3. Head Trauma In Child Abuse Outline V D

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VISUAL DIAGNOSIS OF CHILD ABUSE ON CD-ROM LECTURE SERIES 3. Head Trauma in Child Abuse Outline Abstract Controversies in Shaken Baby Syndrome/ Shaken Impact Syndrome Learning Objectives Outcomes in Shaken Baby Syndrome/Shaken Impact Syndrome Incidence and Prevalence The Biomechanics of Head Injury Types of Head Injuries Anatomy and Characteristics of the Infant Head Types of Extracranial Injuries Types of Skull Fractures Types of Intracranial Injuries Shaken Baby Syndrome/Shaken Impact Syndrome (SBS/SIS) Mechanism of Injury Lesions Seen Associated Injuries Retinal Hemorrhages and Shaken Baby Syndrome Theories of Etiology of Retinal Hemorrhages Characteristics of Retinal Hemorrhages Differential Diagnosis of Retinal Hemorrhages Signs and Symptoms of Shaken Baby Syndrome Imaging Techniques Laboratory Studies Data Collection 1 Visual Diagnosis of Child Abuse on CD-ROM Lecture Series 3. HEAD TRAUMA IN CHILD ABUSE Abstract 60% of inflicted injury deaths.3 Annegers4 estimated that in the United States, children between the ages of 1 year and 15 years die of head trauma-related injuries at a rate of 10 per 100,000, a rate 5 times the death rate of childhood leukemia, the next leading cause of death. In 1985, there were approximately 7,000 brain injury deaths—about 29% of all injury deaths in this age group.5 In a 1990 study,6 17% of all brain injuries and 56% of serious brain injuries in children younger than 1 year were caused by assault. In a 1985 study of 84 head-injured infants ranging in age from 3 weeks to 11 months, 64% of injuries were attributed to accidents and 36% were the result of abuse.2 In a recent study of 287 head-injured children younger than 6.5 years of age, abusive head trauma accounted for 19% of the total. When restricting the age group to children younger than 3 years, one third of the head-injured children had sustained their injuries as a result of abuse. When injuries subsequent to motor vehicle crashes were excluded (easily distinguished from possible abuse), 49% of the head-injured children had sustained their injury from abuse.7 The mortality rate in the child abuse group was 13% versus 2% for the accident group. In another retrospective review of medical records submitted to the National Pediatric Trauma Registry during the 10-year period from 1988 through 1997,8 children categorized as victims of child abuse were younger (mean age 12.8 months versus 27.5 months for the unintentional trauma group), had a higher mortality rate than the unintentional group (12.7% versus 2.6%), and the child abuse survivors were more severely injured (Injury Severity Scores between 20 and 75 in 22.6% of the child abuse group versus 6.3% in the unintentional group). Ewing-Cobbs and colleagues9 found a similar age distribution (10.6 months in the abuse group versus 35.6 months in the accident group). There is more mortality and morbidity from nonaccidental head trauma than from any other single cause of child physical abuse. Knowledge of basic cranial anatomy and the properties of the tissues of the various layers of the head is necessary to understand how biomechanical forces can affect those tissues. Types of head injuries can be roughly classified into extracranial injuries, skull injuries, and intracranial injuries. Each of these categories is further subdivided according to the severity and involvement of the injured structures. Shaken baby syndrome (SBS) and shaken impact syndrome (SIS) are specific entities produced by specific biomechanical forces and have characteristic signs and symptoms and physical and radiologic findings. Shaking and impact lead to rupture of bridging veins and collection of blood in the subdural and/or subarachnoid spaces, traumatic, vascular, hypoxic, and biochemical injuries to the brain; extensive retinal hemorrhages (RHs); and diffuse axonal shearing of brain substance. Abusive head trauma can be distinguished from other etiologies of head injury by careful attention to the history of the injury, the resulting signs, symptoms, imaging studies, and clinical course. Learning Objectives • To differentiate abusive from non-abusive head injuries • To identify the types of scalp injuries associated with abuse • To differentiate simple from complex fractures of the calvarium • To identify mechanisms of intracranial bleeding • To define and describe SBS/SIS • To differentiate abusive and non-abusive mechanisms of RHs and their significance • To compare computed tomography (CT) and magnetic resonance imaging (MRI) for use in diagnosing head injuries There are no firm statistics regarding the incidence of SBS/SIS because there are no central reporting registries to collect these data. Estimates range from 600 to 1,400 per year. Shaken baby syndrome/ SIS occurs in babies, usually younger than 1 year, but has been described in children considerably older.10,11 Recent papers in the medical literature have reported confirmed cases of shaking in adults leading to the same clinical and pathological findings as in infant shaking cases.12 Incidence and Prevalence Craniocerebral trauma is the most common cause of mortality and long-term morbidity in physically abused children, and it is second only to vehiclerelated injuries as a cause of traumatic mortality in the United States.1,2 Intracranial injury is found in 2 Visual Diagnosis of Child Abuse on CD-ROM Lecture Series 3. HEAD TRAUMA IN CHILD ABUSE The subgaleal space is not truly a “space” until blood or other material separates the overlying tissue from the skull. The Biomechanics of Head Injury Hymel et al13 have advanced the understanding of biomechanics in head trauma. There are contact (the head striking or being struck by an object) and noncontact (acceleration/deceleration) types of injury. Contact forces cause focal strain that tends to be limited to the site of impact. Contact can cause scalp injury and/or skull fracture as well as more distant injuries, such as hemorrhages and parenchymal disturbances. Noncontact forces can cause the brain to deform, causing rupture of bridging veins and strains within the parenchyma. The skull is the bony calvarium, with an outer and inner table surrounding a small marrow cavity. The epidural space also is a potential space, overlying the dura mater. The dura mater is a relatively tough membrane overlying the intracranial contents. Within the dura runs an extensive network of dural sinuses containing venous blood returned from the brain by the bridging veins. These are numerous small veins arising from the surface of the brain and connecting to the dural sinuses. They are fixed to the brain and to the dura, so that they have no mobility. They run through the subdural and the subarachnoid spaces. Skull fractures are contact injuries and may occur with or without accompanying brain injury. Cranial impact over a large surface causes linear skull fractures. Cranial impact over a small area may result in a depressed skull fracture. The subdural space, another potential space, lies beneath the dura mater. Epidural hemorrhage may occur below a cranial impact. Subdural hemorrhage may occur as a contact or a noncontact (acceleration/deceleration) injury. The piarachnoid membrane is a lacy (spiderweblike) membrane, more delicate than the dura mater, and following the sulci and gyri of the brain. The cerebrospinal fluid (CSF) is contained within the subarachnoid space and circulates throughout the central nervous system (CNS) with nutritional and excretory function. Crushing injuries of the head result from slow, distributed mechanical loading, allowing severe strain conditions but inducing minimal cranial acceleration. Patients with crush injuries to the head often recover well. Diffuse brain injuries are primarily the result of shearing strains created by cranial acceleration, but contact strains from cranial impact play a significant role in the production of these injuries and are thought by some14,15 to be of primary importance in producing the lesions seen in abusive head trauma. The brain substance (parenchyma) lies beneath the subarachnoid space. The brain parenchyma is made up of millions of neurons, the basic cell of the nervous system. Each neuron has one axon and several dendrites. Axons carry efferent (outgoing) nerve impulses and dendrites carry afferent (incoming) nerve impulses. The neurons are gathered into nerve bundles and tracts going to the various parts of the body. The gray matter of the brain consists of the neuron cell bodies and the white matter consists primarily of the nerve bundles and tracts. Blood vessels (arterioles, venules, and capillaries) are everywhere within the brain substance. Types of Head Injuries Anatomy and Characteristics of the Infant Head Understanding the anatomy of the infant head is central to grasping the concepts of injury. In its most simple terms, the head can be viewed as a series of layers, each consisting of different types of tissues. Each of these tissues has unique properties, and they differ from each other in major ways. Because of this, each of these layers reacts to trauma in a different manner, leading to differing manifestations of injury. A protein-rich material, myelin, is laid down around the components of the CNS over the first 18 months of life. This substance makes the brain of an older child and adult much firmer than the brain of an infant or young child. The other characteristic of the infant brain, and another reason for its fragility, is that the infant brain contains approximately 25% more water than the brain of an older child and adult. Pathologists describe the infant brain as being gelatinous in consistency. The scalp consists of the skin and its appendages, subcutaneous tissue, and underlying fascia, the galea. 3 Visual Diagnosis of Child Abuse on CD-ROM Lecture Series 3. HEAD TRAUMA IN CHILD ABUSE Types of Intracranial Injuries FIGURE 3-1. TYPES OF EXTRACRANIAL INJURIES Bleeding within the skull can occur in the • Epidural space • Subdural space • Subarachnoid space • Brain parenchyma (brain tissue itself) • Intraventricular space Bleeding in the epidural space may be due to venous or arterial injury, but is usually is due to dural venous tears.16–18 It usually is associated with a skull fracture.17 An epidural hematoma on CT appears as a hyperdense, lenticular-shaped extraaxial mass. If it is arterial in origin, it can accumulate rapidly and, if not diagnosed and treated promptly, can lead to coma and death. An epidural hematoma is more often accidental rather than abusive in origin, but it can be seen as a consequence of abuse. Prompt medical attention and, in some cases, evacuation of the hematoma usually results in the rapid resolution of symptoms and signs and has a good prognosis. Types of Extracranial Injuries • Bruises (visible externally) • Bruises (intracutaneous and subcutaneous; not visible externally) • Lacerations • Abrasions Bleeding in the subdural and/or the subarachnoid spaces is due to the shearing and breaking of the veins going from the surface of the brain to the dural sinuses.19 These veins are fixed to the brain and to the dural membrane. When the brain moves within the skull, these veins are stretched, and when they exceed their elasticity, they break and bleed. • Subgaleal hematomas • Alopecia (hair loss secondary to hair-pulling) Types of Skull Fractures Simple: Linear—not crossing suture lines Temporoparietal constitute the vast majority Bleeding within the brain substance (parenchyma) is primarily due to trauma to the brain itself. Less than 2 mm separation Complex: Linear—crossing suture lines Shaken Baby Syndrome/Shaken Impact Syndrome (SBS/SIS) Linear—>2 mm separation Branching or stellate Mechanism of Injury Comminuted (isolated fragments of bone) The injuries result from violent shaking and/or shaking plus impact. Recent data have supported the concept that shaking and, in many cases, impact by throwing the child against a surface and resultant deceleration are the responsible forces producing the subdural hematoma, subarachnoid bleeding, cerebral trauma, and diffuse axonal shearing with consequent cerebral edema leading to raised intracranial pressure.20 There has been much discussion about whether shaking by itself is sufficient to produce these injuries or whether shaking plus impact is required to generate the forces causing the lesions seen in SBS/SIS. This Depressed (comminuted with bone fragments impinging on the brain) Compound (overlying laceration) Diastatic (growing) 4 Visual Diagnosis of Child Abuse on CD-ROM Lecture Series 3. HEAD TRAUMA IN CHILD ABUSE body, particularly the brain. The infant brain, with much higher water content than an adult brain, is much softer than an adult brain, having the consistency of gelatin. The absence of myelin, the protein covering of the nervous tissue, contributes to the relative softness. These factors make the brain more easily distorted and compressed within the skull. discussion really began with the 1987 article from Duhaime and colleagues15 in which they described a retrospective study of 48 cases of SBS at their institution. Of these, 62% had clinical evidence of blunt trauma to the head (bruising, skull fracture), and postmortem evidence of blunt trauma was present in all of the fatal cases. In this article, they also studied the forces generated when 3 types of dolls were shaken. Using a strain gauge measuring forces during shaking, they were unable to demonstrate enough force from shaking to account for the extent of damage seen in clinical cases. The authors concluded that impact with rapid deceleration of the intracranial contents was necessary for these lesions. This discussion has continued, with some investigators citing the absence of evidence of impact in a substantial number of their reported cases 21,22 The criticism of the required impact theory cites the crudeness of the doll models used in the study by Duhaime et al and the fact that no good data exist to inform us about what magnitude of forces are required to injure the structures of the head, particularly the infant brain. There is no way to obtain experimental evidence to measure the forces required to produce damage to the infant brain, and without such information this question cannot be adequately answered. However, by comparing data obtained from cases of accidental head injury, where the histories of injury are known (such as in motor vehicle crashes [MVCs], where there is knowledge of the time of the crash, and ambulance records are detailed as to the condition of the victims), certain information is available about the clinical courses, imaging studies, and timing of injuries, and this can be used to enhance our understanding of abusive head trauma. Lesions Seen Shaking and the sudden deceleration of the head at the time of impact do several things 1. The veins that bridge from the brain to the dura mater, a tough, inelastic membrane inside of the skull, are stretched and, exceeding their elasticity, tear open and bleed, creating the subdural hematoma and/or subarachnoid hemorrhages common in SBS/SIS. 2. The brain strikes the inner surfaces of the skull, causing direct trauma to the brain substance itself and resultant brain swelling (cerebral edema). 3. Other structures of the brain, the axons, can be broken, shearing off during the commotion to the brain causing diffuse axonal shearing injuries. 4. The lack of oxygen (hypoxia) during shaking causes further irreversible damage to the brain substance. 5. Damaged neurons release their intracellular proteins that cause vasospasm. This adds to the oxygen deprivation in the brain and also causes more destruction of adjacent brain cells.23 6. The combined effect of this cascade of injury, hypoxia, and brain swelling is massive destruction of the brain tissue, causing enormous increases in intracranial pressure. This causes compression of the blood vessels, thereby further decreasing the oxygen supply to the brain. The usual trigger for shaking is thought to be inconsolable crying by the infant. Frustrated by attempts to console the baby, the perpetrator loses control and grabs the infant, either by the chest, under the arms, by the arms, or by the neck, and violently shakes the baby. The duration of the shaking varies, usually ranging from around 5 seconds to 15 or 20 seconds. It has been estimated by video recordings of a person shaking a doll that the number of shakes ranges from 2 to 4 per second. During the shaking, the head rotates wildly on the axis of the neck creating multiple forces within the head. The infant stops crying and stops breathing during the shaking, causing decreased oxygen supply to the It is these insults to the brain, not the subdural or subarachnoid blood, that cause the signs, symptoms, and course of SBS/SIS. The bleeding in the subdural and subarachnoid spaces are markers of the tremendous forces brought to bear on the head during shaking and/or impact. 5 Visual Diagnosis of Child Abuse on CD-ROM Lecture Series 3. HEAD TRAUMA IN CHILD ABUSE Associated Injuries single fresh hemorrhage in 1 eye. Kanter,29 however, reported on 54 children, 45 of whom had had a traumatic event prior to resuscitation. Six had RHs, 5 of whom were victims of abusive head trauma. The one child with RHs after CPR with no preceding traumatic event had had a seizure at home, arterial hypertension in the hospital, and subsequently died. There was no description, however, of the type and extent of the RHs. His conclusion was that RHs should not be attributed to CPR. Gilliland and Luckenbach30 performed postmortem examinations of the eyes of 169 children. One hundred thirty-one had resuscitation for 30 minutes or more. No RHs were found in 99 children, 70 of whom had had resuscitation. Retinal hemorrhages were found in 70 children, 61 of whom had been resuscitated. Of these 61, 56 had craniocerebral trauma, both intentional and unintentional, 3 had CNS causes of death (tumor, infection), and 1 had sepsis—all conditions known to be associated with RHs. One died of undetermined causes. The authors concluded that no case in this study was found to support the hypothesis that RHs are caused by CPR. Odum et al31 examined the retinas of 43 hospitalized children who had received at least 1 minute of CPR. One patient with a coagulation defect had small punctate RHs that were morphologically different from the RHs found in SBS/SIS. Fackler et al32 produced cardiac arrest in 6 newborn piglets, followed by controlled mechanical CPR for 50 minutes. After sacrificing the animals, postmortem examinations of the eyes revealed no RHs. The overwhelming conclusion from all of these studies is that CPR is rarely, if ever, associated with the production of RHs and that classic Purtscher’s retinopathy is distinctly different from the retinopathy of SBS/SIS. Bruising and/or skeletal injuries are associated with some cases of SBS but not all.7,85 Posterior rib fractures, classic metaphyseal lesions of the long bones, and other associated fractures of abuse should be sought by skeletal survey. Retinal Hemorrhages and Shaken Baby Syndrome THEORIES OF ETIOLOGY OF RETINAL HEMORRHAGES The pathogenesis of RHs is the subject of controversy. There are 3 major etiologic theories advanced by those studying the phenomenon. The first suggests that they are due to increased intracranial pressure arising from transmission of cardiothoracic pressure (Purtscher’s retinopathy). This condition is a hemorrhagic retinal angiopathy characterized by preretinal hemorrhages and RHs, retinal exudates, and decreased visual acuity. It has been described in adults following a sudden compression of the thoracic cage and is postulated to be the result of transmission of an acute increase in intravascular pressure to the head and eyes giving rise to RHs.24,25 There has been only one pediatric case of Purtscher’s retinopathy reported in the literature26 prior to the 1975 report of Tomsai and Rosman27 who described Purtscher’s retinopathy in 2 battered children with clinical signs of traumatic brain injury. These cases were seen and treated before CT head scans came into common usage and were probably SBS/SIS. The RHs as described in this paper are not classic Purtscher’s retinopathy, which is associated with cotton-wool exudates and superficial hemorrhages. The theory of increased cardiothoracic pressure causing transmitted intravascular pressure to the head and resultant RHs led clinicians to consider the possibility of cardiopulmonary resuscitation (CPR) causing such a chain of events. Goetting and Sowa28 reported on 20 children who had received CPR, 2 of whom had RHs. One of those children, a 2-year-old, had been immersed in water, resuscitated by emergency medical personnel en route to the hospital, and remained in a coma for 4 days until death. Autopsy showed no preceding traumatic events. No information was given as to the brain findings but one can assume there was cerebral edema giving rise to raised intracranial pressure before death. The case, an infant of 1.5 months, died of sudden infant death syndrome and had a A second theory concerning RHs holds that they are the result of increased intracranial pressure. In 1975, Khan and Frenkel33 attributed RHs to acute intracranial hypertension following cerebral injury, resulting in retinal venous hypertension. Lambert et al34 stated that “it seems likely that a sudden rise in intracranial pressure significantly contributed to [the occurrence of RHs] in our patient.” Older accounts in the adult literature claim intracranial hypertension to be responsible for intraocular hemorrhage.35,36 In 1993, Munger and colleagues37 examined the eyes of 12 infants with RHs who had died subsequent to suspected violent shaking. Ten had subdural hematomas and cerebral edema; 6 Visual Diagnosis of Child Abuse on CD-ROM Lecture Series 3. HEAD TRAUMA IN CHILD ABUSE 9 had subarachnoid bleeding. Retinal detachment, with the formation of retinal folds, was found in 5. The authors leaned toward the concept of increased intracranial pressure as the pathogenetic mechanism. any other cause.1,2,7,10,15,38,44,46-51 Retinal hemorrhages in SBS/SIS usually involve the posterior pole in the nerve fiber and ganglion cell layers, but may involve any retinal layer. They usually are flame-shaped rather than dot-, blot-, or boat-shaped hemorrhages typical of intraretinal or preretinal hemorrhages.46,39 The time of resolution of RHs varies, ranging from 10 days to several months.50 If RHs are caused solely by increased intracranial pressure, one would expect to see them in accidental head trauma to the same extent as in inflicted head injury. Johnson et al38 reported on 140 children whose head injuries were thought to be accidental (MVCs and long falls in 90%). Retinal hemorrhages were seen in only 2 patients, both of whom were in the back seat of a motor vehicle impacted from the side. These data are borne out in numerous other studies,1,7,11,30,39,40 and clinical experience has instructed that most children with head injuries who have increased intracranial pressure do not often have RHs. Although RHs are the most commonly found ocular lesion in SBS/SIS, other ocular lesions also may be seen. These include retinal detachment, optic nerve injury, and cupping of the optic nerve secondary to raised intracranial pressure. DIFFERENTIAL DIAGNOSIS OF RETINAL HEMORRHAGES Vaginal delivery—Occurring in 40% of children delivered vaginally, these fine petechial preretinal hemorrhages usually resolve within 10 to 14 days of delivery leaving no residual. A third theory—traumatic retinoschisis—suggests that the forces of shaking are responsible for the RHs in SBS/SIS. According to this theory, one of the effects of shaking is to make the lens move forward and back within the ocular fluids.41 Elner and associates 42 believed that the full-thickness hemorrhagic retinal necrosis in 5 of their study subjects and retinoschisis and perimacular folds in 4 suggested that severe anteroposterior acceleration-deceleration forces directly produced retinal injuries in abused children who die of blunt head injury, and further that blunt head trauma may be necessary to produce significant vitreoretinal traction resulting in the constellation of severe retinal injuries seen in such children. Gaynon et al43 suggest that retinal folds may be a hallmark of shaking injuries in child abuse victims. Bleeding disorders—Isolated RHs in coagulopathies have not been described. When they occur in patients with bleeding or clotting disorders, they are associated with other sites of bleeding. Arteriovenous malformations—Arteriovenous malformations are extremely rare in infancy and, when present, are seldom associated with RHs. Increased intracranial pressure—This is present in most cases of SBS/SIS, but current thinking is that if increased intracranial pressure caused RHs, they would be present in all cases of increased intracranial pressure secondary to all causes. This is not supported by medical literature describing accidental head trauma with increased intracranial pressure. Retinal hemorrhages have not been found as the result of seizures in childhood.44,45 Meningitis—Increasingly rare in pediatrics, it is not likely meningitis would be overlooked after clinical assessment, culturing, and examination of CSF. CHARACTERISTICS OF RETINAL HEMORRHAGES Accidental head trauma—Recent literature on the incidence of RHs in accidental head trauma indicates that RHs are seldom seen in cases of accidental origin. Retinal hemorrhages seen in SBS/SIS are many in number, are distributed widely over the entire retina, are not associated with papilledema, and involve multiple layers of the retina. Retinal hemorrhages seen in other conditions usually are closer to the surface, so-called preretinal hemorrhages, and resolve quickly. The incidence of RHs in SBS/SIS is reported to be between 50% to 100% depending on the series reported, and they may be unilateral or bilateral, although they more commonly are bilateral. Retinal hemorrhages are overwhelmingly more common as the result of abusive head trauma than Signs and Symptoms of Shaken Baby Syndrome Symptoms and physical findings vary depending on the length and severity of the shaking and whether the infant was thrown onto a surface. The syndrome can be seen as a continuum from a short duration of shaking with little or no impact, 7 Visual Diagnosis of Child Abuse on CD-ROM Lecture Series 3. HEAD TRAUMA IN CHILD ABUSE to severe, prolonged shaking and major impact. The resulting signs and symptoms may run the gamut from decreased responsiveness, irritability, lethargy, and limpness—through convulsions, vomiting from increased intracranial pressure, increased respiratory rate, hypothermia, and bradycardia—to coma with fixed and dilated pupils—to death. All of the symptoms are caused by generalized brain swelling, increased intracranial pressure, and, in most cases, diffuse axonal shearing. These are the direct result of trauma and anoxia, and the signs and symptoms begin almost immediately after the shaking and reach their peak within 4 to 6 hours.52,53 COMPARISON OF CT AND MRI IN HEAD INJURIES Advantages of CT Delineates subarachnoid hemorrhage better than MRI Better imaging of cranial injuries Ease of performance in unstable patients Advantages of MRI Better in subacute and chronic cases Better for deep cerebral injuries Able to determine age of extracerebral fluid Will detect smaller subdural hematomas LABORATORY STUDIES IMAGING TECHNIQUES Children with head trauma severe enough to be admitted to the hospital also should have laboratory studies to support diagnoses of associated trauma in other organ systems, anticipate hematological and biochemical alterations sometimes attendant to head trauma, and seek the manifestations of their neurological status. These studies are displayed in Table 3-1. In most instances of moderate to severe head injury, the first imaging modality should be CT scanning without contrast because it is readily available in most hospitals and can be performed safely with life support systems operating during the procedure. Bone windows should be employed along with the standard scan. Plain radiographs of the skull will usually show existing skull fractures more clearly than CT. Magnetic resonance imaging is ordinarily used as a confirmatory test rather than an initial one due to the longer scan times and need for life support, but MRI gives superior detail in showing parenchymal changes and smaller subdural hematomas. A recent study54 examining coagulopathy in pediatric abusive head trauma found that there were prothrombin time prolongations in 54% of patients with parenchymal damage and in 20% of those without demonstrable parenchymal damage. Other coagulation markers (partial thromboplastin time, platelet counts, and fibrinogen levels) also were altered. The authors hypothesize that these abnormalities in coagulation elements are due to tissue Although head injury may capture the attention of providers because of the altered levels of consciousness resulting from it, trauma to other parts of the body must be considered during the initial assessment. Computed tomography scans of the abdominal viscera are valuable when there are reasons to believe that intra-abdominal injury may coexist with head injury. TABLE 3-1. LABORATORY STUDIES • CBC with morphology, serial hematocrits • Serum electrolytes, BUN, creatinine, serum and urine osmolality Skeletal surveys are recommended in serious head trauma in children younger than 3 years because the diagnosis of abuse may be made or supported if unsuspected or occult traumatic injuries are found in other parts of the appendicular skeleton. Such accompanying skeletal fractures are seen in roughly half of the cases of abusive head injury. Posterior rib fractures are present in some cases of shaken infants and can be demonstrated either with bone scintigraphy for fresh fractures or with follow-up thoracic films in 10 to 14 days to see callus formation at the site of the fractures. • Urinalysis • Liver function studies (AST, ALT, alkaline phosphatase) • Serum and urinary amylase • Creatine phosphokinase (CPK) • Cultures of blood, urine, cerebrospinal fluid (if safe to perform lumbar puncture) • PT, PTT, TT, platelet count, fibrinogen, and FDP • Stool for blood • Arterial blood gases 8 Visual Diagnosis of Child Abuse on CD-ROM Lecture Series 3. HEAD TRAUMA IN CHILD ABUSE presence of bruises on the back, thighs, or in the perineum also should be noted. Photodocumentation of such injuries is highly desirable. factor release from damaged parenchymal cells that, when complexed with factor VII, activate coagulation via the extrinsic pathway, leading to disseminated intravascular coagulation. The examination of the fundi is of utmost importance. This should be carried out ideally by pupillary dilation and indirect ophthalmoscopy, or at the very least by direct ophthalmoscopy. Although RHs are the most common finding in child abuse, other lesions also may be seen. These include retinal detachment, optic nerve injury, and cupping of the optic nerve (papilledema secondary to raised intracranial pressure). DATA COLLECTION While a child with a serious head injury is being evaluated and treated medically, it is crucial for a detailed, analytical—but not challenging or accusatory—history to be obtained from the caretakers. The person collecting the history should ideally be someone with experience in child abuse cases and one who does not have immediate responsibility for the medical treatment required by the child. It is the rule that abusing parents will tell a misleading story about how the “accident” happened and are sometimes quite inventive in describing the event. Thus the skill of interviewing becomes an important foundation on which to build the diagnostic formulation. Gentle probing, with inquiries and request for clarification on questionable portions of the history, sometimes called “the Columbo Approach,” often will elucidate the mechanism of injury and show discrepancies in the history. The history of the pregnancy, labor and delivery, neonatal course, as well as a history of family diseases is important, with particular attention to bleeding and clotting disorders, neurological diseases, metabolic and bone disease, or other genetic conditions of the family. This comprehensive evaluation will save returning to the caretakers for missing data as the case ages. The medical history of the child, including previous injuries and serious illnesses or hospitalizations, along with a review of systems should be obtained. Exploration of the social milieu with attention to the living arrangements and the relationships of household members should be done. Controversies in Shaken Baby Syndrome/Shaken Impact Syndrome Shaking versus shaking plus impact—In 1987, Duhaime et al15 reported on 48 cases of SBS in which two thirds of the subjects had external evidence of head trauma, and all of the infants who died had external trauma. Using 3 doll models implanted with accelerometers to measure the forces developed during shaking, Duhaime and colleagues concluded that shaking alone was insufficient to produce the forces seen in the injuries. In 1968, Ommaya and colleagues55 showed that subdural hematomas could be experimentally produced in rhesus monkeys by rotational displacement of the head on the neck alone, without significant direct head impact. Gennarelli et al56 confirmed this in 1982 and concluded that “it is apparent that nothing need strike the head in order for acute subdural hematomas to occur. It is sufficient that the head undergo the appropriate acceleration strain-rate conditions, since in this animal model nothing strikes the head. Thus those mechanical events that result from an object contacting the head are not necessary for acute subdural hematoma (ASDH). Although impact to the head is certainly the most common cause of clinical ASDH, it is the acceleration induced by the impact and not the head contact per se that causes the ASDH.” Others, however, believe that shaking in and of itself is sufficient to cause the lesions seen in SBS.7,21,22,42,51,57–64 The major problem in this controversy is that no one has been able to devise a model that even closely approximates the head and neck of the human infant. There are so many properties of the scalp, skull, meninges, brain, blood vessels, and neck musculature that are unknown In conducting a physical examination of the child with a head injury, there is the risk of overlooking less urgently compromised organ systems. Bleeding visceral organs are the most glaring and potentially disastrous omissions, but overlooking cutaneous injuries can deprive the diagnostician of important clinical data because of the fleeting nature of these injuries. Likewise, inspection of the oral cavity looking for intraoral lesions and a search for hidden head lesions under the hair should be done. The neck should be carefully inspected for signs of injury (strangulation, hand or finger bruising). The 9 Visual Diagnosis of Child Abuse on CD-ROM Lecture Series 3. HEAD TRAUMA IN CHILD ABUSE and variable from infant to infant that an attempt to determine the amount of force required to produce particular injuries is difficult. setting and in the courts. The so-called lucid interval in adults has been described in the adult medical literature and refers to that period of time between a significant head injury and the onset of signs and symptoms commensurate with the seriousness of the head injury. A comparable phenomenon has not been described in children in the pediatric literature. In one study, Willman and colleagues53 reviewed the case histories of 95 fatally injured children 16 years of age and younger. The head injuries were all accidental and involved blunt, non-penetrating forces. All cases had been witnessed, and the time of injury ascertained. Injuries included subdural hematoma; subarachnoid hematoma; extradural hematoma; cerebral, cerebellar, or brainstem contusions; skull fractures; and cerebral edema. Thirty cases had CT scans. The shortest interval between injury and CT scans demonstrating severe brain swelling was 1 hour, 17 minutes. Six cases showed evidence of mild swelling among those with head CT scan performed less than 3 hours post-injury. In only 1 case of a CT scan being done in less than 3 hours was there no brain swelling. Computed tomography scans done later than 3 hours after injury demonstrated various degrees of brain swelling. In only 1 case was there a “lucid interval”: an 11-year-old boy with an epidural hemorrhage who died of a surgical complication. Neck injuries—Cervical spine injuries occur in 1% to 2% of most large series of abusive head injuries. It is surprising that this incidence is not higher, given the large acceleration-deceleration forces applied to the head and by reflection to the cervical spine and neck musculature. In autopsy and clinical appraisals of children dying from SBS/SIS, there is little reporting of significant neck and cervical spine injuries. Hadley and colleagues65 reported subdural and epidural bleeding in 6 fatally injured infants. Feldman et al66 sought to determine the utility of MRI screening for cervical spine and cord abnormalities in 12 cases of abusive head trauma. In this series, 5 children had died of their head injuries and 4 of them had small subdural or subarachnoid hemorrhages at the level of the cervical spine. Magnetic resonance imaging had not identified any of these lesions. The authors questioned the efficacy of screening MRIs as a method for detecting cervical injuries in children with head injuries. Two cases of cervical spine injury, suffered as the result of hyperflexion of the neck, were reported by Rooks et al.67 By more careful attention to head injuries, it may be found there are more injuries than have been reported in the past. Serious head injuries resulting from falls—Many cases of abusive head trauma have histories of short falls as the reason for the head injury. However, there is a vast literature demonstrating that short falls (less than 10 feet) rarely, if ever, produce life-threatening head injuries, except in the cases of epidural hematomas. These latter intracranial injuries are easily distinguished from subdural and subarachnoid hematomas on CT and/or MRI imaging studies.68–79 Outcomes in Shaken Baby Syndrome/ Shaken Impact Syndrome There are too few studies analyzing outcome of SBS/SIS, but those that do indicate that long-term morbidity is high.80–83 The most common sequelae include tetraplegia, hemiplegia, blindness, cognitive impairment, neurobehavioral disorders, hemiparesis, and psychomotor delay. Spasticity, lack of coordination, and ataxia are the most common forms of psychomotor impairments.84 The few long-term follow-up studies lead to the conclusion that the full implication of such injuries takes more than 5 years to appreciate. The “lucid interval” and the time of injury to onset of signs and symptoms—This phenomenon has been the subject of argument both in the hospital 10 Visual Diagnosis of Child Abuse on CD-ROM Lecture Series 3. HEAD TRAUMA IN CHILD ABUSE References 18. Barkovich A. Destructive brain disorders in childhood. In: Barkovich A, ed. Pediatric Neuroimaging. 2nd ed. New York, NY: Raven Press; 1995:107–175 1. Duhaime AC, Alario AJ, Lewander WJ, et al. Head injury in very young children: mechanisms, injury types, and ophthalmologic findings in 100 hospitalized patients younger than 2 years of age. Pediatrics. 1992;90:179–185 19. Yamashima T, Friede RL. Why do bridging veins rupture into the virtual subdural space? J Neurol Neurosurg Psychiatry. 1984;47:121–127 2. Billmire E, Myers P. Serious head injury in infants: accident or abuse? Pediatrics. 1985;75:340–342 20. Duhaime AC, Christian CW, Rorke LB, Zimmerman RA. Nonaccidental head injury in infants—the “shaken-baby syndrome”. N Engl J Med. 1998;338(25):1822–1829 3. Weston JT. The pathology of child abuse and neglect. In: Kempe CH, Helfer RE, eds. The Battered Child. Chicago, IL: University of Chicago Press; 1980:241–271 21. Alexander R, Sato Y, Smith W, Bennett T. Incidence of impact trauma with cranial injuries ascribed to shaking. Am J Dis Child. 1990;144(6):724–726 4. Annegers J. The epidemiology of head trauma in children. In: Shapiro K, ed. Pediatric Head Trauma. Mt. Kisko, NY: Futura Publishing; 1983:1–10 22. Gilliland MG, Folberg R. Shaken babies—some have no impact injuries [see comments]. J Forensic Sci. 1996;41(1):114–116 5. Kraus J, Fife D, Cox P, Ramstein K, Conroy C. Incidence, severity and external causes of pediatric head injury. Am J Dis Child. 1986;140:687–693 6. Kraus J, Rock A, Hemyari P. Brain injuries among infants, children, adolescents and young adults. Am J Dis Child. 1990;144:684–691 23. Zauner A, Bullock R. The role of excitatory amino acids in severe brain trauma: opportunities for therapy: a review. In: Bandak F, Eppinger R, Ommaya A, eds. Traumatic Brain Injury. Bioscience and Mechanics. Larchmont, NY: Mary Ann Liebert, Inc.; 1996:97–104 7. Reece RM, Sege R. Childhood head injuries: accidental or inflicted? [see comments]. Arch Pediatr Adolesc Med. 2000;154(1):11–15 24. Marr W, Marr E. Some observations on Purtscher’s disease: traumatic retinal angiopathy. Am J Ophthalmol. 1962;54:693–705 8. DiScala C, Sege R, Li G, Reece RM. Child abuse and unintentional injuries: a 10–year retrospective [see comments]. Arch Pediatr Adolesc Med. 2000;154(1):16–22 25. Purtscher O. Noch unbekannte Befun nach Schaeltrauma. Ber Dtsch Ophthalmol Ges. 1910;36:294–301 26. Morgan O. A case of crush injury to the chest associated with ocular complication. Trans Ophthalmol Soc UK. 1945;65:366–369 9. Ewing-Cobbs L, Kramer L, Prasad M, et al. Neuroimaging, physical, and developmental findings after inflicted and noninflicted traumatic brain injury in young children. Pediatrics. 1998;102(2 Pt 1):300–307 27. Tomsai L, Rosman N. Purtscher retinopathy in the battered child syndrome. Am J Dis Child. 1975;129:1335–1337 10. Ludwig S, Warman M. Shaken baby syndrome: a review of 20 cases. Ann Emerg Med. 1984;13(2):104–107 28. Goetting M, Sowa B. Retinal hemorrhage after cardiopulmonary resuscitation in children: an etiologic re-evaluation. Pediatrics. 1990;85:585–588 11. Duhaime AC. Head trauma. Thousand Oaks, CA: Sage Publications, Inc; 1997 29. Kanter R. Retinal hemorrhage after cardiopulmonary resuscitation or child abuse? J Pediatr. 1986;108:430–432 12. Pounder DJ. Shaken adult syndrome. Am J Forensic Med Pathol. 1997;18(4):321–324 30. Gilliland MGF, Luckenbach MW. Are retinal hemorrhages found after resuscitation attempts? A study of the eyes of 169 children. Am J Forensic Med Pathol. 1993;14:187–192 13. Hymel KP, Bandak FA, Partington MD, Winston KR. Abusive head trauma? A biomechnics-based approach. Child Maltreatment. 1998;3(2):116–128 31. Odum A, Christ E, Kerr N, et al. Prevalence of retinal hemorrhages in pediatric patients after in-hospital cardiopulmonary resuscitation: a prospective study. Pediatrics. 1997;99(6):E3 14. Ommaya AK, Hirsch AE. Tolerance for cerebral concussion from head impact and whiplash in primates. J Biomech. 1971;4:13–23 15. Duhaime AC, Gennarelli TA, Thibault LE, Bruce DA, Margulies SS, Wiser R. The shaken baby syndrome. A clinical, pathological, and biomechanical study. J Neurosurg. 1987;66(3):409–415 32. Fackler J, Berkowitz I, Green R. Retinal hemorrhages in newborn piglets following cardiopulmonary resuscitation. Am J Dis Child. 1992;146:1294–1296 16. Schutzman S, Barnes P, Mantello M, Scott R. Epidural hematoma in children. Ann Emerg Med. 1993;22:535–541 33. Khan SG, Frenkel M. Intravitreal hemorrhage associated with rapid increase in intracranial pressure (Terson’s syndrome). Am J Ophthalmol. 1975;80(1):37–43 17. Shugerman RP, Paez A, Grossman DC, Feldman KW, Grady MS. Epidural hemorrhage: is it abuse? Pediatrics. 1996;97(5):664–668 34. Lambert SR, Johnson TE, Hoyt CS. Optic nerve sheath and retinal hemorrhages associated with the shaken baby syndrome. Arch Ophthalmol. 1986;104(10):1509–1512 11 Visual Diagnosis of Child Abuse on CD-ROM Lecture Series 3. HEAD TRAUMA IN CHILD ABUSE 35. McCrae M, Teasell R, Canny C. Bilateral retinal detachments associated with Terson’s syndrome. Retina. 1994;14:467–469 52. Gilliland MGF. Interval duration between injury and severe symptoms in nonaccidental head trauma in infants and young children. J Forensic Sci. 1998;43(3):723–725 36. Muller P, Deck J. Intraocular and optic nerve sheath hemorrhage in cases of sudden intracranial hypertension. J Neurosurg. 1974;41:160–166 53. Willman KY, Bank DE, Senac M, Chadwick DL. Restricting the time of injury in fatal inflicted head injuries. Child Abuse Negl1997;21(10):929–940 37. Munger CE, Peiffer RL, Bouldin TW, Kylstra JA, Thompson RL. Ocular and associated neuropathologic observations in suspected whiplash shaken infant syndrome. A retrospective study of 12 cases. Am J Forensic Med Pathol. 1993;14(3):193–200 54. Hymel KP, Abshire TC, Luckey DW, Jenny C. Coagulopathy in pediatric abusive head trauma. Pediatrics. 1997;99(3): 371–375 55. Ommaya AK, Faas F, Yarnell P. Whiplash injury and brain damage: an experimental study. JAMA. 1968;204(4): 285–289 38. Johnson D, Braun D, Friendly D. Accidental head trauma and retinal hemorrhage. Neurosurgery. 1993;33:231–235 39. Betz P, Puschel K, Miltner E, Lignitz E, Eisenmenger W. Morphometric analysis of retinal hemorrhages in the shaken baby syndrome. Forensic Sci Int. 1996;78:71–80 56. Gennarelli TA, Thibault LE, Adams JH, Graham DI, Thompson CJ, Marcincin RP. Diffuse axonal injury and traumatic coma in the primate. Ann Neurol. 1982;12(6):564–574 40. Elder JE, Taylor RG, Klug GL. Retinal haemorrhages in accidental head trauma in childhood. J Paediatr Child Health. 1991;27:286–289 57. Kirschner RH. The pathology of child abuse. In: Helfer ME, Kempe RS, Krugman RD, editors. The Battered Child. 5 ed. Chicago, IL: The University of Chicago Press; 1997:248–295 41. Greenwald M, Weiss A, Oesterle C, Friendly D. Traumatic retinoschisis in battered babies. Ophthalmology. 1986;93: 618–625 58. Budenz D, Farber M, Mirchandani H, Park H, Rorke LB. Ocular and optic nerve hemorrhages in abused infants with intra–cranial injuries. Ophthalmology. 1994;101:559–565 42. Elner SG, Elner VM, Arnall M, Albert DM. Ocular and associated systemic findings in suspected child abuse: a necropsy study. Arch Ophthalmol. 1990;108:1094–1101 59. Frank Y, Zimmerman R, Leeds N. Neurological manifestations in abused children who have been shaken. Dev Med Child Neurol. 1985;27:312–316 43. Gaynon MW, Koh K, Marmor MF, Frankel LR. Retinal folds in the shaken baby syndrome. Am J Ophthalmol. 1988; 106(4):423–425 60. Giangiacomo J, Khan J, Levine C, Thompson V. Sequential cranial computed tomography in infants with retinal hemorrhages. Ophthalmology. 1988;95:295–299 44. Levin A. Ocular manifestations of child abuse. In: Reece R, Ludwig S, eds. Child Abuse: Medical Diagnosis and Management. Baltimore, MD: Lippincott Williams and Wilkins; 2001 61. Kleinman PK, Barnes PD. Head trauma. In: Kleinman PK, ed. Diagnostic Imaging of Child Abuse. 2nd ed. St. Louis, MO: Mosby; 1998:285–342 45. Sandramouli S, Robinson R, Tsaloumas M, Willshaw H. Retinal hemorrhages and convulsions. Arch Dis Child. 1997;76:449–451 62. Riffenburgh R, Sathyavagiswaran L. Ocular findings at autopsy of child abuse victims. Ophthalmology. 1991;98: 1519–1524 46. Annable W. Ocular manifestations of child abuse. In: Reece R, editor. Child Abuse: Medical Diagnosis and Management. Malvern, PA: Lea and Febiger; 1994:138–49 63. Wilkinson WS, Han DP, Rappley MD, Owings CL. Retinal hemorrhage predicts neurologic injury in the shaken baby syndrome. Arch Ophthalmol. 1989;107(10):1472–1474 47. Buys YM, Levin AV, Enzenauer RW, Elder JE, Letourneau MA, Humphreys RP, et al. Retinal findings after head trauma in infants and young children. Ophthalmology. 1992;99(11): 1718–1723 64. Zepp F, Bruhl K, Zimmer B, Schumacher R. Battered child syndrome: cerebral ultrasound and CT findings after vigorous shaking. Neuropediatrics. 1992;23:188–191 48. Eisenbrey A. Retinal haemorrhages in the battered child. Child’s Brain. 1979;5:40–44 65. Hadley MN, Sonntag VK, Rekate HL, Murphy A. The infant whiplash-shake injury syndrome: a clinical and pathological study. Neurosurgery. 1989;24(4):536–540 49. Han DP, Wilkinson WS. Late ophthalmic manifestations of the shaken baby syndrome. J Pediatr Ophthalmol Strabismus. 1990;27(6):299–303 66. Feldman K, Weinberger E, Milstein J, Fligner C. Cervical spine MRI in abused infants. Child Abuse Negl. 1997;21: 199–205 50. Levin A. Ocular manifestations of child abuse. Ophthalmol Clin North Am. 1990;3:249–264 67. Rooks V, Sisler C, Burton B. Cervical spine injury in child abuse: report of two cases. Pediatr Radiol. 1998;28:193–195 51. Zimmerman RA, Bilaniuk LT, Bruce D, Dolinskas C, Obrist W, Kuhl D. Computed tomography of craniocerebral injury in the abused child. Radiology. 1979;130:687–690 68. Barlow B, Niemirska M, Gandhi RP, Leblanc W. Ten years of experience with falls from a height in children. J Pediatr Surg. 1983;18(4):509–511 12 Visual Diagnosis of Child Abuse on CD-ROM Lecture Series 3. HEAD TRAUMA IN CHILD ABUSE 69. Chadwick DL, Chin S, Salerno C, Landsverk J, Kitchen L. Deaths from falls in children: how far is fatal? J Trauma. 1991;31(10):1353–1355 79. Smith MD, Burrington JD, Woolf AD. Injuries in children sustained in free falls: an analysis of 66 cases. J Trauma. 1975;15(11):987–991 70. Helfer RE, Slovis TL, Black M. Injuries resulting when small children fall out of bed. Pediatrics. 1977;60:533–535 80. Bonnier C, Nassagne M, Evrard P. Outcome and prognosis of whiplash shaken infant syndrome: late consequences after a symptom–free interval. Dev Med Child Neurol. 1995;37:943–56 71. Joffe M, Ludwig S. Stairway injuries in children. Pediatrics. 1988;82(3 Pt 2):457–461 81. Duhaime AC, Christian C, Moss E, Seidl T. Long–term outcome in infants with the shaking-impact syndrome. Pediatr Neurosurg. 1996;24(6):292–298 72. Kravitz H, Driessen G, Gomberg R, Korach A. Accidental falls from elevated surfaces in infants from birth to one year of age. Pediatrics. 1969;44(suppl):869–876 82. Fischer H, Allasio D. Permanently damaged: long–term follow-up of shaken babies. Clin Pediatr. 1994;33:696 73. Lehman D, Schonfeld N. Falls from heights: a problem not just in the Northeast. Pediatrics. 1993;92:121–124 83. Haviland J, Russell R. Outcome after severe non-accidental head injury. Arch Dis Child. 1997;77:505–507 74. Lyons TJ, Oates RK. Falling out of bed, a relatively benign occurrence. Pediatrics. 1993;92:125–127 84. Wharton R, Rosenberg S, Sheridan R, Ryan D. Long–term medical consequences of physical abuse. In: Reece R, ed. Treatment of Child Abuse: Common Ground for Mental Health, Medical and Legal Professionals. Baltimore, MD: Johns Hopkins University Press; 2000:117–134 75. Meller JL, Shermeta DW. Falls in urban children. A problem revisited. Am J Dis Child. 1987;141(12):1271–1275 76. Musemeche CA, Barthel M, Cosentino C, Reynolds M. Pediatric falls from heights. J Trauma. 1991;31(10): 1347–1349 85. Atwal GS, Rutty GN, Carter N, Green MA. Bruising in non–accidental head injured children; a retrospective study of the prevalence, distribution and pathological associations in 24 cases. Forensic Sci Int. 1998;96(2–3):215–230 77. Nimityongskul P, Anderson L. The likelihood of injuries when children fall out of bed. J Pediatr Orthop. 1987;7: 184–186 78. Selbst SM, Baker MD, Shames M. Bunk bed injuries. Am J Dis Child. 1990;144(6):721–723 13