachments at the sutures) than subcutaneous or subgaleal collections, and the latter may be extensive and contribute to circulatory compromise. The spectrum of cranial injury includes fractures and suture splitting. Fractures may be simple (e.g., single, linear, nondisplaced) or complex including bilateral, multiple, diastatic, depressed, or growing (e.g., leptomeningeal cyst). Localized suture splitting may indicate traumatic diastasis (e.g., by fracture extension), whereas diffuse or multiple suture splitting indicates increased intracranial pressure (e.g., edema, expanding collection, hydrocephalus). Intracranial fluid collections: Abnormal collections may be subarachnoid, intraventricular, subdural, or epidural. Subarachnoid (and intraventricular) collections may contain hemorrhage, cerebrospinal fluid (e.g., hygroma, hydrocephalus), or both. Subdural and epidural collections may contain hemorrhage (e.g., hyperacute, acute, chronic, combined), protein, CSF (e.g., acute subdural hygroma or chronic subdural hematoma), or a combination of these. Subarachnoid and subdural collections may be localized or extensive, and occur about the convexities, interhemispheric (along or within the falx), or along the tentorium between the cerebrum above (for example, supratentorial), the cerebellum and brainstem below (for example, infratentorial or posterior fossa), or within the leaves of the tentorium (for example, intratentorial, usually related to the dural venous sinuses and connecting veins). Subarachnoid collections are more specifically identified when extending into the cisterns, fissures, and sulci. Epidural hemorrhage, whether arterial or venous in origin, tends to be more localized (limited by the periosteal layer of the dura mater along the inner calvarial table, about the dural venous sinuses, or within the tentorium or falx) and usually appears as a lentiform collection. Convexity subarachnoid and subdural collections tend to be crescentic and follow the contour of the subjacent cerebrum or cerebellum. Occasionally, a collection cannot be determined to be specifically subarachnoid, subdural, or epidural, and collections in multiple spaces may be present. Brain damage: The range of brain injury includes acute to subacute (e.g., contusion, shear injury, intracerebral hemorrhage, edema, hypoxia-ischemia) and chronic injury (e.g., atrophy, encephalomalacia, mineralization) 11 24 84. Contusions may be hemorrhagic or nonhemorrhagic, typically occur in cortical gray matter along brain surfaces next to hard tissues (e.g., bone, dura), and may appear near or opposite the point of impact (coup vs. contracoup, respectively). Shear injury occurs deeper in the brain within the subcortical and periventricular white matter at gray-white matter junctions, is more often nonhemorrhagic than hemorrhagic, and may appear as gross tears or as more subtle axonal injury. This injury has been previously referred to as "diffuse axonal injury", but is more properly termed multifocal or traumatic axonal injury, since diffuse axonal injury is more characteristic of hypoxic-ischemic damage. Edema or swelling may be traumatic, hyperemic, hypoxic-ischemic, or related to other factors (e.g., seizures, metabolic) 11 24 84. Traumatic edema is related to direct traumatic effects such as contusion, shear, or vascular injury (associated with dissection or herniation). Malignant brain swelling in children with head trauma may also occur due to cerebrovascular congestion (hyperemia) as a vasoreactive rather than an autoregulatory phenomenon. Global hypoxia (e.g., apnea, respiratory failure) or ischemia (e.g., cardiovascular failure) is likely a major cause of, or contributor to, brain edema in the child with head trauma. Other contributors to edema or swelling include such complicating factors as seizures (e.g., status epilepticus), fluid-electrolyte imbalance, or other systemic or metabolic derangements (e.g., hypoglycemia). The type and pattern of edema conforms to the nature and distribution of the causative insult. Traumatic edema is often focal or multifocal in areas of contusion, shear, or hemorrhage. Hyperemic edema is often diffuse and may appear early as accentuated gray-white matter differentiation. Hypoxic-ischemic injury may have a diffuse appearance acutely with decreased gray-white differentiation throughout the cerebrum (e.g., white cerebellum sign), and then evolve to a more specific pattern (e.g., borderzone or watershed , basal ganglia / thalamic, cerebral white matter necrosis, reversal sign). The subacute to chronic sequelae of traumatic brain injury include hydrocephalus, atrophy, encephalomalacia, gliosis, mineralization, and chronic extracerebral collections. Malignant brain swelling in children with head trauma may also occur due to cerebrovascular congestion (hyperemia) as a vasoreactive rather than an autoregulatory phenomenon. Global hypoxia (e.g., apnea, respiratory failure) or ischemia (e.g., cardiovascular failure) is likely a major cause of, or contributor to, brain edema in the child with head trauma. Other contributors to edema or swelling include such complicating factors as seizures (e.g., status epilepticus), fluid-electrolyte imbalance, or other systemic or metabolic derangements (e.g., hypoglycemia). The type and pattern of edema conforms to the nature and distribution of the causative insult. Traumatic edema is often focal or multifocal in areas of contusion, shear, or hemorrhage. Hyperemic edema is often diffuse and may appear early as accentuated gray-white matter differentiation. Hypoxic-ischemic injury may have a diffuse appearance acutely with decreased gray-white differentiation throughout the cerebrum (e.g., white cerebellum sign), and then evolve to a more specific pattern (e.g., borderzone or watershed , basal ganglia / thalamic, cerebral white matter necrosis, reversal sign). The subacute to chronic sequelae of traumatic brain injury include hydrocephalus, atrophy, encephalomalacia, gliosis, mineralization, and chronic extracerebral collections. Spine injury: The spectrum of spine injury in NAI significantly overlaps that of accidental injury and is presented in greater detail in other references 24. This spectrum often differs with age (degree of spinal development) and includes either single or multiple lesions involving the cervical, thoracic, lumbar, or sacral level. The mechanisms of injury include: Hyperflexion Hyperextension Axial loading or rotation Distraction Such injuries may not be apparent on plain films (e.g., SCIWORA - spinal cord injury without radiographic abnormality) and require CT and/or MRI for complete evaluation. MRI is particularly important for evaluating ligamentous injury and intraspinal injury. The range of intraspinal injury includes displaced bone or disk fragments and hematomas (e.g., epidural) with spinal cord or nerve root compression. There may be edema, contusion, hemorrhage, or transection of the spinal cord, or avulsion of one or more nerve roots. CT or MR angiography may be needed to evaluate for vascular injury (e.g., dissection). Cervical spinal cord injury may be associated with head injury or may be the unsuspected cause of encephalopathy (such as in unexplained respiratory failure with hypoxic-ischemic brain injury). It should be ruled out in all cases of "head injury", whether accidental or NAI. Imaging CT: Regarding the dating or timing of CNS injury, CT and MRI are the primary modalities used in this regard. US with Doppler may occasionally be useful in the very young infant and at the bedside 11 24 84. In general, CT is primarily used to identify acute or subacute hemorrhage, other collections, edema, skull fracture, and scalp injury 11 23 24 33 84. Bone CT algorithms and display techniques are used along with skull films to evaluate for scalp and skull injuries. Scalp and skull injuries are difficult to precisely time by CT, again unless there are serial CTs available, and depending upon the nature and number of traumatic events 11 24 84. Unless there is direct injury to a scalp vessel that results in a hematoma, and particularly if the child is in a state of circulatory compromise, only subtle findings of scalp injury may be present acutely. Such injury may not be apparent unless the soft tissue and bone windows are carefully examined in addition to the skull films. With accumulation over time, the abnormal scalp collection or edema may not be obviously present until several hours later or the next day. Skull fractures are also difficult to time by both plain films and CT because of the lack of periosteal reaction during healing. A simple skull fracture in an infant may require 6 months for complete healing. In an older child and adult, this may require up to a year. In acute neurologic presentations, CT is indicated emergently to evaluate the need for immediate neurosurgical intervention (e.g., an expanding hemorrhagic collection) and as an additional guide for the medical management of increased intracranial pressure (e.g., cerebral edema). Repeat or serial imaging may be necessary. CT, particularly as a single examination, often cannot provide precise information with regard to the character and age of collections, particularly in the presence of anemia or coagulopathy, and depending upon the nature and number of traumatic events. Acute to subacute clotted hemorrhage appears high density (age range: 3 hours to 7 days, or sometimes up to 10 days). Hyperacute "unclotted" hemorrhage ( < 2-3 hours old), very chronic hemorrhagic collections ( > 10-14 days old), and nonhemorrhagic collections (e.g., subdural effusions or hygromas) all appear hypodense, or occasionally isodense, depending upon cell and protein content. Benign Macrocrania of Infancy The subarachnoid CSF spaces may also be prominent in infants (e.g., normal infantile subarachnoid spaces, benign external hydrocephalus, or benign extracerebral collections) and also appear low density on CT. US with Doppler may be used to separate out the fluid compartments but MRI is usually needed for more definite evaluation 11 24 84 86-89. Particularly in the unstable infant, initial and repeat cranial US with Doppler (e.g., transcranial Doppler - TCD) at the bedside may not only be an effective method of evaluating structural abnormalities (e.g., white matter tears), but may also be used for monitoring alterations in cerebral blood flow and intracranial pressure. MRI Multiplanar MR is probably the most important technique for assessing the pattern, extent, and timing of the injury (or injuries), particularly in the absence of characteristic findings on CT 11 23-24 32-33 77 85-86. MRI should be done as soon after the presentation as the child's condition allows, and a follow-up examination within 7-10 days may be needed. T1 and T2 spin echo sequences are necessary for characterizing the nature and timing of hemorrhages and other collections as to hyperacute, acute, subacute, or chronic using established criteria STAGE BIOCHEMICAL FORM SITE T1-MRI T2-MRI Hyperacute* (+edema) [< 24 hours] Fe II oxyHb Intact RBCs Iso-Low I High I Acute (+edema) [1-3 days] Fe II deoxy Hb Intact RBCs Iso-Low I Low I Early Subacute (+edema) [3-7 days] Fe III metHb Intact RBCs High I Low I Late Subacute (-edema) [1-2 weeks] Fe III metHb Lysed RBCs (extracellular) High I High I Early Chronic (-edema) [>2 weeks] Fe III transferrin Extracellular High I High I Chronic (cavity) Fe III ferritin & hemosiderin Phagocytosis Iso-Low I Low I The radiologist must also be aware of certain conditions that are known to have clinical and imaging features that may mimic abuse 11 17 24 84. These include: Trauma of labor and delivery Accidental injury Coagulopathies Vascular diseases (e.g., venous thrombosis) Infectious or postinfectious conditions (e.g., postvaccinial) Metabolic disorders Neoplastic diseases Certain therapies Some congenital and dysplastic disorders The physician should not only rule them out, but also must consider the possibility of combined, or multifactorial, mechanisms with synergistic effects (such as an underlying condition with superimposed non-accidental, or accidental, trauma).