Wouter A. Karst

Abusive head trauma in young children in the Netherlands: evidence for multiple incidents of abuse

We investigated the prevalence of risk factors for and the prevalence of prior abuse in abusive head trauma victims in the Netherlands.

Using the table in the Swedish review on shaken baby syndrome will not help courts deliver justice

1.Department of Forensic Medicine, Section on Forensic Pediatrics, Netherlands Forensic Institute, The Hague, The Netherlands 2.Institute of Legal Medicine/University Hospital of Cologne, Cologne, Germany 3.Department for Pediatric and Adolescent Medicine, Child Protection Center, Klinikum Kassel, Germany 4.Department of Forensic Medicine, Netherlands Forensic Institute, The Hague, The Netherlands 5.Forensic Pathology, University Medical Center, Maastricht, The Netherlands 6.Forensic (Paediatric) Radiology, Amsterdam Medical Center, Amsterdam, The Netherlands 7.Department of Legal Medicine, University Medical Center, Hamburg-Eppendorf, Germany 8.Forensic Pathology and Clinical Forensic Medicine, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway

Abusive head trauma: Differentiation between impact and non-impact cases based on neuroimaging findings and skeletal surveys

OBJECTIVES To determine whether imaging findings can be used to differentiate between impact and non-impact head trauma in a group of fatal and non-fatal abusive head trauma (AHT) victims. METHODS We included all AHT cases in the Netherlands in the period 2005-2012 for which a forensic report was written for a court of law, and for which imaging was available for reassessment. Neuroradiological and musculoskeletal findings were scored by an experienced paediatric radiologist. RESULTS We identified 124 AHT cases; data for 104 cases (84%) were available for radiological reassessment. The AHT victims with a skull fracture had fewer hypoxic ischaemic injuries than AHT victims without a skull fracture (p=0.03), but the relative difference was small (33% vs. 57%). There were no significant differences in neuroradiological and musculoskeletal findings between impact and non-impact head trauma cases if the distinction between impact and non-impact head trauma was based on visible head injuries, as determined by clinical examination, as well as on the presence of skull fractures. CONCLUSIONS Neuroradiological and skeletal findings cannot discriminate between impact and non-impact head trauma in abusive head trauma victims.

Racial and Ethnic Disparities and Bias in the Evaluation and Reporting of Abusive Head Trauma

Objective To characterize racial and ethnic disparities in the evaluation and reporting of suspected abusive head trauma (AHT) across the 18 participating sites of the Pediatric Brain Injury Research Network (PediBIRN). We hypothesized that such disparities would be confirmed at multiple sites and occur more frequently in patients with a lower risk for AHT. Study design Aggregate and site‐specific analysis of the cross‐sectional PediBIRN dataset, comparing AHT evaluation and reporting frequencies in subpopulations of white/non‐Hispanic and minority race/ethnicity patients with lower vs higher risk for AHT. Results In the PediBIRN study sample of 500 young, acutely head‐injured patients hospitalized for intensive care, minority race/ethnicity patients (n = 229) were more frequently evaluated (P < .001; aOR, 2.2) and reported (P = .001; aOR, 1.9) for suspected AHT than white/non‐Hispanic patients (n = 271). These disparities occurred almost exclusively in lower risk patients, including those ultimately categorized as non‐AHT (P = .001 [aOR, 2.4] and P = .003 [aOR, 2.1]) or with an estimated AHT probability of ≤25% (P < .001 [aOR, 4.1] and P < .001 [aOR, 2.8]). Similar site‐specific analyses revealed that these results reflected more extreme disparities at only 2 of 18 sites, and were not explained by local confounders. Conclusion Significant race/ethnicity‐based disparities in AHT evaluation and reporting were observed at only 2 of 18 sites and occurred almost exclusively in lower risk patients. In the absence of local confounders, these disparities likely represent the impact of local physicians’ implicit bias.

Non-Accidental Injury in Infants and Children: Evidence-Based Emergency Imaging

Child abuse is a world-wide problem, with both short and long term consequences, and the radiologist can be one of the first to suggest a diagnosis of child abuse. Timely detection of physical child abuse can be important to prevent further harm to the child in question. In this chapter radiological findings in young children, e.g. subdural hematoma and posterior rib fractures, which are strong indicators for child abuse are discussed and the evidence base is presented.

More on the strength of evidence in forensic pathology

We would like to respond to the Commentary entitled ‘‘On the strength of evidence in forensic pathology,’’ by Pollanen [1]. He brings up the issue of the strength of evidence in forensic pathology. More specifically, he discusses the strength of evidence required to draw conclusions about the cause of death, and three issues that make this a thorny topic: First, the legal system will apply legal standards such as ‘‘balance of probabilities’’ and ‘‘beyond a reasonable doubt’’ while it is unusual for pathologists to formulate their opinions based on a legal standard. Second, logic would require the severity of the legal outcome to be linked to a higher medical evidential standard for an opinion. This could make the required evidential standard vary from case to case. Third, different pathologists can seemingly vary widely in their opinion in difficult areas of pathology, based on a possibly small variation in their interpretation of the evidence and the standard they apply to reach a conclusion. We think Pollanen is correct in pointing out these issues. In this contribution we want to demonstrate how the application of logic can solve them, and clarify the role of the forensic pathologist. The issues mentioned stem from the idea that the forensic pathologist should report a conclusion (categorical or otherwise) rather than the strength of evidence. For a physician who observes hypertension in a patient and prescribes some medicine this makes sense, since the physician has all the information available and has the task to make a decision on treatment: the physician is assuming both the task of the scientist and the equivalent of the task of the trier of fact (judge or jury) to decide. In contrast, the pathologist’s goal is to support the decision of someone else, the trier of fact, who has all the information and other evidence available in the case and the task to decide on the issues. The solution lies in the realization that the task of the forensic pathologist is to report the evidential strength, nothing more, nothing less [2]. The evidential strength communicates everything that the medical evidence can tell us (through the expertise of the pathologist dealing with the case), and allows the trier of fact to combine it with all the other evidence and information in the case. The other evidence and information is outside the area of expertise of the pathologist. It is therefore up to the trier of fact (not the pathologist) to decide whether the total of the evidence reaches the amount required to decide one way or another. This solution solves Pollanen’s first issue. Note that non-medical evidence can influence the probability of medical hypotheses concerning the cause of death. Suppose the pathologist is considering two competing causes of death where one is considered a natural cause while the other is crime-related. Information from an eye witness claiming to have seen violence occur could support the hypothesis of the crime-related cause of death. This information would clearly not be for the pathologist to take into account, but for the trier of fact to combine with the evidence from the pathologist and all other evidence and information in the case. This is properly done when the forensic pathologist reports on the evidential value of the medical findings only, and not on the probability of the medical hypotheses. Pollanen rightly points out that the total amount of evidence required would logically depend on the severity & Charles E. H. Berger c.berger@nfi.minvenj.nl

Mast cells in the human dura: effects of age and dural bleeding

To the Editor, We read with great interest the manuscript by Varatharaj and colleagues[2] regarding the presence of mast cells in the human dura. The authors should be applauded for their continued efforts to try to bring clarity to an area which remains opaque and complex; timing of subdural haemorrhage (SDH) collections. The central feature of their study is the presence of mast cells in the dura. It is important to note, as the authors indicate, immunologically active cells and angiogenic factors have been identified as part of the reparative reaction to subdural haemorrhage for decades. The authors note Sarkar and colleagues[1] demonstrated the presence of eosinophils the chronic SDH in 2002. Sarkar and colleagues report the finding having been discovered by Yamashima and colleagues[3] demonstrating this finding as early as 1985. The most recent contribution by Varatharaj and colleagues[2], evaluating mast cell density within postmortem dural samples, is quite compelling, but given what is already known about the presence of eosinophils in subdural haemorrhage, some of the conclusions are unsupported by the data presented. The current study was aimed to determine the density of the mast cell population in the dura mater of humans. The authors also wanted to describe changes in the density of the mast cells between fresh and old SDH. It appears that the intention of the investigators, in part, is to assess a “profile” that mast cells may have as related to the age of the subdural collection. What remains unclear from the methods section is if the assessment of the mast cell density was done by an assessor blinded to clinical information. If there were no blinding in the assessment of mast cell density then there is significant opportunity for investigator bias. Varatharaj and colleagues[2] note that the density of mast cells was nearly statistically related to the age of the SDH, although it remains unclear what statistical analysis was being performed. The standard error ranges of the average mast cell density, as shown in Fig. 4, are relatively large. Given the small sample size, it is not surprising the absence of a statistically significant. Despite the lack of statistical significance, a relation between the mast cell density and the age of the SDH would confirm the findings of Yamashima and colleagues. In evaluating dural membrane samples of 50 subjects (10-87 years), Yamashima and colleagues noted that the density of eosinophils was related to the age of the SDH as opposed to the age of the subject. In addition they noted lymphocytes, histiocytes and mast cells in various distributions according to age of the SDH. These authors concluded that eosinopshils were part of a broader cellular inflammatory response to injury and contributed to the healing as well as the angiogenesis associated with “chronic” SDH. We would contend that the findings of Varatharaj and colleagues is quite consistent with these findings, and that any apparent association of mast cell density to age of the subject is confounded by the age of the SDH and small sample size. To help resolve the apparent discrepancy we suggest some clarifications. First, it would be helpful for the authors to present the ages of the subjects and the ages of the SDH collection in tabular form. We would anticipate that the apparent trend of mast cells to the age of the subject is related to the over representation of “old” SDH in younger subjects. Additionally, it is unclear why 200 months (16 years and 8 months) was used as the age cut off. It would be helpful to the reader to have the ages represented in a more standardized fashion (years or developmental stage; i.e. infant, toddler, adolescent, adult...). We anticipate that the apparent age relationship with mast cell density would be readily resolved by a reformatting of the data. Overall, we find the work of Varatharaj and colleagues quite intriguing. We would propose that the relationship of mast cell density is simply a function of inflammatory response to injury as has been reported earlier and that the need for a more complex explanation for these findings (trigemino-cardiac reflex) is unwarranted and remains unsupported.

Letter to the editor: Unexplained fractures: child abuse or bone disease: a systematic review.

To the editor We read with interest the article by Pandya et al. [9]. Their review of the medical literature for bone diseases mimicking child abuse and neglect (CAN) is helpful with the very important interpretation of unexplained fractures. However, we do not understand why the study by Paterson et al., in which they introduced a variant form of osteogenesis imperfecta (OI) which they called ‘temporary brittle bone disease’ (TBBD) [11], was not excluded from the study. Paterson et al. suggested a temporary deficiency of an enzyme, involved in the posttransitional processing of collagen, as the underlying problem of TBBD in infants [11]. Others have suggested decreased fetal movement in utero might be the reason of temporary brittle bones [8]. No single clinical or laboratory study supports one of these theories. TBBD is not clinically validated nor generally accepted by expert professionals [4, 5, 7]. The Supreme Court in the United Kingdom concluded in a 2001 case that Paterson’s TBBD theory had no scientific basis and the investigation was subjective, unreliable, nonscientific, and nonproven [1]. In 2004 the General Medical Council removed Paterson from their register of practicing physicians in the United Kingdom because “he ignored crucial evidence to advance his own controversial theories on bone disease” [3]. Paterson recently published five more cases on infants with multiple rib fractures [10], which he presented as evidence for the existence of TBBD. Letters to the editor showed once again the complete lack of validation for the entity [6, 12]. Crucial additional information in these cases, such as data from brain imaging, eye examinations, or a complete skeletal survey, were not provided [10]. There was no review of the radiologic images by a pediatric radiologist [10]. In four cases there were no data on examination for skin injury [10]. Being unaware of the lack of scientific basis for the existence of TBBD is dangerous, as the important evaluation of fractures in young children might lead to incorrect conclusions, possibly resulting in ongoing risk for the child or other children. In our opinion TBBD should be considered a theory without any scientific basis. This background information should have been provided in the otherwise instructive review by Pandya et al. [9].