Whether New York City social workers and agency officials should face liability for wrongfully or mistakenly removing children from allegedly abusive homes was at the center of oral arguments yesterday at the U.S. Court of Appeals for the Second Circuit.
Judges Jose A. Cabranes and Roger Miner, and Southern District Judge Jed S. Rakoff, sitting by designation, heard argument in four cases concerning the proper degree of legal exposure for the city and employees of its Administration for Children’s Services (ACS).
Carolyn Kubitschek of Lansner Kubitschek Schaffer & Zuccardy in Manhattan, arguing for parents, foster parents and children who have been wrongfully removed from their homes, called the city agency “out of control.” She contended that agency officials should be liable under federal civil rights law for relying on a doctor criticized for over-reporting child abuse, and that caseworkers should be held liable for prematurely removing a child or failing to act quickly in returning them once the parent or foster parent has been cleared of responsibility for the child’s injury.
But in arguing for immunity, Deborah Brenner of the New York City Law Department told the court that caseworkers should not be held liable for decisions they make under pressure. “Caseworkers walk a very fine line every day,” she said. “They have to balance the right of the parent to family integrity” versus the safety of the children. New York City was represented by four senior counsels with the Law Department’s Appeals Division: Tahirih Sadrieh argued Green v. Mattingly, 08-4636-cv; Ms. Brenner argued V.S. v. Mattingly, 08-5157-cv; Drake Colley argued Graham v. Mattingly, 08- 5271-cv; and Janet Zaleon argued Cornejo v. Bell, 08-3069-cv.
The panel was openly skeptical about Ms. Zaleon’s argument in Cornejo that caseworkers and ACS lawyers should have absolute immunity for their actions. In Cornejo, caseworkers removed a baby who later died from injuries that included a fractured rib allegedly suffered when the mother was not home. It was later revealed the child died of a birth defect. Agency lawyers stuck by the removal in Family Court even after some staff said it should drop the case. The attorneys continued, the court was told, because there remained a belief the father may have shaken the baby.
“That’s a novel theory we don’t have any support for,” Judge Cabranes said. Judge Miner said, “Absolute immunity is a pretty heavy concept.” He also wanted to know if there is “any historical or common law basis for this assertion?” Ms. Zaleon said the situation with caseworkers and lawyers at ACS was unique because, unlike police officers and prosecutors, they work for the same agency and are supposed to assist the court in determining what is in the best interests of the child on an ongoing basis. But Ms. Kubitschek said the attorneys in Cornejo “stepped out of that function when they resisted their clients’ efforts” to drop the case, she said. “They were acting contrary to the
instructions as given” by caseworkers and supervisory staff.
A central figure in the arguments was Dr. Deborah Esernio-Jenssen of Long Island Jewish Hospital, who has been criticized by Family Court judges for incorrect diagnoses of Shaken Baby Syndrome. The issue is whether ACS workers, knowing about Dr. Esernio-Jenssen’s reputation, could be held liable for relying on her opinion in what turned out to be the mistaken removal of a child. Ms. Brenner said it “can’t be the correct constitutional standard” to require “that ACS has to look into a history of over-reporting.” “The plaintiffs would ask this court to place the onus on the ACS” and demand that caseworkers in a situation of likely child abuse look into a doctor’s history, she said. But Ms. Kubitschek said Dr. Esernio-Jenssen “has a long history of giving incorrect diagnoses,” and the agency should have gotten a second opinion. Simply because a doctor has a medical degree, she said, “does not entitle caseworkers whose duty is to do what’s best for children to rely on a doctor who is biased.”
Ms. Brenner countered that it was enough that Dr. Esernio-Jenssen “was qualified by the state of New York and she has given ACS a list of injuries and a diagnosis.” Judge Miner asked, “Suppose she had been wrong on a number of cases and ACS knew it,” would that be enough? “Yes,” Ms. Brenner responded. “ACS has some very serious responsibilities here. ACS simply as a matter of policy can’t be required to check on a doctor’s reputation.” In the Graham case, a woman unsuccessfully sued the city after she had three grandchildren and five children removed from her home. The woman had been asleep two floors away while a friend of a relative attacked one of the children, an 11 year-old girl, and Ms. Kubitschek said the agency removed all the children even though the person the girl “accused of abusing her had been arrested and the other children weren’t in danger.”
This ran contrary to the holding in another case Ms. Kubitschek and partner David Lansner had handled, Nicholson v. Scopetta, 344 F.3d 154 (2003), where the circuit, with guidance from the New York Court of Appeals, held in part that ACS should not insist on keeping the child out of the home once the danger had been removed. She also told the judges that ACS has a number of practices and policies that conflict with court holdings on due process and other violations.
She said the agency does not provide pre-deprivation hearings before removal, the agency “resolves any ambiguity in favor of removing the children,” officials make it “acceptable to misrepresent facts” in Family Court, and the “parent is required to explain how a child was injured even if the parent wasn’t present during the injury and someone else was caring for the child.” The law department’s Mr. Colley countered that, in the Graham case, a jury had correctly found that “the defendants’ lawful actions were shown not to violate procedural due process rights” and the Fourth Amendment claim brought by the grandmother “was rightfully dismissed.”
Mr. Colley said the grandmother missed the 11-year-old’s injuries, which were only discovered by school officials the following day. Ms. Kubitschek responded that the grandmother “could not have been expected to anticipate this would happen” and the 11 year-old child “said it hadn’t happened to her before.”
@|Mark Hamblett can be reached at email@example.com.
Letters to the Editor
In our August 2009 issue, we published the article “Challenging an Assumption” (p. 29), which
was a profile of Dr. John Plunkett, a Minnesota pathologist who questions the validity of the
shaken baby syndrome diagnosis. In January, we received and published a letter critical of our
article and of Dr. Plunkett’s views (p. 5). That letter was signed by members of the international
advisory board of the National Center on Shaken Baby Syndrome. Since then, we have received
numerous letters taking issue with their letter and the views of its signers. Clearly, we have
touched a nerve in writing about this issue. Our intent for the story about Dr. Plunkett was
neither to validate nor to denigrate his work. We merely wanted to highlight the fact that a
Minnesota physician is taking part in a highly controversial debate that has ramifications for
medicine and the legal system. Below are some of the letters we have received recently on this
topic. Others can be viewed online at http://www.minneotamedicine.com.
Growing Body of Contrary Evidence
In your January 2010 issue, nine doctors, a prosecutor, and a police detective—all of whom are
associated with the National Center on Shaken Baby Syndrome, an advocacy group devoted to
the promotion of “shaken baby” theory—attacked Dr. John Plunkett, who was featured in the
August 2009 issue of Minnesota Medicine. Dr. Plunkett has spent his recent career applying
basic biomechanical and medical principles to shaken baby syndrome (SBS) and testifying, if
needed, when accused parents or caretakers are confronted with unproven or demonstrably
incorrect medical claims. Because of his work and research by others, the literature on SBS has
changed substantially since 2000, forcing major changes in the SBS position papers of the major
medical organizations. In their 2010 letter, the representatives of the National Center on Shaken
Baby Syndrome claim that Dr. Plunkett’s findings are based on “belief” rather than “evidence.”
In fact, doctors have been diagnosing SBS for nearly 40 years without an adequate scientific
basis—and in the face of a growing body of contrary evidence.
In the 1970s, “shaking” was advanced as a theory to explain a triad of findings (subdural
hemorrhage, retinal hemorrhage, and/or brain swelling) that is sometimes seen in infants or
children who have no signs of trauma. The theory was that shaking caused these findings by
rupturing bridging veins and tearing the axons within the brain. In 1987, Dr. Ann-Christine
Duhaime, a neurosurgeon working with biomechanical engineers at the University of
Pennsylvania, attempted to prove that shaking could cause these injuries. However, her study
showed the opposite: The forces of shaking fell well below established injury thresholds and
were 1/50th the force of impact, including impact on soft surfaces.1
Despite these findings, many doctors continued to testify that shaking was the primary or sole
cause for the triad of symptoms and that it would take a fall from a multistory building to cause
these findings. In 2001, Dr. Plunkett disproved this premise in an article that included a
videotaped fall of a toddler from a 28-inch plastic indoor play structure that resulted in subdural
hemorrhage, retinal hemorrhage, and death.2 This videotape proved definitively that short falls
can cause the triad and are sometimes fatal. Although SBS proponents initially suggested that
the videotape had been altered, Dr. Case (one of the signatories to the attack on Dr. Plunkett) has
acknowledged the validity of the videotape, which has been shown in courtrooms and at teaching
seminars in the United States and England.3 Numerous biomechanical studies have further
confirmed that the force from short falls meets the injury thresholds, while shaking does not.4-6
Short falls are not the only cause of medical findings previously attributed to shaking. Studies
by Dr. Jennian Geddes published in Brain, England’s leading neurology journal, from 2001 and
2003 found that the brain injuries of allegedly shaken children were generally hypoxic rather
than traumatic in origin, and that subdural hemorrhages are also found in natural deaths.7,8 In
2002, Drs. Hymel, Jenny, and Block (two of whom signed the attack on Dr. Plunkett) listed the
alternative causes for findings previously attributed to shaking or inflicted head trauma as
accidental trauma; medical or surgical interventions; prenatal, perinatal, and pregnancy-related
conditions; birth trauma; metabolic, genetic, oncologic, or infectious diseases; congenital
malformations; autoimmune disorders; clotting disorders; the effects of drugs, poisons, or toxins;
and other miscellaneous conditions.9 A 2006 text on abusive head trauma in infants and children
(co-edited by Dr. Alexander, another signatory to the attack on Dr. Plunkett) and a 2007 review
article by Patrick Barnes, professor of radiology at Stanford University and chief of pediatric
neuroradiology at Lucile Salter Packard Children’s Hospital, are in accord.10 Despite this
consensus, hundreds to thousands of parents and caretakers have been imprisoned based on
testimony by doctors that subdural hemorrhages, retinal hemorrhages, and/or brain swelling are
diagnostic of abuse, with little or no regard to the alternatives, including short falls and natural
At the same time, many doctors and academics have recognized that the real problem lies in the
lack of an evidence base for shaken baby theory. In 2003, a review article by Dr. Mark Donohoe
found that “[T]he evidence for SBS appears analogous to an inverted pyramid, with a small data
base (most of it poor-quality original research, retrospective in nature, and without appropriate
control groups) spreading to a broad body of somewhat divergent opinions.” 12 In 2006, the
National Association of Medical Examiners withdrew its position paper on shaking, and its
annual conference included presentations with titles such as “‘Where’s the Shaking?’: Dragons,
Elves, the Shaking Baby Syndrome, and Other Mythical Entities” and “Use of the Triad of Scant
Subdural Hemorrhage, Brain Swelling, and Retinal Hemorrhages to Diagnose Non-Accidental
Injury is Not Scientifically Valid.” In subsequent publications, Dr. Waney Squier of Oxford
University, one of England’s leading neuropathologists, and Dr. Jan Leestma, author of the
textbook Forensic Neuropathology, similarly concluded that the evidence base for shaken baby
syndrome is lacking.13,14 None of this material is addressed or cited in the attack on Dr. Plunkett.
The problem, in short, is not that Dr. Plunkett was wrong; the problem is that he was right. Over
the past decades, hundreds to thousands of caretakers—many of whom are innocent—have been
convicted based on theories that lack a scientific basis. These convictions must now be revisited.
Of course children are abused. But there are many ways to abuse children, one of which is
ripping them from their families and imprisoning their parents and caretakers based on
misdiagnoses of abuse. We therefore urge the medical profession to join us in developing a
calm, rational and evidence-based approach to pediatric head injury and child death.
Heather Kirkwood, J.D.
Barry S. Scheck, J.D.
Co-director, Innocence Project
Benjamin N. Cardozo School of Law
New York City
Keith Findley, J.D.
President, Innocence Network
Co-director, Wisconsin Innocence Project
University of Wisconsin Law School
Bridget McCormack, J.D.
Co-director, Michigan Innocence Clinic
University of Michigan Law School
Ann Arbor, Michigan
Julie Jonas, J.D.
University of Minnesota Innocence Clinic
Managing Attorney, Innocence Project of Minnesota
Jacqueline McMurtrie, J.D.
Director, Innocence Project Northwest Clinic
University of Washington School of Law Seattle, Washington
1. 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):409-15.
2. Plunkett J. Fatal pediatric head injuries caused by short-distance falls. Am J Forensic Med Pathol 2001;22(1):1-12.
3. Seventh North American Conference on Shaken Baby Syndrome (Abusive Head Trauma), Vancouver, B.C. October
4. Ommaya AK, Goldsmith W, Thibault L. Biomechanics and neuropathology of adult and paediatric head injury. Br J
5. Prange MT, Coats B, Duhaime AC, Margulies SS. Anthropomorphic simulations of falls, shakes, and inflicted impacts
in infants. J Neurosurg 2003;99(1):143-50.
6. Goldsmith W, Plunkett J. A biomechanical analysis of the causes of traumatic brain injury in infants and children. Am
J Forensic Med Pathology 2004;25(2):89-100.
7. Geddes JF, Hackshaw AK, Vowles GH, Nickols CD, Whitwell HL. Neuropathology of inflicted head injury in children,
I and II. Brain. 2001;124(part 7):1290-8.
8. Geddes J, Tasker RC, Hackshaw AK, et al. Dural haemorrhage in non-traumatic infant deaths: does it explain the
bleeding in ‘shaken baby syndrome’? Neuropathol Appl Neurobiol 2003;29:114-22.
9. Hymel KP, Jenny C, Block RW. Intracranial hemorrhage and rebleeding in suspected victims of abusive head trauma:
addressing the forensic controversies. Child Maltreat 2002:7(4):329-48.
10. Frasier L, Rauth-Farley K, Alexander R, Parrish R. Abusive Head Trauma in Infants and Children: A Medical,
Legal, and Forensic Reference. G.W. Medical Publishing, Inc.; St. Louis, MO: 2006.
11. Barnes PD, Krasnokutsky M. Imaging of the central nervous system in suspected or alleged nonaccidental injury,
including the mimics. Top Magn Reson Imaging 2007;18:53-74.
12. Donohoe M. Evidence-based medicine and shaken baby syndrome part I: literature review, 1966-1998. Am J Forensic
Med Pathol 2003;24(3):239-42.
13. Squier W. Shaken baby syndrome: the quest for evidence. Dev Med Child Neurol 2008;50(1):10-4.
14. Leestma J. Forensic Neuropathology, Second ed. CRC Press; Chicago: 2009.
We read with interest Kate Ledger’s article “Challenging an Assumption: A pathologist
questions shaken baby syndrome” (Minnesota Medicine, August 2009) and the response of Drs.
Alexander, Barr, Block, et al. (January 2010).
Dr. Block and his cosigners complain that Ms. Ledger ignored the enormous body of
international peer-reviewed medical literature about shaken baby syndrome. Much of this
literature exhibits circular reasoning, selection bias, or misrepresents the data. Of the 14
references they cite, six are unsystematic reviews or consensus statements that mingle opinion
with fact and add no original supporting evidence. Two are based on data described by the
authors as “explorative.” Those authors suggest that “further surveillance … and modelling will
be required.” Two are invalidated by insufficiently robust criteria to reliably diagnose abuse and
one by failure to address the fundamental methods on which the study was based.
Dr. Block and his cosigners suggest that this literature “consistently and repeatedly supports the
concept of shaken baby syndrome.” We do not disagree with this but would point out, as Ms.
Ledger clearly did, that supporting a concept is far from demonstrating the scientific basis for it.
Just as disturbing as the literature Block and his cosigners cite is the indignation they expressed
that someone should challenge their opinions as medical “experts” in a court of law—as if they
are somehow exempt from the human tendency for cognitive errors in medical decision making.
What scientist is afraid of debate that is crucial to our understanding of evolving ideas?
Fortunately, medicine has never been static. There is much to learn about the pathophysiology of
infant brain trauma. We cannot make up for this lack of knowledge by reiterating opinion and
poor data: Ignoring new evidence and failing to question and engage in debate is a dereliction of
our duties to our patients and their families.
Waney Squier, FRCP FRCPath
John Radcliffe Hospital
Oxford, United Kingdom
Julie Mack, M.D.
Assistant professor of radiology
Penn State Hershey Medical Center
Patrick E. Lantz, M.D.
Professor of pathology
Wake Forest University
Winston-Salem, North Carolina
Patrick D. Barnes, M.D.
Chief of pediatric neuroradiology
Lucile Packard Children’s Hospital
Stanford University Medical Center
Irene Scheimberg, M.D.
Paediatric and perinatal pathologist
The Royal London Hospital
James T. Eastman, M.D.
Clinical professor of pathology and laboratory medicine
University of Wisconsin
Marta Cohen, M.D.
Sheffield Children’s Hospital NHS Foundation Trust
Sheffield, United Kingdom
Peter J. Stephens, M.D., FCAP
Burnsville, North Carolina
Darinka Mileusnic-Polchan, M.D., Ph.D.
Medical Examiner for Knox and Anderson Counties
Regional Forensic Center
University of Tennessee Medical Center Knoxville, Tennessee
Persuasive Evidence and a Theory
I serve on occasion as an expert witness for the defense in shaken baby syndrome (SBS) cases.
That is a matter I disclose as a potential conflict of interest. I wish the writers of the letter in your
January 2010 issue had done the same.
When I cast doubt on the validity of SBS, I cite the original literature. In my judgment, SBS is so
lacking in evidence, it is hard to understand how the hypothesis ever gained traction.1,2
I cite a review of seminal SBS literature up to 1998. It concluded the evidence was inadequate.3 I
cite Ommaya, et al., who did the original work on whiplash biomechanics that debunks the SBS
hypothesis.4 I cite experimental work that indicates forces generated by manual shaking are an
order of magnitude less than forces of impact, and less than the threshold for injury.5 I cite an
article that states the neck should be destroyed if manual shaking were capable of producing
brain damage.6 I have seen no case in which neck injury was observed.
Finally, I cite my own hypothesis. It is untested, just as the SBS hypothesis is untested. If the
forces of shaking are sufficient to cause brain damage, the thumbs of the shaker and the places
where the thumbs are applied on the victim should be conspicuously injured. They are not.
Edward N. Willey, M.D.
St. Petersburg, Florida
1. Guthkelch AN. Infantile subdural haematoma and its relationship to whiplash injuries. Br Med J 1971;2(5759):430-1.
2. Caffey J. On the theory and practice of shaking infants. Its potential residual effects of permanent brain damage and
mental retardation. Am J Dis Child 1972;124(2):161-9.
3. Donohoe M. Evidence-based medicine and shaken baby syndrome: part I: literature review, 1966-1998. Am J Forensic
Med Pathol 2003;24(3):239-42.
4. Ommaya AK, Goldsmith W, Thibault L. Biomechanics and neuropathology of adult and paediatric head injury. Br J
Neurosurg 2002;16(3): 220-42.
5. Duhaime, AC, Gennarelli TA, Thibault LE, et al. The shaken baby syndrome. A clinical, pathological, and
biomechanical study. J Neurosurg 1987;66(3): 409-15.
6. Bandak FA. Shaken baby syndrome: a biomechanics analysis of injury mechanisms. Forensic Sci Int 2005;151(1):71-9
Overrepresentation of Males in Traumatic Brain Injury of Infancy and in Infants With Macrocephaly: Further Evidence That Questions the Existence of Shaken Baby Syndrome
Miller, Rubin BA; Miller, Marvin MD
Shaken baby syndrome (SBS) has been thought to be caused by violent shaking of an infant and is characterized by the triad of findings: subdural hematoma (SDH), retinal hemorrhages, and neurologic abnormalities. The triad is not specific for SBS and can be seen in accidental trauma and in certain medical conditions. Recent observations, however, question whether SBS exists. Herein, we review the gender differences in 3 groups of infants with traumatic brain injury:
(1) neonates with SDH from birth trauma,
(2) infants with SDH from accidental trauma, and
(3) infants with SDH from SBS.
Gender differences are also presented in a fourth group of infants with macrocephaly related to increased extra-axial fluid spaces (IEAFS). Compared with the expected male frequency of 51.4% in newborns, there was a statistically significant overrepresentation of males in each of the 4 groups-65.3%, 62.2%, 62.6%, and 68.8%, respectively. We believe that the most likely explanation for these findings relates to the larger head size of the male compared with the female which has several relevant consequences. First, the larger head circumference of a male newborn compared with a female newborn may increase the likelihood that a male newborn will incur a small SDH from the minor trauma of the birthing process that can later rebleed and present with a symptomatic SDH that could be misdiagnosed as SBS and child abuse. Second, a short fall would have a greater likelihood of causing a SDH in a male infant than a female infant who could subsequently become symptomatic from hours to weeks later and could thus present as an unexplained SDH. Third, infants with macrocephaly related to IEAFS may be at increased risk for developing a SDH from the larger head size and greater tautness of the bridging vessels in the extra-axial fluid spaces. We believe that many infants who have been diagnosed with SBS have been given incorrect diagnoses of child abuse. Rather, their SDH may occur as a result of a small SDH from the birthing process that enlarges during early infancy, a short fall, or from macrocephaly with IEAFS.
Unexplained fractures in infancy: looking for fragile bones
1Academic Unit of Child Health, University of Sheffield, Sheffield Children’s Hospital, Sheffield, UK
2Sheffield Children’s NHS Foundation Trust, Sheffield Children’s Hospital, Sheffield, UK
3Sheffield Molecular Genetics Service, Sheffield Children’s NHS Foundation Trust, Sheffield Children’s Hospital, Sheffield, UK
Dr N Bishop, Academic Unit of Child Health, University of Sheffield, Sheffield Children’s Hospital, Sheffield S10 2TH, UK; firstname.lastname@example.org
- Accepted 13 October 2006
A fracture occurs when the force exerted on a bone exceeds the ability of the bone to absorb the force by deforming. Fractures in children are common—approximately one third of children will have a fracture by 16 years of age, with more boys experiencing fracture than girls.1 This differentiation in fracture risk is apparent from 2 years of age. Before the age of 2 years, fracture incidence is equal and occurs at a rate of approximately 80/10 000 person years. For the UK, therefore, approximately 4800 infants will have a clinically evident fracture before their first birthday each year.
Some long-bone fractures may occur at birth2 in association with events such as shoulder dystocia3; skull fractures may occur during forceps4 and ventouse delivery.5 Some may (uncommonly) occur as a result of clearly defined trauma such as road accidents.6 Most, however, fall into the “unexplained” category. This article reviews our current approach to identifying bone disease in the infant presenting with more than one unexplained fractures, and discusses the recognised disease processes that result in increased bone fragility.
The history should include inquiry into specific areas as listed in the box. The two most frequently recognised underlying disease processes causing bone fragility in infancy are metabolic bone disease of prematurity7 and osteogenesis imperfecta, and directed questioning is appropriate for these conditions. For premature infants, the features commonly associated with fracture are delivery at <28 weeks of gestation, necrotising enterocolitis, late (>30 days) establishment of full enteral feeds, conjugated hyperbilirubinaemia, chronic lung disease, and use of furosemide.8,9 For a proportion of infants with osteogenesis imperfecta, there will be a family history either of osteogenesis imperfecta itself or of features that suggest osteogenesis imperfecta. The other elements of the history relating to the …
Differentiating osteopenia of prematurity from child abuse
- Chandan Gupta, Senior House Officer Neonates
Mayday University Hospital, Croydon CR7 7YE, United Kingdom
The review on fractures in infancy is brilliant and very informative. I would like to take this opportunity to stress the sensitive issue of fractures due to osteopenia of prematurity that many a times needs differentiating from child abuse.
Reports of osteopenia/rickets of prematurity are on the increase because of improved survival rates of low birthweight infants.2 The incidence of osteopenia among infants born before 28 weeks of gestational age are as high as 30%. 1 The contributory factors are prematurity, lack of activity, chronic lung disease, use of diuretics, prolonged parenteral nutrition and iatrogenic factors that are unavoidable in neonatal intensive care. Iatrogenic injuries are frequently the result of physiologic or anatomical response to proper and lifesaving treatment. The most serious of these are found in the premature infant, who may suffer chronic lung disease or, more seriously, brain damage.3
The diagnosis of osteopenia of prematurity remains difficult as there is no screening test which is both sensitive and specific.5 Such infants sometimes go undiagnosed of fractures from the neonatal unit and when they come back with reasons like excessive crying and the x-rays show multiple healing fractures, the differential of child abuse, unfortunately, tends to take the top position. Due to the obvious reasons and the sensitivity of the issue, clinicians have shown concerns about the mistaken diagnosis of child abuse.4
I agree with the authors that the plain film radiography is not the final arbiter of bone fragility in infancy; as with the other forms of investigation discussed in the article, it is a part of the overall approach to discriminating between a diagnosis of bone fragility and one of non-accidental injury.Dual energy X-ray absorptiometry and quantitative ultrasound has been employed by some neonatal units to determine the mineral density of the bone but it is still not universal due to the issues like ionising radiation and the difficulty to interpret data.5
As a result, the clinicians, especially the junior doctors who happen to be the first contact with the carers need to keep osteopenia of prematurity high on their list of differentials especially when a NICU graduate presents without an official diagnosis of it.
1. Kocsis I, Kis E, Szabó A, et al. Osteopenia of Prematurity. Orv Hetil. 2005; 146:2491-7.
2. Caksen H, Oztürk A, Kurtoðlu S, et al .Reports of osteopenia/rickets of prematurity are on the increase because of improved survival rates of low birthweight infants. J Emerg Med 2002; 23:305-6.
3. Singleton EB. Intentional and unintentional abuse of infants and children. Curr Probl Diagn Radiol 1986; 15:277-330
4. Blumenthal I. Osteogenesis imperfecta, non-accidental injury, and temporary brittle bone disease. Arch Dis Child 1996; 74:91
5. McDevitt H, Ahmed SF. Quantitative ultrasound assessment of bone health in the neonate. Neonatology 2007; 91:2-11.
Toddler fracture question
My son is a very active 3 and 7 months. After spending the morning running, jumping and saving the world, he started limping. The limping quickly progressed to pain when touching the leg. I took him to the ER where x-rays showed a small line on the tibia. They put him in a cast and told me it was a toddlers fracture”. There was never a moment when he fell or yelled in pain. Is this common? I always thought bone breaks were after a trauma. There is no bruising or swelling either and is it common for bones to just break in young healthy kids?
Children differ from adults in many ways. Compared to adults, children’s bones are more porous than are adult bones, which are well calcified and hard. Children’s bones are more prone to fractures because of their porosity and because their ligaments are stronger than their bones. It is the reverse in adults. Adults suffer sprains while children suffer fractures.
Children also have different types of fractures than do adults because of these bony differences. Children experience greenstick fractures, which are a partial crack through the bone rather than a full separation of the bone segments. They also have buckle fractures where the more porous bone is basically compressed downwards in one area but the bone is not broken through. They also have bend fractures where a long bone is clearly bent but not cracked through.
Unlike adults, children also have growth plates that actively lengthen bones throughout life. Adults have no active growth plates in their bones. Fractures through these growth plates are called Salter-Harris fractures. These are particularly difficult fractures because a child may lose all or part of their bone’s growth plate causing uneven growth of the bone as well as a difference in bone length from one side of the body to the other. This results in obvious problems in movement and appearance that are difficult to correct.
Happily your son saw a good pediatric doctor who recognized his fracture and casted him. Even when the bone is not separated, a fracture is still very painful and feels a lot better when it is immobilized in a cast. As a young child, he will also heal quickly.
While it is possible that your son could have an underlying problem with his bones, that is unlikely. If he has more fractures after little impact or malformed teeth, then it is worth discussing a possible problem with his doctor. Otherwise, he is just a normal, active little boy with a normal child’s more fracture-prone bones.
I hope he heals quickly and uneventfully!
McMillan et al. (Eds.) (2006). Oski’s Pediatrics: Principles and Practice (4th Edition). Philadelphia: Lippincort, Williams, and Wilkins.
|Mary M. Gottesman, PhD, RN, CPNP, FAAN
Associate Professor, Specialty Program Director
Pediatric Nurse Practitioner Program
College of Nursing
The Ohio State University
Child skull fracture
My daughter is 3 1/2 years old, and we were involved in an accident where the impact was on the front passenger side of the vehicle. She had a bruise on her right eye which led me to believe that her car seat may have shifted towards the impact of the wreck. However, she was taken to the hospital 4 days later when she developed black eyes and it was found that she had a skull fracture and some bleeding. The skull fracture was on her left side of her head, which is very puzzling. Is this possible? If so are there documented medical cases, and where could I find such cases or articles?
Yes, it is possible as a result of what is called the coup-contrecoup type of closed head injury. In this situation the brain suffers damage directly under the area of impact, but a second injury of equal or greater magnitude occurs directly opposite the point of contact. This occurs because the brain is suspended in the cranium or skull in cerebral spinal fluid with long nerve tracts extending from deep within the brain down into the spinal cord. When the head suffers a blow, the brain is first injured directly beneath the point of impact and then secondarily on the opposite side as the brain hurtles across the skull and slams into the bony plates opposite the point of impact, bouncing back yet again to the original site of injury. Children’s bones are much more porous than adult bones and hence are far more likely to fracture than are adult bones.
In addition to the direct injury and secondary injury, such a severe blow also results in what is called diffuse axonal injury from the stretching and shearing of nerves in the brain as they move to the contrecoup injury site across the skull. This may result in abnormal brain function for sometimes lengthy periods as the nerves swell in response to the injury and then eventually heal. It is not possible to know what the exact outcomes of any injury will be, particularly for children, since their brains have more flexibility in healing (plasticity) and in the transfer of skills to other neurons than do the brains of adults. There is no way to predict how many cells are affected or their degree of recovery.
Your daughter’s injury highlights the critical importance of using optimal restraint systems for children precisely in order to protect their brains, the most likely body part to be injured in a motor vehicle accident. Because children’s heads are so large and heavy compared to the rest of their bodies, their heads function like bullets in an accident, pulling the child forward toward impact. Children should be in approved and properly installed car seats and booster seats until they are 80 pounds in weight AND 4 feet 9 inches in height. Research shows that up to 80% of child restraint systems are installed or used incorrectly.
If you are interested in reading more, enter coup-contrecoup injury or diffuse axonal injury or closed head injury into a search engine – these terms should lead you to additional information. I hope this information is helpful.
Child skull fracture
my child and I were involved in a car accident. As far as I know, she may have hit her head on her right side as she had a bruise on her right eye. However, she sustained a skull fracture on her left side. Is this possible?
Yes, it is absolutely possible because of a phenomenon known as rebound injury, wherein the brain opposite the injury is also damaged. When the force that directly impacts the skull is significant, it causes the brain, it’s blood vessels, nerves, and cushioning fluid to move swiftly across the space inside the skull and literally smash up against the other side of the bony skull. This applies shearing or tearing forces to all of these tissues as they move at high velocity to slam into a the bony skull barrier and then rebound again to inflict more damage at the original site of impact.
I don’t know how old your child is, but the bony plates that make up the skull do not fuse completely with one another until sometime after 10 years of age. This allows for the rapid growth of brain tissue that occurs in the first decade of life that is necessary for normal development and learning. In younger children bones are also more likely to fracture than they are in adults because they are less calcified.
Your experience highlights the critical need for the proper restraint of all children in appropriate car seats and booster seats until they meet the weight AND the height criteria for moving into standard seatbelt usage. These milestones are 80 pounds and four feet nine inches. Use of booster seats and car seats reduces serious injury by 60-80%. Regular seat belts used on smaller individuals result in cutting across the trachea or windpipe,potentially collapsing it or the esophagus as the windpipe is driven back into the esophagus or food pipe, making swallowing and eating painful and difficult. They also can inflict significant bruising injury on the abdominal organs leading to internal bleeding as well as painful bruising over bony areas.
I hope both you and your daughter heal quickly and consistently use good restraint practices when back out on the road.
Mary M. Gottesman, PhD, RN, CPNP, FAAN
Associate Professor, Specialty Program Director
Pediatric Nurse Practitioner Program
College of Nursing
The Ohio State University
Predilection sites of infantile skull fractures following blunt force
Previous investigations on calvarial fractures in infants have shown that the flexibility and displacement of the infant calvarial are not sufficient to avoid fractures as a result of fall. From a table height onto hard ground – and in special cases, fractures cannot be avoided even after falls onto softly cushioned ground. The skull fractures are located in paper-thin, transparent, single-layer bone areas without diploe. The results of previous literature were compared with investigations of the skulls of 82 infants (from neonates up to infants 14 months of age). Congenital fissures, cranioschisis, locally retarded ossification in the cranium and craniotabes are all weak points where fracture has a tendency to occur even if the impact is minor. These ossification defects are increased in the ossa parietalia, but can also be found in the os frontale or in the os occipitale. The location is not always the same but can be detected by locating the skull transparency using diaphanoscopy.
Biomechanical fragility of the infant skull
Following previous experiments on postmortem skull fractures of infants, falls from 82-cm heights onto stone (A), carpet (B) and foam-backed linoleum (C), 35 further falling tests were carried out onto softly cushioned ground. In 10 cases a 2-cm thick foam rubber mat (D) was chosen and in 25 further cases a double-folded (8-cm-thick) camel hair blanket (E). Hence the results of altogether 50 tests could be evaluated. In test groups A-C on a relatively hard surface, skull fractures of the parietale were observed in every case; in test group D this fracture was seen in one case and in test group E in four cases. Measurements along the fracture fissures showed bone thickness of 0.1-0.4 mm. The fracture injuries originated in paper-thin single-layer bone areas without diploe, which can also be considered the preferred regions for skull fractures of older infants following falls from low heights. These results indicate that it is no longer possible to assume that the skull of infants is not damaged after falls from table height.