Sports injury prevention programmes from the sports physical therapist's perspective: An international expert Delphi approach.

OBJECTIVE: To provide consensus on how to plan, organize and implement exercise-based injury prevention program (IPP) in sports. DESIGN: Delphi. SETTING: LimeSurvey platform. PARTICIPANTS: Experienced sports physical therapists from the International Federation of Sports Physical Therapy member countries. MAIN OUTCOME MEASURES: Factors related to sports IPP planning, organization and implementation. RESULTS: We included 305 participants from 32 countries. IPP planning should be based on an athlete's injury history, on pre-season screening results, and on injury rates (respectively, 98%, 92%, 89% agreement). In total 97% participants agreed that IPP organization should depend on the athlete's age, 93% on the competition level, and 93% on the availability of low-cost materials. It was agreed that IPP should mainly be implemented in warm-up sessions delivered by the head or strength/conditioning coach, with physical training sessions and individual physical therapy sessions (respectively, 94%, 92%, 90% agreement). CONCLUSION: Strong consensus was reached on (1) IPP based on the athlete's injury history, pre-season screening and evidence-based sports-specific injury rates; (2) IPP organization based on the athlete's age, competition level, and the availability of low-cost materials and (3) IPP implementation focussing on warm-up sessions implemented by the strength/conditioning coach, and/or individual prevention sessions by the physical therapist.

Congenital rickets due to vitamin D deficiency in the mothers.

BACKGROUND & AIMS: We wished to review all published reports of congenital rickets to identify the causes and characteristics. METHODS: 25 cases were identified in 19 published reports in which there was radiological and/or histological evidence of rickets in the first two weeks after birth. Cases of rickets associated with maternal renal failure were excluded as were infants born at less than 32 weeks gestation. RESULTS: There was evidence of maternal deficiency in 24 of these cases. In 16 cases the diagnosis of the rickets led to the identification of symptomatic osteomalacia in the mothers. Of the 12 mothers who had assays for serum 25-hydroxyvitamin D (25OHD) 11 had values less than 10 ng/mL. Presentations in the infants included craniotabes, wide skull sutures, rachitic rosaries, enlargement of the wrists, tetany and convulsions. In two cases rickets had been suspected from antenatal X-rays. In five cases fractures were found at the time of initial presentation. Of the 16 infants with serum calcium assays 15 had values lower than 8.8 mg/dL. Of 13 infants who had serum alkaline phosphatase assays 12 had abnormally high levels. Of the seven infants in whom serum 25OHD was measured before treatment, all had values less than 10 ng/mL. CONCLUSIONS: These reports provide strong support for the view that maternal deficiency leads to overt bone disease from before birth. Maternal deficiency probably also leads to impairment of bone quality in postnatal life. The importance of ensuring adequate vitamin D nutrition in pregnancy is emphasised.

Clinical and laboratory features of temporary brittle bone disease.

Temporary brittle bone disease has been described since 1990. It is a syndrome characterised by multiple unexplained fractures in early childhood. There is growing evidence that it has natural causes and does not represent inflicted trauma. We report the clinical and laboratory features of 104 patients investigated personally between 1985 and 2000. These patients had in aggregate 976 fractures or fracture-like lesions. Our patients included disproportionate numbers of infants born preterm or as a result of multiple pregnancy. The fractures were mainly identified in the first 6 months of life and entirely within the first year of life. Most fractures were asymptomatic, particularly the many rib fractures and metaphyseal lesions. Few patients had evidence of bruising at presentation; none had clinical evidence of inflicted injury commensurate with the fractures found. In 22 patients the fractures were found in the course of investigation for unrelated symptoms. In several cases fractures took place while the children were in hospital. Unexplained bruising and sub-conjunctival haemorrhages also occurred in hospital, suggesting collagen defects. Hernias were recorded; in most these resolved spontaneously, again suggesting transient collagen defects. Among the unexplained symptoms of the patients was a history of vomiting, often projectile vomiting. Some patients had unusually blue or grey sclerae for the child's age. Many patients had abnormally large anterior fontanelles. Laboratory findings included anaemia, neutropenia and an exceptionally high serum alkaline phosphatase. Our findings reinforce the view that children with temporary brittle bone disease have a distinctive and identifiable syndrome which probably includes osteopathy of prematurity. These patients do not have osteogenesis imperfecta and are not the victims of non-accidental injury. While the causes of this syndrome remain uncertain, its distinctive features should now be more readily recognised.

Enhancing skills of critical reflection to evidence learning in professional practice.

Professional organisations and regulatory bodies are making critical reflection a mandatory component of professional practice. Reflection is a vital part of learning from experience and is central to developing and maintaining competency across a practitioner's lifetime. This paper will discuss key educational theories to illustrate why reflection is important. Kolb's and Gibbs' reflective cycles are used to structure the process of critical reflection. Elements of the educational tradition of Bildung are discussed and integrated to enrich the understanding of self and to facilitate the reader's ability to enhance their professional practice.

Temporary brittle bone disease: association with intracranial bleeding.

We report 20 infants aged between 1 month and 6 months found to have subdural bleeding and also multiple unexplained fractures in a pattern similar to that described earlier as temporary brittle bone disease. Child abuse seemed unlikely as a cause of the fractures as in no case was there clinical evidence of injury commensurate with the fracturing, as some patients had fractures while in hospital and as metaphyseal lesions, when present, were often symmetrical in distribution. Abuse seemed unlikely to have been the cause of the subdural bleeding in several patients; three had clear histories of accidental injury and five had evidence that the initial bleeding was likely to have taken place at birth. Abuse also seemed unlikely as the cause of the syndrome; the nine patients who were returned to their parents had no subsequent allegations of abuse with a mean follow-up period of 15.8 years. The finding of hypermobile joints in the parents of eight of the children is an additional pointer to a natural cause for this condition. The cause of this combination of fractures and subdural bleeding is not yet clear but it is important to be aware that it can result from natural disease.

Joint laxity in the parents of children with temporary brittle bone disease.

One controversial cause of unexplained fractures in young children is temporary brittle bone disease. Contributory factors for this disorder include the following: premature birth, twin pregnancy and diminished foetal movement. Heritable factors may also be important. Infants with findings consistent with temporary brittle bone disease were identified from clinical and medico-legal referrals. The routine evaluation of each family included examination of both parents where available for joint laxity using the nine-point Beighton scale. Of 81 children in whom both parents had been examined personally, 40 had at least one parent with a Beighton score of four or more, conventionally regarded as indicative of the hypermobility syndrome. We found no significant difference in laxity when we compared the whole group of mothers with the controls (P = 0.081). The fathers were significantly different from their control group (P = 0.013). When we compared the figures for the most flexible parent of each child, there were significant differences from control subjects both in the mothers and in the fathers (P = 0.042 and P = 0.0065, respectively). We draw attention to the likely autosomal dominant inheritance of this risk factor for temporary brittle bone disease as well as the potential value of assessing parental joint laxity in evaluating children with fractures.

Temporary brittle bone disease: relationship between clinical findings and judicial outcome.

There is a wide differential diagnosis for the child with unexplained fractures including non-accidental injury, osteogenesis imperfecta and vitamin D deficiency rickets. Over the last 20 years we and others have described a self-limiting syndrome characterised by fractures in the first year of life. This has been given the provisional name temporary brittle bone disease. This work had proved controversial mostly because the fractures, including rib fractures and metaphyseal fractures, were those previously regarded as typical or even diagnostic of non-accidental injury. Some have asserted that the condition does not exist. Over the years 1985 to 2000 we investigated 87 such cases with fractures with a view to determining the future care of the children. In 85 of these the judiciary was involved. We examined the clinical and radiological findings in the 33 cases in which there was a judicial finding of abuse, the 24 cases in which the parents were exonerated and the 28 cases in which no formal judicial finding was made. The three groups of patients were similar in terms of demographics, age at fracturing and details of the fractures. The clinical similarities between the three groups of patients contrast with the very different results of the judicial process.

Vitamin D deficiency: a diagnosis often missed.

Vitamin D deficiency causes rickets in children and osteomalacia in adults. These are common today but often not recognized. This article summarizes the clinical features, investigation and treatment of these disorders and examines the factors contributing to failures of diagnosis.

Vitamin D deficiency rickets and allegations of non-accidental injury.

UNLABELLED: Vitamin D deficiency rickets has long been recognized as a cause of fractures and fracture-like appearances in young children. Often seen in the early 20th century, rickets has recently been regarded as uncommon; the radiological appearances, familiar to previous generations, may not be recognized for what they are. This article reports four children with unexplained fractures initially attributed confidently to non-accidental injury. In each case, the later evidence of vitamin D deficiency led to a reconsideration of that diagnosis. CONCLUSION: It is important to be aware of this bone disorder in the differential diagnosis of fractures, to investigate appropriately and to recognize that the radiological appearances may be misleading. A mistaken diagnosis of abuse does real harm, not least to the child itself.