Recognising Child Maltreatment and Steps to Safeguarding Children and Young People in the Emergency Department

recognizing child maltreatment

Safeguarding Children and Young People

In the busy and stressful environment of the emergency department (ED), it is often easy for us to miss the inexplicit signs or calls for help from children and young people! When looking at it from a broader view, the paediatric population is sometimes a part of the category of vulnerable patients who cannot ask for help, and may at times not realise they need it. Of the millions of children that pay visits to the ED a year, some present with non-accidental or non-intentional illnesses that had been brought upon by abuse or neglect. The ED can often be the first contact these children have with healthcare professionals, making it imperative that we notice the faint signs of maltreatment that may direct us towards acting for their protection.

The term safeguarding, as described by the government document, Working Together, encompasses the act of protecting children and young people from maltreatment, ensuring children and young people are growing up in a safe and healthy environment, and ensuring the best outcomes for all children and young people.

Who’s at Risk?

Parental issues, including alcohol/substance misuse, mental health problems, and domestic abuse, can indicate an unsafe environment for children. Additionally, poverty, poor housing, poor relationships with carers/parents, and a lack of support for the child can increase the risk of child maltreatment. Babies and disabled children are at an even greater risk of physical abuse.

Whose Responsibility is it to Protect and Safeguard Children and Young People?

According to various legislations, including the Children Act 2004, all healthcare staff and organisations must respond in times of suspected child maltreatment and take effective action to safeguard and protect these children. All healthcare staff should be prepared to amend their practice into a child-focused approach if there is any recognition of the risk of abuse or neglect in a child.

All NHS Trusts will have a specifically allocated doctor or nurse for safeguarding. Make sure to know who this is; they will be your point of contact if you have any concerns on safeguarding and child protection issues! This named healthcare professional will have the expertise to advise other professionals on the appropriate action to take.

What to do if a child reveals abuse:

  • Listen attentively
  • Let them know they have done the right thing by telling you
  • Tell them it is not their fault
  • Tell them you take them seriously
  • Do not confront the alleged abuser
  • Explain what you will do next
  • Report what the child has told you as soon as possible

Recognising Maltreatment

There are many forms of maltreatment a child may suffer from, including physical, emotional and mental. Many of these signs and symptoms don’t always point towards maltreatment immediately. The background history and presentation of the child will often be key to identifying issues. However, it may be worth considering child maltreatment if you notice the following:
 
  • A child that regularly has injuries (– check their records!)
  • Previous or current involvement with Children Social Care
  • The pattern of injury doesn’t make sense or match the history/explanation
  • A delay in seeking medical help (without appropriate explanation)
  • If the parent/carer leaves with the child before they are seen at the ED
      • Although there may be credible reasons for this, the Trust was responsible for ensuring all children in their care have a safe discharge. If the child leaves without the staff having been informed, action is required to ensure their safety.
  • Child missing appointments
  • Child not being registered with a GP

Physical symptoms of abuse:

  • Bruises/Swelling
  • Burns or scalds
  • Bite marks
  • Broke or fractured bones
  • Scarring
  • Signs of poisoning (vomiting, drowsiness, seizures)
  • Difficulty breathing  (as a result of drowning, suffocation, poison)
  • Evidence of neglect (unkempt, malnourished, smelly, dirty) 

Behavioural symptoms of abuse:

  • Anti-social behaviour
  • Anxiety, depression, suicidal thoughts
  • Drug/alcohol use
  • Eating disorders
  • Aggression/Tantrums
  • Bed-wetting, insomnia
  • Problems in school (slow development)

Next Steps if Maltreatment is Suspected

When abuse is suspected, a referral to social care must be made within 24 hours (the sooner, the better). Make sure records are kept! The child will have registered with the reception staff and given their demographics, but it is important that he child’s GP and school details are in the system, as well as recording the details and relationship of the person(s) accompanying the child. Have a look through previous history/attendances for any potential indicators of reoccurring/previous child maltreatment.

To prepare for making a social care referral, first discuss the concerns with a senior staff member in the ED. Ensure some of the indicators of child maltreatment (such as those listed above) are present to support the referral decision. Consider previous information available about the child that is relevant (such as those on previous medical attendances). The child’s demographics should be known and recorded, and then contact the Local authority of the area the child normally resides to see if the child is subjected to a child protection plan or maybe previously known to children’s care services. Carry out any relevant lateral checks (GP, school nurse, etc.) Consider looking at the Trust’s local Thresholds for referral document before continuing to make the referral. If any further advice is needed, the safeguarding team can be contacted.

Children presenting with self-harm or suicidal issues
Children (ages 0-16) should be referred to a paediatrician/child psychiatrist if they present with thoughts or acts of self-harm or suicide. Trust guidelines on dealing with self-harm in children 16 years and under are available at your local Trust, as well as by NICE guidelines. All children (aged 0-18) presenting with substance misuse issues or emotional issues should be further referred to CAMHS.

Upon discharge, all children should be given the appropriate resources within the department so they know who to contact for support or further information (this could include leaflets, phone numbers, etc.)

Safeguarding Children and the Data Protection Act 1998

The law permits the disclosure of confidential information when necessary to safeguard a child. Personal information (about the child or family) is confidential. Healthcare professionals are subjected to a legal duty of confidence. However, information that is relevant, pertinent, and justified in the child’s interest may be disclosed without consent.

References and Further Reading

Cite this article as: Nadine Schottler, Great Britain, "Recognising Child Maltreatment and Steps to Safeguarding Children and Young People in the Emergency Department," in International Emergency Medicine Education Project, February 3, 2021, https://iem-student.org/2021/02/03/child-maltreatment-and-safeguarding/, date accessed: February 25, 2021

Recent Blog Posts by Nadine Schottler, Great Britain

Immediate Management of Paediatric Traumatic Brain Injury

Traumatic brain injury (TBI) has been noted as a leading cause of death and disability in infants, children, and adolescence (Araki, Yokota and Morita, 2017). In the UK alone, it’s approximated 1.4 million individuals attend the emergency department (ED) with head injury, and of those, 33%-50% are children under the age of 15; on top of this, a fifth of those patients admitted have features suggesting skull fracture or brain damage – that’s no small figure (NICE, 2014)! The particular importance of TBI in the paediatric population is that the treatment and management approach differs to adults; this is largely due to the anatomical and physiological differences in children. Furthermore, neurological evaluation in children proves more complex. All in all, children are complicated, and it is of great importance that we are aware of these differences when a paediatric patient arrives at the ED with TBI presentations.

Why is the paediatric population at risk for TBIs?

To delve slightly deeper into physiology and anatomy, there are several reasons children are at high risk of acquiring serious injury from TBIs. The paediatric brain has higher plasticity and deformity. As such, their less rigid skulls and open sutures allow for greater shock absorbance and response to mechanical stresses (Ghajar and Hariri, 1992). This ‘shaking’ of the brain inside the skull can stretch and tear at blood vessels in the brain parenchyma, resulting in cerebral haemorrhage.

Children also have a larger head-to-body size ratio, making the probability of head involvement in injury consequently higher (in comparison to adults); the head is also relatively heavier in a child, making it more vulnerable (especially in injury caused by sudden acceleration).

Young children have weaker neck muscles on top of having relatively heavier heads. Ligaments in the neck are relied on for craniocervical stability more so than the vertebrae. Hence, not only are TBIs more likely, but craniocervical junction lesions can also result from traumatic injury.

How does TBI in children come about?

The common causes of TBI in the paediatric population varies with age (Araki, Yokota and Morita, 2017). Some of these causes can be seen in the table below, which has been adopted from Araki, Yokota, and Morita (2017).

Table 1 Injury characteristics according to age and development

How can TBI in children present?

  • History: dangerous mechanism of injury (e.g. road traffic accidents or fall from a height greater than 1 meter)
  • Glasgow Coma Scale (GCS) less than 15 (at 2 hours after injury)
  • Visible bleeding, bruise, swelling, laceration
  • Signs of base-of-skull fracture:
    •  ‘Panda’ eyes – haemotympanum
    • Battle’s sign – cerebrospinal fluid leakage from ear or nose
  • Seizure (ask about history of epilepsy)
  • Focal neurological deficit
  • Vomiting
  • Loss of consciousness
  • Amnesia lasting more than 5 minutes
  • Abnormal drowsiness 

Note some children won’t have any of these signs, but if there is any suspicion of possible TBI, it should be investigated further.

Immediate management

There are various causes to paediatric TBI – also subdivided into primary and secondary TBI. Primary TBI includes skull fractures and intracranial injury. Secondary TBI can be caused by diffuse cerebral swelling. Primary and secondary TBI will be managed similarly in initial treatment (i.e. in the ED). The goal of baseline treatment is to:

  1. maintain blood flow to the brain
  2. prevent ischaemia (and possible secondary injury)
  3. maintain homeostasis 

Analgesia, Sedation, Seizure Prophylaxis

A level of anaesthesia needs to be achieved to allow for invasive procedures, such as airway management and intracranial pressure (ICP) control. Normally opioids and benzodiazepines are using in combination for analgesia and sedation in children. Instances where a child presents with a severe TBI (defined as a ‘brain injury resulting in a loss of consciousness of greater than 6 hours and a Glasgow Coma Scale of 3 to 8’), a neuromuscular block is used to improve mechanical ventilation, stop shivering, and reduce metabolic demand.

Anticonvulsants have been used in children, in particular infants, as they have a lower seizure threshold. Risk factors for early onset of seizures in infants under the age of 2 include hypotension, child abuse, and a GCS of ≤ 8; note, all of which may occur as a result of, or preceding, a TBI! For severe paediatric TBI cases, immediate prophylactic administration of anticonvulsants has been recommended.

Maintaining Cerebral Perfusion

The gold standard to measure ICP is an external ventricular drain (EVD); which can be used not only to measure ICP but can also be opened to drain additional CSF to reduce ICP. An intraparenchymal intracranial pressure sensor is an immediate invasive method used to detect early increased ICP in children with TBI. Monitoring of both ICP and cerebral perfusion pressure (CPP) is considered standard practice in TBI management in both paediatric and adult populations, as it is associated with better outcomes.

CPP is the pressure gradient which allows for cerebral blood flow. If this pressure is not maintained, the brain will lose adequate blood flow (Ness-Cochinwala and Dwarakanathan, 2019). Elevated CPP can accelerate oedema and increase chances of secondary intracranial hypertension.

Cerebral Perfusion Pressure (CPP) = Mean Arterial Pressure (MAP) – Intracranial Pressure (ICP)

A CPP of around 40-60 mmHg (40-50mmHg in 0-5 year-olds and 50-60mmHg in 6-17 year-olds) is considered ideal. Achieving an adequate CPP can be done by increasing MAP or reducing ICP (using the above equation). Hence it is necessary to have a good understanding of what good target values for MAP and ICP are.

A good target value for MAP is the upper end of ‘normal’ for the child’s age. Reaching this can be done by using fluids (if fluid deficient) or by use of inotropes. The recommended ICP target is < 20mmHg (normal is between 5-15 mmHg and raised ICP is regarded as values over 20mmHg).

When thinking about ICP, it’s useful to remember a mass in the brain; a mass being possible haemorrhage or any other space-occupying lesion. In TBI, oedema is most prominent at around 24-72 hours post-injury. As a result of increased mass, the initial consequence is a displacement of cerebrospinal fluid (CSF) into the spinal cord. Following this, venous blood in the cranium will also be displaced.

If ICP is further elevated, herniation can result – which is serious and often fatal! Signs of uncal herniation can present as unilateral fixed and dilated pupil. Signs of raised ICP can include pupillary dilatation and series of responses known as the ‘Cushing’s Triad’: irregular, decreased respiration (due to impaired brainstem function), bradycardia, and systolic hypertension (widened pulse pressure). Cushing’s triad results from the response of the body to overcome increased ICP by increasing arterial pressure.

Using the Monroe-Kellie Doctrine as a guide, we can predict how to reduce ICP. One management is head positioning. Head-of-bed should be elevated to 30˚, with the head in mid-line position, to encourage cerebral venous drainage. The EVD can also be used to drain CSF.

Commonly, intravenous mannitol and hypertonic saline are used to manage intracranial hypertension in TBI. Mannitol is traditionally used at a dosage of 20% at 0.25-1.0 g/kg – this is repeatedly administered. The plasma osmolality of the patient needs to be kept a close eye on; it should be ≤ 310 mOsm/L. 3% NaCl can be used to raise sodium levels to 140-150 mEg/L – this is slightly higher than normal sodium levels as a higher blood osmolarity will pull water out of neurons and brain cells osmotically and reduce cerebral oedema (Kochanek et al., 2019). Mannitol works in the same manner, however, use with caution as mannitol, being an osmotic diuretic, can cause blood pressure drops and compromise CPP! In last-resort emergency cases, where ICP need to be immediately reduced, a decompressive craniotomy can be performed.

Intravascular Volume Status

Measuring the patient’s central venous pressure (CVP) is a good indicator of the child’s volume status; 4-10 mmHg have been used as target thresholds. Alternatively, you can also monitor urine output (>1mL/kg/hr), blood urea nitrogen, and serum creatinine. Low volume status should be corrected with a fluid bolus. If the patient’s volume status is normal or high, but they remain hypotensive, vasopressors may improve blood pressure. At all costs, hypotension must be avoided, as if can lead to reduced cerebral perfusion and lead to brain ischaemia; on the other end, hypertension can cause severe cerebral oedema and should also be kept an eye on.

Other considerations​ - There have been reports of pituitary dysfunction in 25% of paediatric TBIs (during the acute phase). Do consider this if the patient had refractory hypotension – keep ACTH deficiency in mind!

Ischaemia

Prevent hypoxia at all costs! Hypoxia goes hand-in-hand with cerebral vasodilation – and as we already know, this increases the pressure in the cranium. Additionally, with hypoxia, there will be ischaemia. A minimum haemoglobin target of 7.0 g/dl is advised in a severe paediatric TBI case.

Other considerations​ - Whilst we are on the blood topic, also take care to correct and control any coagulopathies.

Ventilation

At a Paediatric Glasgow Coma Scale (PGCS) of less than 8, airways must be secured with a tracheal tube and mechanical ventilation commenced. SpO2 should be maintained at greater than 92%.

Of course, hypercapnia (CO2 > 6 kPa) and hypocapnia (CO2 < 4 kPa) are both not ideal, and we should maintain paCO2 at 4.5 – 5.3 kPa. However, some sources have suggested a quick fix to reduce ICP is to acutely hyperventilate the patient (as low CO2 results in cerebral vasoconstriction) – it’s suggested that paCO2 can safely go as low as 2.67 kPa before ischaemia kicks in! Mild hyperventilation is recommended (3.9 – 4.6 kPa)(Araki, Yokota and Morita, 2017).

Decreasing Metabolic Demand of the Brain

Body Temperature

What we want is to prevent hyperthermia, as it increases cerebral metabolic demands. Normothermia (36.5˚C – 37.5˚C) can be maintained by use of cooling blankets or antipyretics. There has been debate on whether therapeutic hypothermia has shown any benefit. Some studies have shown that moderate hypothermia for up to 48 hours, followed by slow rewarming, has prevented rebound intracranial hypertension as well as decreased ICP, however, there have not been any confirmed functional outcomes or decreased mortality rates benefits of this method (Adelson et al., 2013; Hutchinson et al., 2008).

Glycaemic control

Persistent hyperglycaemia (glucose > 10 mmol/L) should be treated. Hypoglycaemia (< 4 mmol/L) is much more dangerous. Persistent hyperglycaemia can be managed by reducing the dextrose concentration in IVF (which is usually administered in the first 48 hours of ICU care), or by starting an insulin drip.

A comment on imaging methods

In the UK, the initial investigation choice for detecting acute brain injuries is a CT head scan. A CT scan should be done within an hour of suspected head injury.
If there are no indications for a CT head scan (i.e. the signs/symptoms listed previously), a CT head scan should be performed within 8 hours of injury (NICE, 2014).

MRI scans are not usually done as the initial investigation, however, they have shown to provide information on the patient’s prognosis.

A final and most important note:

Don’t ever forget Safeguarding in children. Unfortunately, child maltreatment is common and can present anywhere. Have a look at the NICE guidelines below for more on how to identify child maltreatment.

Further reading

References

  • Adelson PD, Wisniewski SR, Beca J, Brown SD, Bell M, Muizelaar JP, Okada P, Beers SR, Balasubramani GK, Hirtz D; Paediatric Traumatic Brain Injury Consortium. Comparison of hypothermia and normothermia after severe traumatic brain injury in children (Cool Kids): a phase 3, randomised controlled trial. Lancet Neurol. 2013 Jun;12(6):546-53. doi: 10.1016/S1474-4422(13)70077-2.
  • Araki T, Yokota H, Morita A. Pediatric Traumatic Brain Injury: Characteristic Features, Diagnosis, and Management. Neurol Med Chir (Tokyo). 2017;57(2):82-93. doi:10.2176/nmc.ra.2016-0191
  • Finnegan R, Kehoe J, McMahon O, Donoghue V, Crimmins D, Caird J, Murphy J. Primary External Ventricular Drains in the Management of Open Myelomeningocele Repairs in the Neonatal Setting in Ireland. Ir Med J. 2019 May 9;112(5):930.
  • Ghajar J, Hariri RJ. Management of pediatric head injury. Pediatr Clin North Am. 1992;39(5):1093-1125. doi:10.1016/s0031-3955(16)38409-7
  • Hutchison JS, Ward RE, Lacroix J, Hébert PC, Barnes MA, Bohn DJ, Dirks PB, Doucette S, Fergusson D, Gottesman R, Joffe AR, Kirpalani HM, Meyer PG, Morris KP, Moher D, Singh RN, Skippen PW; Hypothermia Pediatric Head Injury Trial Investigators and the Canadian Critical Care Trials Group. Hypothermia therapy after traumatic brain injury in children. N Engl J Med. 2008 Jun 5;358(23):2447-56. doi: 10.1056/NEJMoa0706930.
  • Kochanek PM, Tasker RC, Bell MJ, Adelson PD, Carney N, Vavilala MS, Selden NR, Bratton SL, Grant GA, Kissoon N, Reuter-Rice KE, Wainwright MS. Management of Pediatric Severe Traumatic Brain Injury: 2019 Consensus and Guidelines-Based Algorithm for First and Second Tier Therapies. Pediatr Crit Care Med. 2019 Mar;20(3):269-279. doi: 10.1097/PCC.0000000000001737.
  • National Institute for Health and Care Excellence. Head injury: assessment and early management. 2014. Available at: https://www.nice.org.uk/guidance/cg176
  • Ness-Cochinwala M., Dwarakanathan D. Protecting #1 – Neuroprotective Strategies For Traumatic Brain Injury. Paediatric FOAMed. 2019. 
Cite this article as: Nadine Schottler, Great Britain, "Immediate Management of Paediatric Traumatic Brain Injury," in International Emergency Medicine Education Project, November 16, 2020, https://iem-student.org/2020/11/16/paediatric-traumatic-brain-injury/, date accessed: February 25, 2021

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The Kawasaki Disease Enigma Continues 150 years Later

kawasaki disease

Kawasaki disease (KD), or mucocutaneous lymph nodes syndrome is an immune-mediated inflammation in the walls of medium-sized arteries throughout the body. It’s complications result in the coronary arteries expanding, heart attacks, and premature death.

As the leading cause of heart disease in North American and Japanese children, KD continues to bewilder clinicians and researchers – even in the midst of a global pandemic. Possible links to SARS-CoV2 has even stirred uneasiness in patients, and physicians making diagnoses.

Beginning in Victorian-era England, a young boy presented to the doctor’s office with symptoms suggestive of scarlet fever; however, noticing heart disease in this child was just baffling. Despite being unaware of this rare disease, it was beyond physicians at the time; since then, progress has been limited as clinicians still fail to comprehend the disease’s root cause.

Dating back to 1874, KD was discovered by Samuel Gee while he was dissecting the cadaver of a seven-year-old boy.

He noticed something strange, “The pericardium was natural. The heart natural in size, and the valves healthy. The coronary arteries were dilated into aneurysms at three places, namely, at the apex of the heart a small aneurysm the size of a pea; at the base of the right ventricle, close to the tip of the right auricular appendix, and near to the mouth of one of the coronary arteries, another aneurysm of the same size; and at the back of the heart, at the base of the ventricles, and in the sulcus between the ventricles, a third aneurysm the size of a horse bean. These aneurysms contained small recent clots, quite loose. The aorta near the valves, and the aortic cusp of the mitral valve, presented specks of atheroma.

From his autopsy, evident was that Gee found aneurysms in the coronary arteries running across the surface of the boy’s heart. He then placed the specimen in a jar and provided it to the Barts Pathology Museum in London. Little did he know, that his specimen marked evidence of the earliest recorded case of KD and sparked worldwide medical curiosity. Unfortunately, when physicians 100 years later were hoping to retrieve samples from the specimen containing the boy’s heart, they were informed that it was missing.

A few years later, the disease was recognized in 1967 by the Japanese physician, Tomikasu Kawasaki. Although some researchers claimed the virus was unknown, others stated KD resulted from a bacterial or fungal toxin. The windborne theory suggested that the disease was seasonal, and as such, the direction of the swaying wind played a role in infection. Others stated that since children’s immune systems are still developing and since they have just lost the protective antibodies from their mothers, they are susceptible to infection. Therefore, in Asian American household’s diets rich in soy put Asian children at greater risk due to the isoflavones. In the 1980s, the Center for Disease Control and Prevention (CDC) suspected chemicals as the cause of KD, inferring that disease stems from agents that trigger an overreaction of the patient’s immune system. No one knew exactly what the mechanism or cause of KD was, although many scientists speculated some theories.

Over the last decade, significant progress toward understanding the pathogenesis, history, and therapeutic interventions of KD has been fruitful. Treatment aimed at the intravenous infusion of gamma globulin antibodies derived from the plasma of blood donations has helped children recover. In contrast, other therapies of corticosteroids for immunoglobulin-resistant patients and tumor inhibitors such as etanercept, infliximab, and cyclosporin A have been other medications providing relief.

The most significant clinical debate was over the possible link between the rash and the cardiac complications seen in Asian American children. Factors responsible for KD were introduced into Japan after World War II and re-emerged in a more virulent form spreading through the industrialized Western world. Advancements in medicine, improvements in healthcare, and, notably, the use of antibiotics reduced the burden of rash and fever illnesses significantly allowing KD to be recognized as a distinct clinical entity.

Nonetheless, the enigma pervades even during the COVID19 pandemic; this time, more pressing as the ever-elusive cause of KD that troubles children’s hearts affects physicians’ sleep and worries parents’ minds. Although the story of Kawasaki disease began decades ago when a young boy’s heart was locked inside a glass specimen, its ending is still being crafted. By the time the heart is found again at the museum, and placed safely for visitors treasuring ancient history, what further knowledge and progress will the scientific community have achieved? How far will humanity have come to find answers to KD and fill in the perplexing missing piece of the puzzle?

For now, there are no answers, but the enigma continues…

Cite this article as: Leah Sarah Peer, Canada, "The Kawasaki Disease Enigma Continues 150 years Later," in International Emergency Medicine Education Project, July 24, 2020, https://iem-student.org/2020/07/24/kawasaki-disease-enigma-continues/, date accessed: February 25, 2021

References and Further Reading

Salter-Harris Fractures

salter harris

Case Presentation

You are a medical student doing your first clinical shift as part of your Emergency Medicine rotation. A 9-year-old boy is brought in by his father after an injury to his left hand approximately 1 hour back. As explained by the father, the child was playing at home with his elder brother when his left index finger became caught in between a door that had quickly slammed shut. Following the injury, the child was reported to be crying due to severe pain, but had no lacerations or other associated injuries. He was rushed to the hospital and presented in the ED as an anxious, weeping boy who held out his left index finger and pointed to the tip as the region of maximal pain. Mild swelling was noted at the distal interphalangeal joint as well as at the tip of the affected finger. After appropriate analgesia was initiated, the child was sent to the Radiology department for X-ray imaging. The images obtained by the department are shown below in Figures 1.1 and 1.2.

Figure 1.1
Figure 1.1
Figure 1.2
Figure 1.2

Findings

Due to the lack of ideal positioning and suboptimal cooperation from the child and his parent, the radiology technician reports back to you stating that the best images they could obtain were the ones displayed above. Although unclear, you can confidently identify a small break in the bone at the base of the distal phalanx. You mention to the father that you see a fracture on the X-ray and report back to your Attending Physician. 

The Attending Physician decides to take a break from his morning coffee and utters the dreaded question: “What kind of fracture is this?” You try to recall a lecture you had about Salter-Harris fractures but cannot recall the classification of these fractures. As if on cue, the father of the patient finds you shuffling your weight in front of the Attending Physician and asks: “You said he has a fracture, will he have to get surgery for his finger?”

“What kind of fracture is this?”

Salter-Harris Fractures

Salter-Harris Fractures refer to fractures that involve the growth plate (physis). Therefore, these fractures are applicable specifically to the pediatric population, occurring most often during periods of rapid growth (growth spurts) when the growth plate is at its weakest, close to age ranges where children tend to participate in high-risk activities (11-12 in girls and 12-14 in boys) [1].

Originally described in 1963 by Dr Robert Salter and Dr Robert Harris [2], the now infamous Salter-Harris fractures are classified by the region of bone that is affected. Figure 2 displays the gross anatomy of a normal distal phalanx similar to the picture we examined in the X-ray, labelled to reflect the different areas of the bone relative to each other. The types of fractures that can occur are outlined below.

SALTER HARRIS ANATOMY
Figure 2
  • Type I Salter-Harris Fractures (Slipped)

    Type I fractures occur when a longitudinal force is applied across the physis, resulting in a displacement (“slip”) of the epiphysis from the metaphysis. Though relatively infrequent (5%), suspicion of this fracture is raised when the epiphysis is seen to either be displaced to the side of its original position relative to the metaphysis or when the gap between the two segments is widened.

Salter-Harris Type I
Salter-Harris Type I
  • Type II Salter-Harris Fractures (Above)

    Type II fractures are the most common (75%) of the Salter-Harris fractures. As with our patient above, this fracture only involves structures “Above” the epiphysis (Metaphysis + Physis/growth plate) with virtually no fracture or displacement of the epiphysis itself. Fortunately, type I and most type II fractures can be managed conservatively with cast immobilization and splinting.

Salter-Harris Type II
Salter-Harris Type II
  • Type III Salter-Harris Fractures (Lower)

    Type III fractures involve both the physis and the epiphysis. Although relatively uncommon (10%), the involvement of the epiphysis and consequent disruption of the growth plate makes this an intra-articular fracture that usually requires surgical fixation.

Salter-Harris Type III
Salter-Harris Type III
  • Type IV Salter-Harris Fractures (Through)

    Continuing the trend of worse outcomes with higher classification types, Type IV fractures involve all three layers (metaphysis, physis and epiphysis) and thus harbor more adverse outcomes and risks, with management primarily consisting of operative internal fixation. Similar to Type III fractures, this is an intra-articular fracture and also occurs at a similar rate of 10%.

Salter-Harris Type IV
Salter-Harris Type IV
  • Type V Salter-Harris Fractures (Rammed/Crushed)

    The rarest of all the Salter-Harris fractures, type V fractures occur due to high impact compression of the growth plate. Potential disruption of the germinal matrix and compromised vascular supply to the growth plate can lead to growth arrest.

Salter-Harris Type V
Salter-Harris Type V

A convenient method to recall the Salter-Harris classifications is outlined below using the mnemonic “SALTR”

Salter-Harris Classification
Salter-Harris Classification

Case Resolution

You ascertain the patient’s fracture to be a type II Salter-Harris fracture, justifying your answer to the Attending Physician by pointing out that the affected region in the X-ray is limited to the metaphysis and physis with no epiphyseal involvement. Recognizing the potential for parental misconceptions surrounding the diagnosis of fractures in pediatric patients [3], you approach the father and explain that, though there is a fracture present, there is likely no need for any surgical intervention. You advise that the left index finger will be immobilized using a splint and further elaborate on the unlikelihood of this injury to manifest any long-term developmental or growth arrest in the affected region.

References and Further Reading

  1. Levine RH, Foris LA, Nezwek TA, et al. Salter Harris Fractures. [Updated 2019 Aug 13]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan
  2. Salter, Robert B.; Harris, W. Robert: Injuries Involving the Epiphyseal Plate, The Journal of Bone and Joint Surgery (JBJS): April 1963 – Volume 45 – Issue 3 – p 587-622
  3. Sofu H, Gursu S, Kockara N, Issin A, Oner A, Camurcu Y. Pediatric fractures through the eyes of parents: an observational study. Medicine (Baltimore). 2015;94(2):e407. doi:10.1097/MD.0000000000000407
Cite this article as: Mohammad Anzal Rehman, UAE, "Salter-Harris Fractures," in International Emergency Medicine Education Project, December 23, 2019, https://iem-student.org/2019/12/23/salter-harris-fractures/, date accessed: February 25, 2021

A 20-months-old head trauma: CT or Not CT?

by Stacey Chamberlain

A 20-month-old female was going up some wooden stairs, slipped, fell down four stairs, and hit the back of her head on the wooden landing at the bottom of the stairs. She did not lose consciousness and cried immediately. She was consolable after a couple of minutes and is acting normal per her parents. She has not vomited. On exam, she is well-appearing, alert, and has a normal neurologic exam. She is noted to have a left parietal hematoma measuring approximately 4×4 cm.

Should you get CT imaging of this child to rule out clinically significant head injury?

PECARN Pediatric Head Trauma Algorithm

Age < 2

Age ≥ 2

  • GCS < 15, palpable skull fracture, or signs of altered mental status
  • Occipital, parietal or temporal scalp hematoma; History of LOC≥5 sec; Not acting normally per parent or Severe Mechanism of Injury?
  • GCS < 15, palpable skull fracture, or signs of altered mental status
  • History of LOC or history of vomiting or Severe headache or Severe Mechanism of Injury?

The PECARN (Pediatric Emergency Care Applied Research Network) Pediatric Head Trauma Algorithm was developed as a CDR to minimize unnecessary radiation exposure to young children. The estimated risk of lethal malignancy from a single head CT in a 1-year-old is 1 in 1000-1500 and decreases to 1 in 5000 in a 10-year-old. Due to these risks, in addition to costs, length of stay and potential risks of procedural sedation, this CDR is widely employed given the frequency of pediatric head trauma ED visits. This CDR has the practitioner use a prediction tree to determine risk, but unlike some other risk stratification tools, the PECARN group does make recommendations based on what they consider acceptable levels of risk. In the less than 2-year-old group, the rule was found to be 100% sensitive with sensitivities ranging from 96.8%-100% sensitive in the greater than two-year-old group.

This algorithm does have some complexity and ambiguity. It requires the practitioner to know what were considered signs of altered mental status and what were considered severe mechanisms of injury. In addition, certain paths of the decision tree lead to intermediate risk zones. In these cases, the recommendation is “observation versus CT,” allowing for the ED physician to base his/her decision to image or not based on numerous contributory factors including physician experience, multiple versus isolated findings, and parental preference, among others.

Other pediatric head trauma CDRs rules have been derived and validated; however, in comparison trials, PECARN performed better than the other CDRs. Of note, in this study, physician practice (without the use of a specific CDR) performed as well as PECARN with only slightly lower specificity.

Case Discussion

For purposes of the case study, the patient falls into an intermediate risk zone of clinically important brain injury. However, a sub-analysis of patients less than two years old with isolated scalp hematomas suggests that patients were higher risk if they were < 3 months of age, had non-frontal scalp hematomas, large scalp hematomas (> 3cm), and severe mechanism of injury. Given the large hematoma in the case study patient and a severe mechanism of injury (a fall of > 3 feet in the under two age group), one might more strongly consider imaging due to these two additional higher risk factors.

Cite this article as: iEM Education Project Team, "A 20-months-old head trauma: CT or Not CT?," in International Emergency Medicine Education Project, May 15, 2019, https://iem-student.org/2019/05/15/a-20-months-old-head-trauma-ct-or-not-ct/, date accessed: February 25, 2021

Ortho Pearls – Salter-Harris Classification

iEM-Infographic-Pearls-Ortho - Salter Harris

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Pediatric fractures affecting growth plate are classified with Salter-Harris classification. It is from I to V. 

What is your opinion about below x-ray? I, II, III, IV or V?

Please give your answer at the comment box below.

428.3 - salter harris 2

iEM Education Project Team uploads many clinical picture and videos to the Flickr and YouTube. These images are free to use in education. You can also support this global EM education initiative by providing your resources. Sharing is caring!

Elbow Pain

In case you didn’t encounter a child with elbow pain today!

iEM Education Project Team uploads many clinical picture and videos to the Flickr and YouTube. These images are free to use in education. You can also support this global EM education initiative by providing your resources. Sharing is caring!