The Journal of Pediatrics
Volume 160, Issue 2 , Pages 199-203, February 2012

Calciferol Deficiency Mimicking Abusive Fractures in Infants: Is There Any Evidence?

  • Ann S. Botash, MD

      Affiliations

    • Division of Child Abuse, Department of Pediatrics, Upstate Medical University and Upstate Golisano Children’s Hospital, Syracuse, NY
    • ,
  • Irene N. Sills, MD

      Affiliations

    • Division of Endocrinology and Diabetes, Department of Pediatrics, Upstate Medical University and Upstate Golisano Children’s Hospital, Syracuse, NY
    • ,
  • Thomas R. Welch, MD

      Affiliations

    • Division of Nephrology, Department of Pediatrics, Upstate Medical University and Upstate Golisano Children’s Hospital, Syracuse, NY
    • Corresponding Author InformationReprint requests: Thomas R. Welch, MD, Upstate Golisano Children’s Hospital, One Children’s Circle, Syracuse, NY 13210.

Received 14 June 2011; received in revised form 27 July 2011; accepted 24 August 2011. published online 13 October 2011.

Article Outline

25(OH)D, 25-hydroxycholecalciferol, 1,25(OH)2D, 1,25-hydroxycholergocalciferol, PTH, Parathyroid hormone

 

The history of calciferol∗ metabolism and biochemistry is tightly intertwined with that of American pediatrics. Rickets was a widespread affliction of children in urban areas in the 19th and early 20th centuries. Mellanby recognized the anti-rachitic properties of a fat-soluble substance that was incorrectly named “vitamin” D. Shortly thereafter, Eliot undertook a seminal clinical trial in New Haven that demonstrated the ability of cod-liver oil to prevent rickets in infants. Within decades, supplementation of nursing infants became nearly universal, and clinical rickets largely disappeared. In the latter part of the 20th century, lax prescribing of calciferol supplements to nursing children, combined with an increasing number of mothers of darkly pigmented infants choosing to breast feed, led to a resurgence of clinical rickets.1

Because we are well into the 21st century, clinical rickets in infants again is largely disappearing. As this has happened, there has been an increasing interest in the possibility that degrees of calciferol deficiency insufficient to cause frank rickets could still have deleterious skeletal effects.2 This interest has been informed by recent information in adults suggesting that levels of calciferol (as assessed by 25-hydroxycholecalciferol [25(OH)D]) we have previously considered normal may actually be low.3 This, in turn, has led to the suggestion that mild degrees of calciferol deficiency, in the absence of actual rickets, could predispose the infant to fractures.4 It is sometimes argued that such subclinical calciferol deficiency could explain some fractures that have been ascribed to abuse.5

Multiple long bone fractures have long been recognized as an indicator for child abuse.6 The implications for the child when fractures caused by abuse are mistakenly attributed to fractures caused by rickets are potentially life-threatening. Similarly, misdiagnosis of abuse in the setting of clinical rickets has significant legal, social, emotional, and clinical implications.

In this commentary, we will provide a review of our current understanding of the metabolism of calciferol in infants. We will then discuss recent data defining normal levels of calciferol at various ages, including in infants. We will examine the fracture risk associated with actual clinical rickets and the evidence that this risk is present with milder degrees of calciferol deficiency. Lastly, we will consider the proposition that mild degrees of calciferol deficiency can predispose infants to fractures mimicking those caused by non-accidental trauma of infants.

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Normal Calciferol Metabolism in Infancy 

Irradiation of 7-dehydrocholesterol in the skin produces cholecalciferol, which is quickly converted in the liver to 25(OH)D. This process is independent of calcium/phosphorus status, and therefore circulating levels of 25(OH)D are the most commonly used measures of calciferol sufficiency. Most dietary calciferol is derived from irradiation of the plant sterol ergosterol into ergocalciferol. 25(OH)D from either source (skin or diet) is equally active in humans.3

The non-skeletal effects of calciferol metabolites are wide-ranging, and our understanding of them is evolving rapidly.7 The skeletal effects of the compounds are generally well understood. The most active calciferol metabolite, 1,25–hydroxycholergocalciferol (1,25[(OH)D), is necessary for absorption of dietary calcium from the intestine. Absent 1,25(OH)2D, only a small fraction of dietary calcium is absorbed, likely by passive diffusion.3

In the fetus and early newborn, 25(OH)D levels reflect maternal concentrations and, consequently, maternal calciferol status.4 From the standpoint of the skeleton, fetal calciferol metabolites are likely unimportant because fetal calcium balance does not depend on intestinal absorption. However, maternal calciferol status directly affects maternal calcium sufficiency, which, in turn, can affect the fetal skeleton.8, 9, 10 Once the infant is born and obtaining oral calciferol and calcium, it has been demonstrated that accretion of mineral into the skeleton is independent of maternal calciferol state.11, 12

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25(OH)D Reference Values 

Calciferol status is determined by circulating levels of 25(OH)D. Defining the reference range of human 25(OH)D concentration has proven to be a challenge. For many biologic anylates, collecting values in “normal” individuals permits the calculation of statistical reference ranges. This approach is not appropriate for 25(OH)D, in that “normal” individuals, especially those residing in areas with compromised sun exposure or with dark skin, should probably not contribute to the reference ranges.3

Recently, it has been recognized that there exists a concentration of 25(OH)D at which there is no longer a stimulus for increasing parathyroid hormone (PTH) concentration. This “cutoff point” has been viewed as a lower limit of normal 25(OH)D, at least for its skeletal effects. For healthy adults, this calculation results in a definition of normal of >31 ng/mL, somewhat higher than what earlier studies suggested.3, 13

For children, however, the reference range for 25(OH)D is much less clear. A recent study in Ireland, for example, observed the 25(OH)D/PTH plateau at approximately 25 ng/mL in a large group of adolescents.14 A similar finding was obtained in a group of Irish children between the ages of 1 and 2 years.15 There are insufficient data comparing 25(OH)D and PTH levels in newborns and infants to permit such a calculation. This is confounded by infants having a calcium/phosphate relationship that is different from that in older individuals. Widely varying calciferol status has been shown to exist in infants and toddlers in multiple regions in the United States and in other countries.16

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The Diagnosis of Rickets 

The clinical presentation of rickets in non-ambulatory infants includes symptoms of hypocalcemia, bone pain, and failure to grow in length along with signs of bone deformity such as metaphyseal changes at the costochondral junctions, ankles, and wrists, delayed closure of fontanelles, and craniotabes. The disease is characterized by 3 stages: (1) initial osteopenia caused by low calciferol levels, subclinical hypocalcemia, and inadequate mineralization of bone; (2) increasing levels of PTH to mobilize calcium from bone to correct serum hypocalcemia; and (3) even higher levels of PTH causing more severe bone changes and evident hypocalcemia. Alkaline phosphatase rises as a marker of the increased bone turnover.17 The diagnosis of rickets depends on the presence of the aforementioned clinical features and radiologic (metaphyseal irregularity, cupping, or both and physeal widening and osteopenia) and laboratory confirmation.

Rickets occurs in infants and toddlers with certain risk factors: inadequate exposure to sunlight, deficiency of dietary calciferol, inability to absorb calciferol enterally, the presence of liver, kidney, or gall bladder disease, or the concomitant administration of medications known to increase the metabolism of 25(OH)D. Congenital rickets has been reported because of low maternal intake of 25(OH)D and calcium. Mothers on strict vegan diets or macrobiotic diets with poor calcium intake and 25(OH)D deficiency may have affected infants with low calcium levels and seizures or tetany in early infancy and rickets.18 Infants <6 months old with 25(OH)D deficiency usually have symptoms of hypocalcemia and no findings of metabolic bone disease.19 However, craniotabes, once thought to be a normal variant of newborns,20 has recently been associated with in utero 25(OH)D deficiency.21

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Fracture Risk with Clinical Rickets 

Fractures are a common accidental injury in childhood. Biomechanical forces, combined with factors of bone and muscle strength, affect susceptibility to fracture, fracture location, and type of fracture. Children with a diagnosis of rickets made on the basis of clinical history, physical examination, and radiographic evidence have increased fracture risk because of poor bone strength caused by demineralization. However, children with overt rickets do not usually have fractures.

In non-ambulatory infants, fractures with rickets are rare. In a recent study of 45 children with rickets between the ages of 2 and 14 months, fractures occurred in 17.5% of the study group.22 Seven children had fractures, and all were mobile and had overt radiographic findings of rickets. However, none of the skeletal fractures that are characteristic of child abuse, classic metaphyseal lesions, or skull fractures were found. In a report of 30 African-American, breastfed infants with radiographic and clinical evidence of rickets in North Carolina, two had fractures, although details were not provided.23 One of these infants was 12 months old, and the other was 5 months old. The 5-month-old infant had an undetectable 25(OH)D level. Fracture as a presenting sign of rickets in infants is notably absent in other reports.19, 24, 25, 26, 27, 28 Fractures in non-ambulatory infants caused by calciferol deficiency appear to be quite rare.

The rate of accretion of calcium and phosphorus in the preterm infant cannot match that which is achieved in utero transplacentally.29 Osteopenia develops in preterm infants mainly because of low intake of calcium and phosphorous, not calciferol deficiency.30, 31 Their bone disease usually presents between the sixth and twelfth postnatal week.32 In very low birth weight premature infants (≤1500 g) fracture rates have been reported to be between 2.1%31 and 24.0%.29 In those infants who survived beyond 6 months, the rate of fracture was 1.2%.33

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Fracture Risk with Milder Degrees of Calciferol Deficiency 

Risk of fracture with milder degrees of calciferol deficiency has been hypothesized. In some cases, metaphyseal fractures have been claimed to be present in the absence of more dramatic signs of rickets. With partial treatment of calciferol deficiency, rickets is more challenging because of less demineralization and normal zones of provisional calcification.34

However, there is no evidence that milder degrees of calciferol deficiency are associated with multiple fractures.35, 36 Schilling et al prospectively studied 118 subjects with fractures and stratified them according to 25(OH)D levels: deficient, insufficient, and sufficient. There was no association between the 25(OH)D levels and the diagnosis of child abuse and the occurrence of multiple fractures, rib fractures, or metaphyseal fractures. None of the children in the calciferol deficient group had radiographic findings of rickets.

An important aspect of the Schilling et al study is the finding that there was no association between calciferol status and the presence of rib or metaphyseal fractures. The authors use these specific fractures because they are considered nearly diagnostic of child abuse.34, 37, 38, 39, 40, 41, 42 Approximately 80% of the children diagnosed with non-accidental fractures had other non-skeletal injuries. Thus, the fractures were not the sole determinants of abuse. Although this study did not use a control group of children without fracture, the incidence of calciferol insufficiency was similar to that of comparable populations of children.3, 16

In a study by Olney et al, 21% of children with fractures and 18% of the control subjects had insufficient 25(OH)D levels.43 Like the Schilling study, calciferol was not a significant factor in determining fracture risk.

Occult bone disease is hypothesized to be a risk for fracture with minimal or no trauma. This is one basis for the hypothesized “temporary brittle bone disease,” an unproven entity.44 Furthermore, occult bone disease caused by calciferol insufficiency or deficiency is unproven. For example, a recent Institute of Medicine report extensively reviewed the literature and showed that there is inconsistent evidence for determining a threshold concentration of 25(OH)D above which rickets does not occur. However, the literature reviewed by this same report did not identify significant bone changes in children with 25(OH)D levels as low as 12ng/dL.45

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Fractures and Child Abuse 

Fractures caused by inflicted trauma may be found in any bone. Although certain fractures and fracture features are more commonly observed in abusive situations, any type of fracture can occur because of child abuse. It has been shown that certain fractures, such as rib fractures and those described as classic metaphyseal lesions, rarely occur accidentally in infants.34, 37, 38, 39, 40, 41, 42 Other fractures that are considered highly specific for abuse include scapula fractures, spinous process fractures, and sternal fractures. These are much less commonly observed, presumably because of the density and location of these bones.46

When a fracture occurs in a child with rickets, the metaphysis is frequently the site of injury.34, 46 Although this may be considered to be a mimic of abuse, rachitic changes in most cases should be differentiated clinically and radiologically from classic metaphyseal lesions observed in situations of child abuse.34 Clinical findings suggestive of rickets do not rule out the possibility that abuse may have also occurred.

Reported case series of children with fractures has been used to support the contention that rickets mimics abuse.47, 48, 49 However, these reports provide limited data on evaluations for abuse. For example, one child appeared to be failing to thrive and likely was calciferol deficient as a result of nutritional deprivation. Trauma, bone disease, or both appeared to be equally as likely in Paterson’s report of 4 cases.47 Other studies have further exposed the limitations in these reports.50, 51

Similarly, published letters to the editor after the case report by Keller and Barnes of 4 children5, 47 outline the multiple concerns about the limitations of their data.52, 53 A significant concern involves selection bias. Both reports demonstrate how limited information can be persuasively presented in the legal arena to disprove abuse.

In other published cases of fractures mistaken for child abuse, the findings are associated with evidence of bone disease. For example, a series of children with fractures and metabolic bone disease caused by biliary atresia has been reported to be associated with calciferol deficiency, clinical features including osteopenia and radiographic features of rickets. The bone disease in these 3 children likely was multifactorial, including defective 25 hydroxylation of calciferol and consequent malabsorption of 25(OH)D, calcium, phosphorus, and magnesium, use of steroids, hyperparathyroidism, hyperbilirubinemia, and other as-yet-unknown causes. In all 3 cases, radiographic bone disease was evident.54

As part of a comprehensive evaluation for risk of abuse, a detailed history reviewing possible mechanisms of trauma is recommended. This should include observations about the incident leading to the fracture, a dietary history, the mother’s dietary intake during pregnancy, a developmental history of the child including capabilities for rolling, walking, running, and climbing, history of risks for abuse and maltreatment, and family history of fractures, stature, and tooth enamel. The fracture work up of any non-ambulatory child should include a skeletal survey to look for occult fractures, non-displaced fractures, or both. The American Academy of Pediatrics recommends that these be performed on children as old as age 2 years when there is a suspicion of abuse.55 A follow-up skeletal survey is recommended at approximately 2 weeks from the incident to look for healing fractures that may have been occult on the first set of radiographic images. When these radiographic studies are correctly performed, the likelihood of missing radiographic evidence of rickets is extremely low.

Evaluation of children with multiple fractures should include a history and physical examination that assesses for underlying bone disease and child abuse.42 When there is a medical concern for calciferol deficiency, testing 25(OH)D levels is appropriate. However, calciferol deficiency in the absence of radiographic bone disease is not associated with fracture risk or with the fractures commonly seen in abuse. Abused children may have coincident but not causal calciferol deficiency.56 A child with one or more fractures from any cause and low 25(OH)D level would likely benefit from treatment with calcium and calciferol to support bone health, repair, and growth.

Although it is recognized that infants may have low calciferol levels for the myriad of reasons described, the likelihood that clinical rickets or mild calciferol deficiency is apt to result in bone fractures in non-ambulatory infants is exceedingly low. Fractures caused by inflicted trauma should not be misdiagnosed as rickets.

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∗Throughout this manuscript, we will use the term calciferol instead of vitamin D, and will use it interchangebly with dietary or endogenous cholecalciferol (vitamin D3) and egrocalciferol (vitamin D2).

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 The authors declare no conflicts of interest.

PII: S0022-3476(11)00882-1

doi:10.1016/j.jpeds.2011.08.052

The Journal of Pediatrics
Volume 160, Issue 2 , Pages 199-203, February 2012

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