Childs Nerv Syst (2007) 23:499–507 DOI 10.1007/s00381-006-0267-4

ORIGINAL PAPER

Nonaccidental head trauma in infants Paula Gerber & Kathryn Coffman

Received: 7 February 2006 / Revised: 25 September 2006 / Published online: 17 March 2007 # Springer-Verlag 2007

Abstract Background Nonaccidental head trauma in infants is the leading cause of infant death from injury. Results and discussion Clinical features that suggest inflicted head trauma include the triad of the so-called shaken baby syndrome, consisting of retinal hemorrhage, subdural, and/or subarachnoid hemorrhage in an infant with little signs of external trauma. Studies have shown that, in general, the average short fall in the home is extremely unlikely to produce either subdural or retinal hemorrhage, although focal injuries such as skull fractures and epidural hemorrhage may be seen. Acceleration/deceleration, especially of the rotational type, is believed to be the most probable mechanism of injury in cases of nonaccidental head trauma. Damage to the cervicomedullary junction and the respiratory centers, with subsequent hypoxia and intracerebral edema, has also been implicated. After the initial trauma and hemorrhage, loss of cerebral autoregulation, breakdown of the blood-brain barrier, and disruption of ionic homeostasis occur, leading to brain edema and cytotoxicity. Cellular damage can involve large volumes of tissue, without respecting vascular territories. Conclusion Overall, a satisfactory biomechanical model is lacking, and the criminal nature of abusive injury makes it

P. Gerber (*) Barrow Neurological Institute, 8th floor, 350 W. Thomas Rd., Phoenix, AZ 85013, USA e-mail: [email protected] K. Coffman Child Abuse Assessment Center, St. Joseph’s Hospital and Medical Center, Phoenix, AZ, USA

difficult to perform systematic, controlled studies. Unfortunately, outcomes are poor, and the rate of repeated abusive episodes is high. Future research should focus on the development of a satisfactory research model and on prevention strategies. Keywords Abuse . Children . Shaken baby syndrome . Nonaccidental trauma

Introduction Trauma is the leading cause of death in children, and nonaccidental head trauma is the leading cause of traumatic death during infancy [15, 40]. This review summarizes the epidemiology, clinical features, biomechanics, imaging, pathology, treatment, and outcomes of inflicted head injury in infants.

Epidemiology The incidence of nonaccidental traumatic brain injury (TBI) in children 2 years or younger is estimated in the United States to be 17/100,000 person–years compared to 15.3/ 100,000 person–years for accidental TBI [40]. In the United Kingdom, a recent study reported the overall annual incidence of subdural hemorrhage and effusion to be 12.54/100,000 for children 0–2 years of age; 57% of these children suffered nonaccidental TBI [32]. The incidence of nonaccidental TBI is higher in male children and in children aged 12 months and younger (compared to older children) [32, 40]. Children of minority groups appear to have a higher incidence of both accidental and non-

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accidental TBI, which may reflect socioeconomic factors [40]. Other risk factors include young and unmarried mothers, a maternal education level of high school or lower, unstable family situations, low socioeconomic status, multiple-birth pregnancies, and disability or prematurity of the child. Having extended family in the home and having a parent in the military also increase the risk of inflicted TBI [15, 40, 49]. Wu et al. [64] reported a higher risk of infant abuse or neglect in children of American mothers who had smoked during pregnancy, were unmarried, were receiving Medicaid benefits, and had more than three children. The risk in children with a low birth weight was also elevated [64]. Starling et al. [61] reported that the most frequent perpetrators are fathers, followed closely by mother’s boyfriends, female babysitters, and mothers. In this series, female babysitters represented 17.3% of the perpetrators, a previously underrecognized culpable group [61].

Clinical presentation The classic presentation of nonaccidental head trauma in infants, the so-called shaken baby syndrome (SBS), is the finding of retinal hemorrhages (RHs), subdural and/or subarachnoid hemorrhage in infants with few signs of external trauma. Other “red flags” that may indicate nonaccidental trauma include a history that changes over time or between caregivers. A developmentally incompatible history (e.g., a 6-month-old child who fell while trying to climb out of a crib) should also raise suspicions [49]. When no history of trauma or only minor trauma is reported to treating physicians, the positive predictive value for abuse is 0.92 [31]. On examination, altered level of consciousness, irritability, a bulging fontanel, focal neurological signs, and seizures all indicate a high likelihood of intracranial injury [59]. Nonaccidental TBI has also been diagnosed in infants who presented with status epilepticus and no history of trauma, and were subsequently found to have retinal and subdural hemorrhage [43]. Children with nonaccidental TBI do not typically present with a lucid interval; they lose consciousness immediately [6]. However, there have been isolated case reports of a lucid interval in young children with fatal diffuse brain injury due to accidental falls. Consequently, this may not always be a reliable distinguishing feature [12, 52]. In a patient with a history suspicious for nonaccidental TBI, external signs of abuse or neglect should be sought, and can help support the diagnosis. They are absent in as many as 50% of cases, however [1]. A radiographic skeletal series is recommended to identify fractures indicating previous abuse. The most common fractures are through the metaphysis of the tibia, distal femora, and

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proximal humeri. Posterior rib fractures are highly specific for abuse [6]. Retinal hemorrhages (RH) have been a subject of controversy. When associated with trauma, they almost always indicate inflicted injury. Yet, they can be associated with a multitude of other conditions, including increased intracranial pressure, subarachnoid hemorrhage, coagulopathy, hematologic disorders, retinal dysplasia, retinopathy of prematurity, galactosemia, and hypertension [26]. A rare metabolic disorder, glutaric aciduria type 1, can also manifest with RH, acute subdural hematoma, and chronic subdural effusion [21]. RH is also a common birth complication. Studies in the United Kingdom and the United States have reported rates of RH in newborns as high as 34%, with wide variation in size and extent [18, 33]. Rates were highest with vacuum-assisted delivery (75– 78%). It is interesting to note that infants born by cesarean section had a small but significant incidence of RH of 7– 8% [18, 33]. RH mostly resolved within 1 month, but in one infant delivered by vacuum, it persisted for 58 days [18]. RH associated with child abuse, in contrast, tends to persist for months [2]. In the past, RH was also considered to be a possible complication of cardiopulmonary resuscitation (CPR). However, Odom et al. [48] performed a prospective study of 43 patients (mean age, 23 months) who received CPR with chest compressions while admitted to the pediatric intensive care unit. Cardiac or respiratory arrest was due to nontraumatic reasons in all cases. Ninety-three percent of the patients had evidence of at least a mild coagulopathy. Patients were evaluated by a pediatric ophthalmologist. Small punctate RH was seen after CPR in only one patient [48]. For a detailed review of pediatric RH, the reader is referred to the recent review by Aryan et al. [2]. If one is able to exclude the above diagnoses, RH is usually considered to indicate trauma and is highly suspicious for inflicted injury, unless the child’s presenting history includes a severe accidental trauma such as a motor vehicle accident [6, 25]. Bechtel et al. [3] reported RHs in only 10% of children less than 24 months old with an accidental TBI compared to 60% with an inflicted TBI. Vinchon et al. [62] described 16 patients with subdural hemorrhage sustained in traffic accidents; only three also had RHs. A controversial paper by Plunkett [52] reported 18 children (aged 12 months to 13 years) with witnessed accidental fatal head injuries caused by falls from playground equipment. Six children had documented funduscopic examinations: Four had bilateral RHs along with acute subdural hemorrhage. The distances that these children fell ranged from 2 to 5 ft [52]. To identify these deaths, however, the author reviewed more than 75,000 playground injury cases over 11.5 years. This speaks to the rarity of significant injury in such cases. Furthermore,

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formal ophthalmologic examinations were not documented in any cases. Finally, the age range for the study was broad, with a median of 4.5 years, and the youngest child was 12 months old. Most cases of nonaccidental TBI occur in children under the age of 12 months [40]. Thus, these data should be interpreted with caution with regard to the typical infant with possible nonaccidental injury. In general, the average fall or injury in the home should be insufficient to cause RH [14, 38]. RH in children with abusive head injury are more likely to be bilateral, intraretinal, to extend to the periphery of the retina, and to be associated with preretinal hemorrhage and premacular retinal hemorrhage. All layers of the retina are often involved [3]. Retinal hemorrhages in these children can also be associated with retinal detachments, tears, folds, and vitreous hemorrhage [6]. In contrast, retinal hemorrhages associated with accidental trauma tend to be unilateral, few in number, and found at the posterior pole [3, 10, 62]. Retinal hemorrhages associated with increased intracranial pressure also tend to be at the posterior pole and associated with papilledema [6, 62]. It is probably most prudent to view retinal hemorrhage, regardless of the pattern, as suggestive of a rotational acceleration injury, while remaining aware of possible exceptions. One must consider the possible biomechanics of the reported trauma and decide if it fits the injury pattern.

Biomechanics Head trauma occurs when a mechanical load, either static or dynamic, is delivered to the head. In most cases, the load is dynamic and of two types: impact or impulsive. An impact load is delivered at a point of impact and can lead to immediate contact effects such as skull fractures, contusions, or epidural hemorrhage. Focal subdural hemorrhage can also underlie a point of impact [34, 35]. Impulse is defined as a change in momentum caused by a force applied over time (i.e., acceleration or deceleration). The acceleration (or deceleration) can be translational, rotational, or angular. Impulsive loads lead to tissue strain, which can be of three types: tension, compression, or shear [24]. Translational acceleration occurs in one plane and is less likely to cause shearing injury than rotational or angular acceleration [6, 14, 52]. In SBS shearing forces on the bridging veins and retina are thought to be the cause of subdural and retinal hemorrhages [5, 6, 24, 34, 35]. The brain has the unique property of viscoelasticity, which means that its tolerance to strain changes with the rate that the strain is delivered. Consequently, not only the magnitude of acceleration or deceleration but also the rate at which it occurs determines the nature of the injury [24]. For instance, falling and striking a hard surface lead to

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rapid deceleration, which can cause a superficial injury such as a skull fracture and possibly an underlying contusion or focal hemorrhage. Deceleration of a higher magnitude, longer duration, or both may cause a diffuse shearing injury. A brief, high-magnitude anteroposterior acceleration/deceleration is thought to cause diffuse subdural hemorrhage (i.e., not directly underlying an impact site). In contrast, relatively lower magnitude but prolonged acceleration/deceleration in the coronal plane is likely to cause diffuse axonal injury [34]. An example is striking the soft cushion of a headrest in a high-speed motor vehicle accident. The focal effects of the impact are reduced, but the duration of deceleration is prolonged [24]. With regards to SBS, in the original description by Caffey in 1972 [5], a nursemaid admitted to shaking several children while holding them by the arms or trunk, leading to the theory that shaking causes shearing of the bridging veins and subsequent subdural and RH. Violent shaking is presumed to cause severe rotational and angular acceleration/deceleration as the head whips back and forth. Infants are especially at risk for acceleration/deceleration injuries because of their relatively large heads, weak neck muscles, and relatively large subarachnoid spaces [16]. Their brains are relatively soft due to immature myelination and the small size of axons. Infants are also at greater risk from impact forces. Their thin, soft skulls more readily transmit impulse forces to deeper structures [6]. While hemorrhage occurs acutely, often the subsequent effects of TBI represent the greatest danger to the patient. After an acute TBI, cerebral autoregulation can be lost and ionic homeostasis disrupted. Both factors contribute to intracerebral edema, which usually develops within the first 24 to 72 h after a TBI. In particular, ipsilateral edema of the entire underlying hemisphere is often associated with an acute subdural hematoma. This phenomenon is not entirely understood. It may be related to loss of autoregulation with increased blood flow, and subsequent disruption of the blood-brain barrier. Defective ion transport and excitatory amino acids, leading to cellular toxicity, have also been implicated. A region of brain with defective autoregulation is also at greater risk for ischemic or hyperemic injury related to changes in cerebral perfusion pressure. Infants appear to be more susceptible to these processes, perhaps due to immature autoregulation and a greater risk for postinjury apnea and hypotension [24, 26, 27, 41, 53]. Some authors disagree that shaking is the primary mechanism of injury in nonaccidental infant head trauma. Duhaime et al. [16] reported that shaking alone is insufficient to cause the pattern of injury seen in these patients; some impact is required. The authors performed a biomechanical study using doll models. The heads were filled with cotton and water to simulate the weight of an actual infant’s head. Several adult male and female

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experimenters shook the models violently. They also shook the models and then struck the heads against both padded and metal objects. In each case, angular acceleration was calculated and compared to primate injury models that had previously determined the acceleration thresholds for certain injuries. They found that the average adult shaking an infant would not achieve the degree of angular acceleration necessary to cause the pattern of injury seen in SBS, whereas shaking followed by impact would. The authors have proposed renaming the syndrome “shaken impact syndrome” [16]. This proposal remains controversial because there is not yet a satisfactory model of the infant head and brain. A doll neck tends to move in the anteroposterior plane, without the same degree of rotational acceleration as that of an infant. The cotton–water model of the brain is of homogenous composition. It fails to simulate the various densities and inertial forces of different parts of the brain and intracranial vessels. Furthermore, regarding the acceleration injury thresholds, the relative head size compared to neck musculature in primates is smaller than in human infants. In support of the impact theory; however, Hanigan et al. [29] described a similar “tin ear syndrome” with unilateral ear bruising, ipsilateral cerebral edema, and RH after blunt trauma to the ear. Another mechanism of injury that has been suggested is damage to the lower brainstem and upper cervical spine. Hadley et al. [27] described a “whiplash-shake syndrome” showing significant cervical spine injury associated with subdural and/or epidural hematomas and contusions of the spinal cord at the cervicomedullary junction. Other autopsy series have reported similar findings [22, 23, 60]. These authors suggest that damage to the cervicomedullary junction, particularly the respiratory centers, may be an important mechanism contributing to morbidity and mortality in nonaccidental TBI in infants [22, 23, 27, 60]. In fact, Geddes et al. [23] recently reported a series of 50 infants aged up to 5 months who suffered nontraumatic deaths (75% with evidence of hypoxia). Seventy-two percent of these infants showed intradural hemorrhage at autopsy; in some cases, hemorrhage had ruptured onto the surface of the dura. The authors proposed that hypoxia (due to damage of the respiratory centers) with severe brain swelling, raised intracranial pressure, and subsequent vascular leakage may be the cause of both subdural and RH in nonaccidental TBI, rather than traumatic rupture of the bridging veins. Donohoe [13] and, more recently, Leestma [42] published literature reviews of studies involving nonaccidental TBI in infants. They pointed out that most of the studies have been retrospective, lacking controls, and furthermore, that a definition of nonaccidental TBI or SBS for research studies has yet to be identified. They also noted that most

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cases of nonaccidental TBI in the literature have been based on inference or on the judgment of physicians and/or social workers involved with the case. There are relatively few studies with cases in which the perpetrators actually confessed to the crime and described the mechanism of injury. In fact, of a total of 324 cases identified between 1969 and 2001, only 54 met these criteria. Of these, only 11 involved shaking alone [42]. These authors discount many of the current theories and assumptions about the nature of nonaccidental infant head injury and SBS. Development of a satisfactory biomechanical model is clearly needed, as randomized controlled trials in humans are ethically impossible. From a clinician’s perspective, however, it is most important to recognize when the severity of injury does not reflect the reported history. Once a child has been abused, the exact mechanism of abuse is moot. Fortunately, data support the idea that minor accidental trauma around the home seldom causes life-threatening injury. Furthermore, these accidents (usually falls) have a different pattern of injury compared to inflicted head trauma. Accidental falls at home are rarely associated with significant injury, particularly intracranial injury. Most injuries are superficial lacerations and hematomas; skull or extremity fractures rarely occur [14, 30, 37, 39, 44, 47, 57, 63]. Williams [63] reported 106 patients younger than 3 years old with a history of a free fall witnessed by two or more people or by a noncaretaker. Of the 106 patients, 77 sustained only mild bruises, abrasions, or simple fractures. Of these 77 patients, 43 had fallen more than 10 ft. Intracranial injury, depressed skull fractures, or compound fractures occurred in 14 patients who fell from 5 to 40 ft. However, in the three patients who fell less than 10 ft, no life-threatening injury occurred [63]. An interesting aspect of this study is that in 53 patients with unwitnessed falls (or falls witnessed by only one caretaker), there were 18 severe injuries, including intracranial injuries, in patients who fell less than 5 ft. This finding suggests that these patients were, in fact, victims of nonaccidental trauma. A similar phenomenon has been noted in other studies [7, 57]. Joffe and Ludwig [37] found no evidence of intracranial hemorrhage in 363 patients, 1 month to 18.7 years old, with a history of having fallen down stairs. In contrast, Chiaviello et al. [9] reported 2 contusions and 1 subdural hematoma in 69 patients less than 5 years old who fell down stairs. The differences could reflect different thresholds for imaging in such cases between 1988 and 1994. In both studies, injuries to multiple body parts were rare as was intracranial hemorrhage [9, 37]. Duhaime et al. [14] reviewed 100 consecutively admitted head-injured patients, 24 months old and younger, and analyzed mechanisms of injury, injury type, and associated injuries. Based on their analysis of patients with accidental injuries, they found that a fall of less than 4 ft (such as from

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a crib) could produce soft tissue injuries, linear skull fractures, or epidural hemorrhage. A fall greater than 4 ft could cause these injuries, plus depressed and basilar skull fractures, subarachnoid hemorrhage, and contusions, but would be unlikely to cause subdural hemorrhage. Severe accidental trauma, such as a motor vehicle accident, would be required to produce diffuse subdural hemorrhage and diffuse axonal injury [14].

Neuroimaging findings Diagnostic imaging modalities in suspected cases of child abuse should include skull radiographs and computed tomography (CT) to evaluate for the presence of skull fractures and intracranial hemorrhage, respectively [54]. Increasingly, magnetic resonance imaging (MRI) is recognized as an important modality because of its sensitivity to hypoxic–ischemic injuries and white matter injuries [8, 51, 54]. Subdural hemorrhage is a characteristic finding of nonaccidental infant head injury. These hemorrhages are most common along the interhemispheric fissure and over the convexities (Fig. 1a–c) [20, 54]. Subarachnoid hemorrhage also may be present, typically along the falx cerebri or focally within sulci along the hemispheres [54]. Epidural hemorrhage and intraparenchymal hemorrhage are less common [19, 54]. Classically, shear injury (diffuse axonal injury) is associated with severe, high-velocity motor vehicle accidents, but it also can be seen in nonaccidental TBI [19, 20, 54]. It is an important marker for demonstrating severe accelerational/decelerational injury [6, 54]. MRI is the

Fig. 1 Axial slices (moving inferiorly to superiorly) from a noncontrast CT scan of a 9-month-old girl show a large right subdural hematoma with right-to-left midline shift. Most commonly, this is seen over the convexities (a–c) or in the interhemispheric fissure (c) [20,

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modality of choice for detecting such injuries. Gradientecho sequences should be included to detect small white matter hemorrhages. Diffusion-weighted imaging can detect nonhemorrhagic injury [8, 54]. Shear injury often involves the subcortical white matter, corpus callosum, brainstem, and internal capsule [54]. Hypoxic–ischemic injury is another important consequence of nonaccidental TBI. It is best demonstrated with diffusion-weighted MRI, which shows diffusion restriction in the area of injury. Injuries may be multifocal and widespread and do not necessarily respect vascular territories. Cerebral edema, related to ischemia or due to the mechanisms described above, is common. On CT there may be diffuse loss of gray–white differentiation and hypodensity in the hemisphere underlying a subdural hematoma, sometimes extending into the contralateral frontal lobe. MRI shows diffusion restriction and T2weighted hyperintensity in areas of edema (Fig. 2) [15, 19, 20, 36, 54]. Children with inflicted injuries are more likely to show enlarged subarachnoid or subdural spaces (often difficult to distinguish radiographically). Enlarged subarachnoid spaces can represent either brain atrophy or communicating hydrocephalus, reflecting previous head injuries [19, 20, 35]. This phenomenon has also been reported to underlie acute subdural hemorrhage. After trauma, subdural fluid collections (hygromas) can develop from a tear in the arachnoid and subsequent accumulation of cerebrospinal fluid [35]. Benign extracerebral fluid collections, also known as benign macrocephaly or external hydrocephalus, are a source of controversy. These collections are defined as asymptomatic enlarged subarachnoid spaces, without ventricular dilatation, in young children with rapidly growing

54]. The varied density of the hematoma may be associated with hyperacute hemorrhage, an evolving subdural hemorrhage, or repetitive trauma with hemorrhage of different ages [35]

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Fig. 2 Axial diffusion-weighted MRI of the brain of a 9-month-old girl within 24 h of admission with a right subdural hematoma shows no diffusion restriction (a) and no T2-weighted (b) signal abnormality in the underlying parenchyma. Diffusion-weighted MRI obtained on

hospital day 6 shows extensive diffusion restriction (c and d) and T2weighted (e–g) changes involving the entire right hemisphere and part of the left inferior frontal lobe. The abnormality crosses multiple vascular territories. MR angiography of the head and neck was normal

heads [46, 56]. They are likely related to immaturity of the arachnoid villi, with transient communicating hydrocephalus [35]. Some authors have reported a predisposition in these children toward subdural hemorrhage after minor

traumas and have argued that this finding may be evidence against inflicted trauma [50, 56]. Based on the width of the extraaxial space, Papasian and Frim [50] developed a mathematical model of potential

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stretch injury to the bridging veins. Their model suggests that the risk of patients with benign extracerebral fluid collections for subdural hemorrhage would be increased after minor traumas compared to the normal population [50]. Others, however, have found no increase in the frequency of subdural hematomas over time in these children, and most children remain asymptomatic [28, 35]. In general, all subdural hemorrhages should be viewed with a high index of suspicion.

Pathology In autopsy series, the most common findings in infants with nonaccidental head trauma are subdural hemorrhages, RHs, and skull fractures. Very young infants (2 to 3 months old) tend to show patterns of apnea and global hypoxia, craniocervical junction injury, skull fractures, and comparatively smaller subdural hemorrhages. Older children tend to show larger subdural hematomas and more severe extracranial injuries. Classic markers for diffuse axonal injury are relatively rare, but some authors suggest that this paucity reflects differences in axonal injury patterns in an immature brain [6, 22, 23, 41]. Typically, the cause of death is increased intracranial pressure related to severe brain edema. Severe hypoxic brain damage is also common [22, 23]. Shannon et al. [60] reported no difference in the frequency of markers of axonal injury between children dying of nontraumatic hypoxic–ischemic encephalopathy and children dying of nonaccidental TBI. Of 11 children with nonaccidental TBI, however, seven had abnormal axons in the cervical spinal cord compared to none of the children in the hypoxic– ischemic group. In these patients, damage at the craniocervical junction may have led to apnea and subsequent hypoxic injury [22, 23, 27, 60].

Treatment A detailed review of the treatment of TBI in infants is beyond the scope of this article. Briefly, initial treatment of these infants should include neuroimaging, and if necessary, urgent neurosurgical evaluation. Patients should be managed in the intensive care unit with fluid resuscitation, anticonvulsants, and intubation and ventilation if necessary [15]. The high rates of repeat abuse mandate strict vigilance on the part of physicians to protect children from further harm or death, and all suspected cases of nonaccidental injury should be reported to the appropriate authorities [17, 45]. Once stabilized, multidisciplinary care involving pediatric intensive care, neurology, neurosurgery, ophthalmology, forensic pediatrics, and social work is recommen-

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ded. If the child survives, he or she will require appropriate rehabilitation for any neurological deficits.

Outcomes Outcomes for children with nonaccidental TBI are poor. Their estimated mortality rate ranges from 15 to 38% [40]. Thirty to 50% of survivors suffer cognitive or other neurological deficits, and 30% have a chance for full recovery [6]. A lower score on the Glasgow Coma Scale at presentation, a prolonged duration of impaired consciousness, and a higher number of lesions on imaging studies all correlate with worse outcomes [55]. Furthermore, the rate of repeated abuse in children who are returned home ranges from 31 to 43% [17, 45]. Data on successful intervention strategies are limited and disappointing [11, 45, 58]. A recent analysis of a broad prevention strategy using individual and community interventions in four cities (the Community Partnerships for Protecting Children) found no consistent, significant benefit between treatment and control groups. Improvements, however, were noted in child welfare workers’ job satisfaction and in parental depression rates [11]. Rubin et al. [58] found that most studies of primary and secondary prevention strategies (mostly involving home visitation programs) showed no benefits. Studies have been limited by small sample sizes, poor follow-up, and a lack of reliable standards for assessing outcomes [58]. Bugental et al. [4] reported positive results with a home visitation strategy incorporating a cognitive therapy component [4]. Clearly, more work is needed in this area.

Conclusions Nonaccidental head trauma in infants is the leading cause of infant death from injury. The high rate of repeated abuse makes identification of potential cases crucial. The underlying biomechanics of injury in this syndrome and the purported sequelae of accidental and nonaccidental trauma remain controversial. Using data from known accidental trauma helps to determine whether a caregiver’s history is a plausible explanation for a particular injury pattern. Once a caregiver’s history is determined to be false, abuse becomes the most likely diagnosis and the exact mechanism of injury is less important. Because the nature of abusive injury makes controlled human studies impossible, development of an appropriate biomechanical model for infant head trauma would be a valuable tool for research. Most importantly, more work is needed to develop effective methods of prevention and intervention.

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