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Protection of the Vulnerable

Special Reports

by Dr Charles Essex

The welfare and protection of the vulnerable are the markers of a civilised society. Paradoxically recognition that children are subject to assault – the battered baby – by parents, the very people whom we would consider are primarily concerned with their welfare, has only been considered in the last few decades. Child abuse, like domestic violence, happens in all strata of society. There is no such thing as parents being a typical or not typical ‘social services family’.

In child protection cases, the stakes are high. If a carer is deemed to have caused the injuries non-accidentally a child may be taken away from an innocent parent, a parent’s nightmare. If the Court decides that the injuries have an innocent explanation, a child may be returned to a potentially murderous situation. Unfortunately child protection can easily become polarised with a relatively small but vociferous group of parents and some journalists and MPs believing that social workers and doctors recommend that children are removed from parents on the flimsiest of evidence.

Although child abuse divided into four areas [physical, sexual, and emotional abuse and neglect], in this article I discuss the findings when physical abuse is suspected, explain the diagnostic process and clarify some misunderstandings.

The history and examination
The role of the paediatrician as an expert witness is to assist the Court by considering the medical evidence and seeing if there is a plausible explanation for the child’s injuries. The process is the same as all medical consultations – history and examination aided by investigations. The history is taken from adult carers, usually the parents, in the case of babies and young children, but also from the child themselves if they are old enough. Even young children can often give a simple explanation if asked gently how they hurt their arm or leg, etc.

It is important not to ask leading questions but simply “How did you get that poorly arm?” or “What happened next?”. If possible one should speak to the child on their own. When using interpreters it is vital to use independent interpreters, not family members.

Doctors are concerned when the history of events does not match the injuries found. Other concerning features are when the history changes significantly. It is not uncommon for parents to remember additional details or make minor changes as the story is retold. However changes such as the injury happening when the baby fell out of the high chair, then later it was when the baby rolled off the changing mat are suspicious. A delay in presenting the child to hospital and multiple attendances at different hospitals are all warning signs.

Bruises, subdural haemorrhages and retinal haemorrhages
Rarely can one say definitively that an injury was caused accidentally or non-accidentally based on its physical appearance alone. One has to take other factors into account such as the age and development of the child, the explanation from the carers, and so on. Very young children who are independently mobile can get bruises. Those bruises are usually are found along a T-shape on the forehead and down the front of the face, or on
the legs, usually below the knee 1  The adage that “children who don’t cruise don’t bruise” means that one must be very suspicious if a very young baby presents with bruises 2
Clearly one cannot do experiments on children to find out exactly what degree of force of contact between a child and an object will cause a bruise or how long the time frames given below are. It is not possible to age bruises 3  Bruises caused at the same time can have different colours and appearances in the same child. This is because of factors such as the force involved, the mechanism of injury, the site of injury [such as whether it is over a bony prominence or if there is lots of subcutaneous fat], etc. Common sense and experience suggest that bruises that are red-blue and are swollen and tender are more recent and bruises that are yellow-brown and are flat and not tender are older bruises but beyond that it is difficult to be precise.

If a reliable witness can say when was the last time they saw that part of the child’s body without bruises then one can say that the event that caused the bruises is likely to have happened after that time, although allowing for the fact that the bruise may have taken some time to appear. Bruises can take one hour to one day to appear although occasionally bruising appears a couple of days later.

Erythema [redness] and grazes [abrasions] are fresher, more recent injuries. Redness usually fades within 24-48 hours or may turn into a bruise. Grazes usually scab over in 24-48 hours.

There are individual variations in terms of response to damage to the skin – an 'injury' [whether accidental or non-accidental]: how the injury will look over time; how it heals; and the final outcome. Injuries to the skin, however caused, can heal with scars of various colours and also, particularly noticeable in dark skinned people such as people of African or Afro-Caribbean descent, with either hyperpigmentation or hypopigmentation [darker skin or lighter skin, respectively, than the person's normal skin colour].

One would imagine that good quality photographs would give an objective record of the physical injury. However individuals can describe colours [of bruises, for example] differently whether seen with the naked eye or in photographs, and the interpretation of, for example, the colour of bruises and skin markings is subjective and different people will describe the same mark in different ways. It is important therefore that the doctor who examines the child gives a careful description in their statement of the size [including measurements] and shape of the injuries.

Causes of bruising and bleeding
Birth injury: I include birth injury as bruising and bleeding can happen during delivery. Babies can sustain subdural haemorrhages [SDHs] and retinal haemorrhages [RHs] during birth. However these resolve by six weeks of age 4
There is no evidence that babies who suffer SDHs and RHs during birth suffer a “re-bleed” some time later.

Vitamin and/or mineral deficiency: Vitamin C deficiency is rare in infants in the UK. Initially they have vitamin C stored from the vitamin C that has been passed to them in pregnancy from their mother. Breastfed babies get vitamin C in the breast milk. Infant formulas are fortified with a variety of vitamins and minerals.

Babies are born with low levels of vitamin K, a necessary component of the human blood clotting mechanism. They can develop the very rare complication of haemorrhagic disease of the newborn [HDN]. Parents are offered that their babies can have vitamin K at birth to lessen the risk of the babies developing HDN. If the baby was given vitamin K then I believe we can discount HDN as the cause of any of bruising or haemorrhages.

Blood clotting disorders: The doctor will request blood tests to check for blood clotting disorders. There are an extended range of blood tests one can request and are increasingly suggested by defence barristers. However if the child has not had a history of difficulty with continued oozing of blood such as after injections such as immunisations, or from the stump of the umbilical cord and there is no family history of bleeding disorders [this does not mean the frequent comment that someone bruises easily], and the child has had no further significant bruising since the index incident then I believe the standard clotting tests are satisfactory.

Accidental trauma: In young children there should be a clear history of an accidental event for significant bruising. Even if the parent were not in the same room at the time, they would hear a loud cry or even scream from a young child if the child has sustained an injury that leads to a large bruise. The doctor has to consider whether the history matches the clinical findings. 

SDHs and RHs caused by an accident in a baby or young infant would have been a very significant event for the parents. The carer(s) would have been well aware of an incident(s). For example, these can be seen following a high speed car crash, which gives an indication of the deceleration and forces involved.

Shaken baby syndrome
Shaken baby syndrome is a phrase used much more by non-doctors than by doctors. It is often used to refer to a combination of SDHs, RHs and an encephalopathy [impaired brain function leading to lethargy and decreased consciousness, poor feeding and poor respiration]. The baby may have fractures. If a baby is violently shaken, because it has weak neck muscles, a large, heavy head relatively to the baby’s size and weight, and because the brain does not fit snugly in the skull but has space around it, the brain ricochets back and forth inside the skull. This causes bleeding on the surface of the brain [SDHs], in the brain substance [parenchymal bleeding], and injury to the brain stem as it is flexed back and forth at the neck near to where the spinal cord leaves the base of the skull. As the baby is often held around the trunk as it is being shaken by the adult the lower half of the baby’s body also shakes and can lead to spinal
SDHs. The baby can develop RHs.  Shaking a baby or infant to dislodge food because one fears the child is choking does not cause SDHs and RHs. Winding a baby on its back after a feed or the baby flopping its head forward against a carer does not lead to SDHs, RHs or even bruises to the baby’s back or face, respectively.

All these features do not need to be present to diagnose that a baby has been shaken. Hence rather than talk about Shaken Baby Syndrome, a doctor will take a history of when the baby became unwell [the baby usually deteriorates immediately after the injury], any accidents or injuries up to that time, and examine the baby physically, looking for any external signs of injury, and neurologically. Investigations will look for signs of infection such as meningitis or a heart abnormality which might have caused the baby to collapse, and a brain scan. When the brain scan shows SDHs, this will raise child protection concerns and lead to further investigations such as blood clotting tests as described, a skeletal survey to look for fractures and an eye examination for RHs and alert the doctor to
the possibility that the baby may have been shaken, rather than attempting to fit everything into the Shaken Baby Syndrome criteria.

Although within the remit of a neurosurgeon and ophthalmologist, respectively, I make the following comments here:

• In babies and infants the size of the SDH is not the cause of neurological dysfunction, as often the SDH is a thin layer of blood on the surface of the brain. Rather it is an indication of what sort of injury happened if no satisfactory explanation is given, namely a probable shaking injury.

• A rare medical condition [glutaric aciduria] can cause shrinkage of the brain and can lead to SDH but the brain scan usually shows a typical pattern of shrinkage of the front of the brain. These brain haemorrhages can happen repeatedly.

• Unlike in adults, in children there is rarely a lucid interval between the event that caused the SDH and the child developing significantly impaired consciousness [an encephalopathy].

• There are medical conditions, albeit rare, that can cause RHs. However extensive RHs and in different layers of the retina and folds in the retina [‘perimacular folds’] are much more likely to be due to non-accidental injury, especially when accompanied by SDHs.

Low level falls
One only has to watch You’ve been framed to see babies and infants sustain low level falls on a regular basis. At the shopping precinct one can see baby buggies tip over backwards when parents put heavy shopping bags on the back and apart from being upset the babies suffer no injuries.

A review of 75 children aged less than 5 years found that falls of under 1 metre did not cause a skull fracture unless there was a small area impact point 5 A review of 207 children who fell out of beds or cots found one fractured skull [even when considering children who had climbed over the bars of the cot] 6  There were no serious, multiple, visceral or life threatening injuries. The Avon Longitudinal Study of Parents and Carers [2001] asked parents to describe any accidents. In 2554 children there were 3357 falls, of which 97% of the injuries involved the head but only 21 resulted in concussion or fractures. Falls from beds or sofas did not result in fractures to the skull. Another review of short falls in infants with an average age of 6 months only found intracranial bleeds in children
in whom abuse was confirmed 7
Hence despite some curious judgements in some cases low level falls of babies rolling off the bed or the sofa and so on are not regarded by most doctors in this field as the cause of RHs and SDHs.

No fracture is diagnostic of a non-accidental injury. Any fracture can be caused accidentally or nonaccidentally. However [depending upon the age of the child] some fractures are so unlikely to happen accidentally that without a convincing history of how the fracture happened one must be suspicious of non- accidental injury. These include fractures of the hands and feet, posterior parts of the ribs, the spine and metaphyseal fractures [at the growth plates of the bones], even in mobile active children. However in young babies and infants a mid shaft fracture of, say, the thigh [femur] would be suspicious especially if the child is not walking.

One has to exclude a medical cause of easy fracturing. These include an underlying metabolic, genetic or medication cause. Deficiency of vitamins C and D, deficiency of copper, and what is frequently termed osteopenia of prematurity, are what might be considered to be the metabolic causes of easy tendency to fracture bones in babies. Osteogenesis imperfecta, [OI] which is a genetic condition, is also a cause. Extensive steroid use is a medication cause.

There are often specific radiological findings in a child with OI but some types of this disorder can have normal radiological findings. Of the severe types leading to fractures very early in life and frequently present at birth, the pattern is different in that there are more frequent fractures and more bones likely to be affected. If fractures occur, it is likely that they will continue to occur unless particular special handling practices are introduced and used.

OI type 1usually presents with a fracture (s) of the longer bones of the arms and legs. It is extremely unusual for it to present with fractures of the fingers, ribs or skull or with metaphyseal fractures. In the history and examination one looks for the child and his parents to see if they have blue sclera [the whites of the eyes being an azure blue], a close family relative having frequent fractures with minimal trauma, or there being a family history of sensorineural deafness in adults in the family. Testing for the COL A1A gene is gaining popularity as this can be defective in OI type 1. However this is only positive in 90% of people with OI type 1. The diagnosis is made predominantly by the history including the family history, the examination of the child, the nature of the fracture(s) and the x-ray findings.

Vitamin C deficiency has been discussed earlier. Interest has now focussed on testing for vitamin D levels and what role it may play in fractures, often without understanding the value of this. A hypothesis was put forward by two American radiologists that low vitamin D levels in babies, which may have occurred secondary to low vitamin D in the mother, is a cause of unexplained fractures in children 8 The authors published four cases of so called “congenital rickets”. Their paper has been subject to many criticisms. These included comments that the clinical details of the cases had been omitted, that the authors did not have clinical care of the children but were paid defence witnesses, and that in three of the four cases Courts found in favour of abuse.

The conventional understanding of rickets [clinical vitamin D deficiency] is that there is a spectrum: low vitamin D, followed by biochemical rickets, followed by radiological rickets [the rickets visible on x-ray] followed by the complication of rickets [that is, fractures]. It is implausible to suggest that even if the child has low vitamin D alone [one end of the spectrum] this could be a cause of fractures as a complication of rickets [at the other end of the spectrum] without the intervening findings.

An up-to-date review of the topic concludes “although it is recognised that infants may have low vitamin D levels for many reasons, the likelihood that clinical rickets or mild vitamin D deficiency is apt to result in bone fractures in non ambulatory infants is exceedingly low” 9
Copper deficiency is very rare and infants have large stores of copper. Children with copper deficiency tend to have delayed development, their muscles tend to lack tone and they frequently have a specific rash. X-ray changes precede fractures and the absence of any changes on the child’s x-rays mean that copper deficiency can be ruled out as a cause of the child’s fracture.

Osteopenia of prematurity is getting rarer as premature babies are monitored carefully and often given phosphate supplements as part of their overall nutrition.

Corticosteroid use is a cause of easy fracture but this is very rare in children. However these need to be ‘potent’ steroids given either directly to the child or the mother within the pregnancy over a period of time. It does not include hydrocortisone cream [which should be used carefully and sparingly in any case] used for, say, eczema.

Thanks to Dr Annie Callaghan for advice on this paper.

1. Maguire S, Mann MK, Sibert K, Kemp A. Are there patterns of bruising in childhood which are diagnostic or suggestive of abuse? A systematic review. Arch Dis Child 2005;90:182-6.

2. Sugar NF, Taylor JA, Feldman KW. Bruises in infants and toddlers: those who don't cruise rarely bruise. Puget Sound Pediatric Research Network. Arch Pediatr Adolesc Med 1999;53:399-403.

3. Maguire S, Mann MK, Sibert J, Kemp A. Can you age bruises accurately in children? A systematic review. Arch Dis Child 2005; 90:187-9.

4. Whitby HE, Griffiths PD, Rutter S, et al. Frequency and natural history of subdural haemorrhages in babies and relation to obstetric factors. Lancet 2004;363:846-51.

5. Johnson K, Fischer T, Chapman S, Wilson B. Accidental head injuries in children under 5 years of age. Clin Radiol. 2005; 60:464-8.

6. Lyons RK, Oates TJ. Falling out of bed – a relatively benign occurrence. Pediatr 1993;92:125-7.

7. Tarantino CA, Dowd MD, Murdock TC. Short vertical falls in infants. Pediatr Emerg Care 1999;15:5–8

8. Keller KA, Barnes PD. Rickets vs abuse: a national and international epidemic. Pediatr Radiol 2008; 38: 1210-16.

9. Botash SA, Sills IN, Welch TR. Calciferol deficiency mimicking abuse fractures in infants: is there any evidence? J Pediatr 2012; 160:199-203.

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