Patrick Aldridge. Wheeze. It’s all in the timing…, Don't Forget the Bubbles, 2019. Available at:
One of the challenges of paediatrics is how to distill a life of experience down to something more tangible. When you are asked “How did you know s/he was sick?” you need to be able to give a better answer than “I just know“. In this session from DFTB19 we challenged three clinicians to explain just why they think the way they do.
Ben, a 14-year-old competitive sprinter, limps into your emergency department complaining of sudden onset severe pain and a “pop” felt in his left hip shortly after the start of his National Athletics 100m Final. He points to a specific area on his pelvis and walks with an antalgic gait. Further examination reveals pain on left hip flexion and an appreciable weakness on active flexion compared to his right side. Mum tells you that Ben has complained of pain during and after heavy training for the last few weeks, but this seems to settle with rest and icing after each session.
Ben and Mum are keen to know what you think of his x-ray.
What is his diagnosis, how are you going to manage it and what are his chances of making the International Schools Team trials in 3 weeks’ time?
Injuries to the apophysis range from recurring painful episodes of apophysitis to avulsion fractures of these secondary ossification centres. Avulsions often present with reports of a “pop” followed by severe pain and weight-bearing difficulties. There is a reported injury predominance in adolescent males of over 70%, with sports involving kicking or sprinting most likely to be involved.
As the participation of adolescents in competitive sport increases so too are reports of apophyseal avulsion injuries. The young athlete is becoming more powerful with stronger muscle groups enhancing physical abilities. Coupled with weaker apophyses, these factors lead to a higher incidence of avulsion fractures in this group.
Early diagnosis and appropriate management is necessary to reduce the risk of chronic pain, disability and reduced participation in physical activity. Apophyseal injuries can be misdiagnosed as “muscle strains” due to a failure to appreciate the anatomical uniqueness of this population making their injury pattern distinct from that of adults. The impact of a delay to diagnosis on long-term health, sports participation and development could be profound.
The apophysis (also known as a traction epiphysis) is a secondary ossification centre that serves as a site for musculotendinous attachment. It arises as a separate bony outgrowth and fuses with the main bone over time. These helpful table illustrations from a publication by Moeller in 2003 highlight the various expected ages of opening and closing of the various pelvic apophyses:
Tensile forces from strong muscular contractions are experienced at the pre-pubescent and adolescent apophysis during sporting activities. We know of several factors which make these structures more susceptible to avulsion injury:
The mechanism of injury in avulsion fractures is based on sudden ballistic movements that are experienced during “explosive” type activities like sprinting, kicking, twisting or jumping. Sudden forceful muscular contractions lead to eccentric loading of the tendon insertion at the apophysis. This then results in the separation and retraction of the apophysis away from its origin at the pelvis or femur.
Ischial tuberosity (54%) and anterior inferior iliac spine (22%) avulsions are the most common types of fractures reported in the adolescent population. Although rare, 5 patients from a study by Rossi and Dragoni in 2001 were reported as having two fractures so be sure to review all apophyseal sites before committing to a final diagnosis.
The various muscles and their corresponding apophyses are shown in the image below:
Most injuries are managed conservatively with initial rest and symptomatic support in the form of ice, protected weightbearing and analgesia. Gradual reintroduction to weightbearing with early range of motion (ROM) and strengthening should be progressed under the guidance of a physiotherapist.
While specifics may vary, a good conservative approach to managing these injuries could be:
Open reduction and internal fixation is considered for fractures with displacement of >2cm or those with chronic pain secondary to painful non-unions. The goal of surgery is to reduce the time to return to pre-injury level of physical activity. Fracture displacement of >2cm has been reported to increase the risk of non-union by up to 26 times, with AIIS and ischial tuberosity fractures also being an increased risk of developing nonunion complications. Sundar and Carty reported significant difficulty in returning to sport in 75% of ischial tuberosity avulsion cases with 25% of these athletes dropping out of sport altogether. A large case series by Schuett et al highlighted that 14% of all patients reported pain more than 3 months post injury, with patients with AIIS avulsions much more likely to report chronic pain.
It is important to counsel patients and parents about the small risk of chronic pain or non-union before disposition from ED and the potential need for delayed surgical intervention in the future.
Thanks to your keen eye for x-rays and knowledge of adolescent sports hip pathology, you diagnose Ben with a left sided ASIS avulsion (“Hip pointer”). You reassure Ben and Mum that this injury is unlikely to require surgery but explain that it will need rehabilitation with his local physiotherapist over the next few weeks. Ben’s devastation is clear for all to see after you express worry that he may not make his important International Schools Trial in three weeks’ time…but thankfully he quickly reassures himself as he has two more years at this age group and fancies his chances next year!
Moeller JL. Pelvic and Hip Apophyseal Avulsion Injuries in Young Athletes. Current Sports Medicine Reports. 2003; 2:110–115
Rossi F and Dragoni S. Acute avulsion fractures of the pelvis in adolescent competitive athletes: prevalence, location and sports distribution of 203 cases collected. Skeletal Radiol. 2001; 30:127–131.
Schuett DJ, Bomar JD, Pennock AT. Pelvic Apophyseal Avulsion Fractures: A Retrospective Review of 228 Cases. Journal of Pediatric Orthopaedics. 2015; 35(6): 617–623
Sundar M and Carty H. Avulsion fractures of the pelvis in children: a report of 32 fractures and their outcome. Skeletal Radiol. 1994; 23:85–90.
We know that the immediate first aid of a burn is to apply cool running water for at least 20 minutes. Fiona Wood reminded us of this in her talk at DFTB18. But just how much evidence is there for its benefit in children.
Natasha, a 13-year old girl, attends the Emergency Department with pain in the right wrist after falling onto her outstretched hand whilst ice skating. There is minimal swelling, but she is reluctant to move the wrist. She is tender on palpation of the anatomical snuffbox and on telescoping of the thumb. A senior colleague suggests this could be a scaphoid fracture and advises some plain radiographs. These show no bony injury, so she is placed in a wrist splint and referred for outpatient follow-up with the orthopaedic surgeons.
The scaphoid lies between the proximal and distal rows of carpal bones, on the radial side of the wrist. Its name comes from the Greek ‘skaphos’, meaning boat, due to its boat-like shape. It starts to ossify between the ages of four and six years, forming two poles (proximal and distal) united by the waist. Ossification occurs from the distal pole and moves proximally. During ossification, it is protected by cartilage. The scaphoid receives its blood supply from the branches of the radial artery, but due to retrograde flow, the blood supply can be interrupted when the bone is fractured, risking avascular necrosis. Full ossification is usually complete by age 13 in girls and 15 in boys.
Scaphoid fractures are uncommon in young children, due to protection of the bone during its ossification by a thick layer of cartilage and soft tissue. Cartilaginous fractures are possible but require reasonable force; simple soft tissue injuries are more common in younger age groups. Bony scaphoid fractures are seen predominantly in older children (ages 12-15). Any fracture diagnosed in the presence of growth plates seen elsewhere on radiographs are classified as paediatric fractures.
The injury pattern for scaphoid fractures is similar to that of adults, with the typical presentation being a fall onto an outstretched hand. Scaphoid fractures may also result from punching against resistance. This injury should also be considered in higher impact trauma, where the wrists are forcefully hyperextended against resistance; a child putting their arms out against a dashboard or front seat in the context of a car accident may lead to scaphoid fracture.
As with any orthopaedic examination, it is time to use the principle of look, feel and, finally, move.
As well as examining the distal radius and ulna, any wrist examination should include consideration of the scaphoid as the area of injury.
Although there is no positive finding which is pathognomonic of a scaphoid fracture, there are clues which should increase our clinical suspicion (see below)
Tenderness in the anatomical snuffbox – located in the first web space.
Tenderness of the scaphoid tubercle – located on the proximal palm at the base of the thumb
Pain elicited on axial loading, or ‘telescoping’ of the thumb.
Bear in mind that other injuries may be present.
Children can be difficult to assess, and if they are behaving as though they have a fracture, it can be difficult to rule out anything based on examination alone. Have a low threshold for imaging an area in which you are suspicious of a bony injury.
NICE recommends MRI as the first line imaging modality in suspected scaphoid fractures. MRI is not only expensive, but most emergency departments have restricted access to this investigation. Plain radiographs miss up to 25% scaphoid fractures across all age groups (Pincus, 2009), but this is our most readily available test.
A scaphoid series of plain x-rays includes four views: postero-anterior (PA), pronated, lateral, and supinated. A further view, PA with a clenched fist, allows some assessment of the scapholunate ligament integrity – although soft tissues cannot reliably be assessed on plain radiographs, a widened space between the scaphoid and lunate may suggest ligamentous disruption.
Plain x-rays are very specific – the presence of a cortical interruption or trabecular abnormality is highly likely to represent a true fracture. However, a normal radiograph is not sensitive enough to rule out a fracture. Patients with normal radiographs, in the presence of clinical symptoms or signs suggestive of a fracture, should be treated as such, and require further imaging, either in the form of repeat films 10-14 days post-injury, or an early MRI.
Due to the scaphoid ossifying from the distal pole proximally, this is the most likely part of the bone to fracture first in children (Gajdobranski, 2014). Unlike in adults, the middle and proximal parts of the bone are less frequently encountered. Similar to other fractures in paediatric patients, scaphoid fractures in this younger age group may be incomplete (uni-cortical) or non-displaced.
There is some overlap in the management in of suspected and confirmed scaphoid fractures based on the initial x-ray.
Paracetamol, ibuprofen and elevation in a sling are all appropriate whilst waiting for radiology.
If there is a confirmed fracture seen on the patient’s initial imaging, they can have a scaphoid cast applied. This is a below elbow backslab with a thumb spica. These patients should be referred to the fracture clinic for further management.
Normal plain radiographs do not exclude a fracture. In this instance, a wrist splint is appropriate to immobilise the affected area. There is no evidence for splinting with the thumb in extension (Dawson-Bowling, 2014). These patients need to be brought back to the fracture clinic for repeat radiography, or more advanced imaging in the form of MRI, dependent on local protocols.
Most scaphoid fractures in children and teenagers are managed conservatively with a cast. Whilst immobilisation time is usually the final remit of the orthopaedic surgeons, it is helpful to be able to offer children and their parents some advice in the Emergency Department as to how long healing will take. As a rule, the more distal the fracture, the quicker the healing process. This is in part due to the blood supply of the scaphoid. Longer immobilisation times will be needed for middle and proximal fractures.
Occasionally, surgical fixation will be required for significantly displaced fractures, or in cases on non-union. This is beyond the scope of Emergency Department management.
Do not miss scaphoid fractures on wrist x-rays – don’t be distracted by other, more obvious fractures. This patient complained of distal forearm pain but the scaphoid region was not specifically examined. A distal radius fracture and an ulnar styloid fracture were spotted on the x-ray. But, if you look at the very top of the film, you’ll also see a fracture through the scaphoid. Children may not complain of pain exactly over the fracture site, especially when there are fractures elsewhere.
Natasha is seen at ten days post-injury in the fracture clinic. Her splint is removed and whilst the swelling has improved, her range of motion is still restricted by pain and she remains significantly tender in the anatomical snuffbox. She is booked for an MRI of the wrist, which shows a non-displaced fracture line through the distal pole of the scaphoid. She is placed into a scaphoid plaster cast and remains immobilised for a total of six weeks. When the cast is removed, she has no residual symptoms and makes a full, uncomplicated recovery.
Abbasi D. Scaphoid Fracture. Orthobullets. Website. Available from: https://www.orthobullets.com/hand/6034/scaphoid-fracture[Accessed 20 April 2019]
Dawson-Bowling S, Achan P, Briggs T, Ramachandran M. 2014. Orthopaedic Trauma. The Stanmore and Royal London Guide. CRC Press. Elhassan B, Shin A. Scaphoid Fracture in Children. Hand Clinics. 2006; 22(1):31-41 Gajdobranski D, Živanović D, Mikov A, et al. Scaphoid Fractures in Children. Srp Arh Celok Lek. 2014; 142(7-8):444-449 Ghane M, Rezaee-Zavareh M, Emami-Meibodi M et al. How Trustworthy Are Clinical Examinations and Plain Radiographs for Diagnosis of Scaphoid Fractures? Trauma Monthly. 2016; 21(5): 1-6 National Institute for Health and Care Excellence (2016) Fractures (non-complex): assessment and management (NICE Guideline 38). Available at: https://www.nice.org.uk/guidance/ng38 [Accessed 12 April 2019]
Jenkins P, Slade K, Huntley J et al. A comparative analysis of the accuracy, diagnostic uncertainty and cost of imaging modalities in suspected scaphoid fractures. Int. J. Care Injured. 2008; 39: 768—774 Pincus S, Weber M, Meakin A. Introducing a Clinical Practice Guideline Using Early CT in the Diagnosis of Scaphoid and Other Fractures. Western Journal of Emergency Medicine. 2009; 4: 227-232(BET 2: Do wrist splints need to have a thumb extension when immobilising suspected scaphoid fractures?Emerg Med J 2011;28:1075-1076.
Abbasi D. Scaphoid Fracture. Orthobullets. Website. Available from: https://www.orthobullets.com/hand/6034/scaphoid-fracture[Accessed 20 April 2019]
Dawson-Bowling S, Achan P, Briggs T, Ramachandran M. 2014. Orthopaedic Trauma. The Stanmore and Royal London Guide. CRC Press.
Elhassan B, Shin A. Scaphoid Fracture in Children. Hand Clinics. 2006; 22(1):31-41
Gajdobranski D, Živanović D, Mikov A, et al. Scaphoid Fractures in Children. Srp Arh Celok Lek. 2014; 142(7-8):444-449
Ghane M, Rezaee-Zavareh M, Emami-Meibodi M et al. How Trustworthy Are Clinical Examinations and Plain Radiographs for Diagnosis of Scaphoid Fractures? Trauma Monthly. 2016; 21(5): 1-6
National Institute for Health and Care Excellence (2016) Fractures (non-complex): assessment and management (NICE Guideline 38). Available at: https://www.nice.org.uk/guidance/ng38 [Accessed 12 April 2019]
Jenkins P, Slade K, Huntley J et al. A comparative analysis of the accuracy, diagnostic uncertainty and cost of imaging modalities in suspected scaphoid fractures. Int. J. Care Injured. 2008; 39: 768—774
Pincus S, Weber M, Meakin A. Introducing a Clinical Practice Guideline Using Early CT in the Diagnosis of Scaphoid and Other Fractures. Western Journal of Emergency Medicine. 2009; 4: 227-232(BET 2: Do wrist splints need to have a thumb extension when immobilising suspected scaphoid fractures?Emerg Med J 2011;28:1075-1076.
One of the many perks of practising in the Emergency Department is the knowledge and experience of managing multiple different types of presentations and injuries involving all parts of human anatomy. This is true except for one small yet crucial part that medicine has historically handed over to another speciality – dentists. However, even though we may have limited experience with the oral cavity and its bony growths, we can still provide appropriate initial management in the Emergency Department.
Evie’s six. She was playing tag with friends, giggling as she twisted and skipped away from being caught. A boy playing football appeared out of nowhere. Evie collided with him and landed face down on the playground floor. One of Evie’s teeth was broken. Evie’s school nurse carefully put the fragment in a glass of milk. Panicked on receiving a phone call from the school, Evie’s mum collected her and brought her straight to your ED. You check Evie over for signs of a head injury. Thankfully all seems ok in this department. Her tongue looks fine with no lacerations. But her tooth is definitely fractured and you’re not sure what to do.
Teeth are divided into the crown (exterior) and root (embedded in the alveolar bone). The tooth is covered in enamel protecting the dentin in which the pulp with the neurovascular supply to the tooth is located. They are held in alveolar bone sockets by the periodontal ligament, a connective tissue covering the root, which forms the socket wall.
You look carefully at Evie’s fractured tooth. You can see an outer white layer, the enamel, surrounding a slightly creamier inner layer, the dentin. Right in the centre of this, you glimpse a pink, vascular layer. This must be the pulp. So Evie has a fracture of her tooth right through the enamel, dentin and into the pulp. But is it an adult or baby tooth?
Baby teeth are called deciduous teeth (although you’ll also hear them called primary and milk teeth). There are 20 deciduous teeth, which start erupting at approximately 6 months of age (although this is very variable – you’ll see many one year olds who still give you a winning gummy smile).
When the child’s about 6 or 7, these deciduous teeth will start falling out, much to the delight of the tooth fairy, making way for the adult, permanent teeth of which there are 28-32 in total.
Don’t confuse your central and lateral incisors from your canines, premolars or molars. Although dentists use a numbering and lettering system, this differs from country to country so, to avoid confusion, it’s easiest to use each tooth’s descriptive term as follows:
Differentiating between whether a tooth is deciduous or permanent is important as it drastically affects management. The patient’s age and a careful history will often make it clear, however, if not teeth can be differentiated according to their characteristics. Deciduous teeth are smaller, white and often with flat smooth edges. Permanent teeth are larger, creamier in colour and can have uneven edges if newly erupted.
Image from Royal College of Emergency Medicine
Evie’s fractured tooth is her front right incisor. All of Evie’s teeth are white with smooth edges. Wide-eyed, Evie tells you that the tooth fairy hasn’t visited her yet as she hasn’t lost any of her baby teeth. You check the surrounding teeth. None are wobbly and Evie’s mum is sure the others look they same as they did this morning when Evie went to school.
Traumatic dental injuries are common amongst small and school-age children with 25% experiencing dental trauma. In the preschool age data shows one-third of children suffer trauma to the deciduous dentition, and one-quarter of children and a third of adults have suffered trauma to permanent teeth. Despite the oral cavity comprising 1% of total anatomy, traumatic dental injuries account for 5% of injuries.
Other injuries should be examined, including mandibular or facial bone fractures. Assess for malocclusion of the jaw, bony tenderness along mandible and facial bones and sensory disturbance or numbness. The inferior alveolar nerve (a branch of the mandibular division of the trigeminal nerve) supplies sensory innervation to the mandibular teeth and via the mental branch to the lower lip and chin. It is often implicated in mandibular fractures, and as such sensory disturbance in these regions should prompt close examination of the mandible. Don’t forget the possibility of a significant head injury. In the case of avulsion, if the tooth can’t be located and there are clues in the history such as choking or coughing, consider ordering a chest x-ray to check it hasn’t been aspirated.
The clinical importance of traumatic injury to deciduous teeth is the impact on the underlying permanent tooth. The apex of the injured deciduous tooth root is in close proximity to the permanent tooth germ, thereby increasing the possibility of injury. Malformation, impaction, eruption disturbance and discolouration are all possible sequelae to injury. As such, management of injuries to deciduous teeth differs to that of permanent teeth as demonstrated below.
Dental injuries fall broadly into five categories: fractures, luxations and subluxations, avulsions and concussions.
Subluxation – the tooth is tender and is mobile
Extrusion – the tooth is almost pulled from the socket so appears longer and is very wobbly
Intrusion – the tooth is impacted into the alveolar bone
Avulsion – the tooth is not in the socket but in the hand
Concussion – just like receiving a bump on the head, the tooth is tender to touch or tapping but does not move
In all cases definitive management and follow up must be performed by dentists, as soon as possible, to prevent complications such as necrosis of the tooth’s pulp and unnecessary patient discomfort. There are, however, a few things we can do in the ED.
You carefully check the inside of Evie’s mouth. There are no lacerations of her cheeks, lips or tongue and the small piece of tooth Evie gingivally hands to you looks like the missing piece of her fractured incisor. You’re satisfied there are no missing fragments of tooth so document there is no need for an x-ray to hunt down any dental foreign bodies.
Dental fractures can be classified as enamel; enamel-dentin and enamel-dentin-pulp fractures. The root can also fracture as can the alveolar bone socket.
Enamel fractures just require the smoothing and sanding down of sharp edges.
Enamel-dentin fractures should be sealed if possible and should be followed up in 3-4 weeks.
Enamel-dentin-pulp fractures are the most serious of the three. If the pulp cavity is not capped off with something like calcium hydroxide paste then apical periodontitis and failure of root maturation may occur. The alternative is just to remove the tooth and be done with it – not a viable option in the case of permanent teeth. There is no evidence that prophylactic antibiotics need to be given in these dental fractures.
Management of deciduous tooth and permanent tooth fractures varies slightly (it’s all to do with whether the tooth fairy is ready for this bit of tooth or not).
Fractured deciduous teeth: the fragment is unsuitable for replacement (the tooth fairy *may* decide it’s worthy of a coin so wrap it in a tissue and give it back to the child). Tell the carer to take their child for dental review so the portion of tooth that remains in situ can be sealed.
Fractured permanent teeth: the broken fragment may be bonded to the tooth if available – this one’s not for the tooth fairy just yet. Store the tooth in milk or saline and advise the child attends a dentist as soon as possible.
Root fractures: Look for bleeding from the gingival sulcus – this might be the only clue that root of the tooth is fractured. If the fragment is displaced, reposition it, bind it with a temporary splint in the ED as soon as possible, and refer to the dentist as soon as possible for assessment for formal splinting.
Alveolar fractures: Alveolar fractures are fractures of the bony socket. They may extend into the mandible – a segment or multiple teeth may be mobile and there may be problems with jaw occlusion. Both will require urgent dental intervention for splinting. Any displaced segment should be repositioned as soon as possible. Discuss with the on-call dental or maxillo-facial team as this is likely to require general anaesthetic.
Extrusions: the tooth is almost pulled from the socket so appears longer and is very wobbly. Management of these again depends on whether the tooth is deciduous or permanent.
Extruded deciduous teeth: treatment depends on the age of the child and severity of the injury. If the extrusion is minor (less than 3mm), it can be repositioned and temporarily splinted in ED. But if it is a major extrusion (more than 3mm), a fully formed deciduous tooth can be extracted with some local anaesthetic and piece of dry gauze or needle holder if the child is able to tolerate this. This tooth will then be ready for the tooth fairy.
Extruded permanent teeth: reposition the tooth if it is obviously elongated, place a temporary splint and advise dental review for permanent splinting. Don’t pull it out.
Intrusions: the tooth is impacted into the alveolar bone.
Intruded deciduous teeth: because the growing maxilla/mandible is relatively demineralised compared to that of an adult, when a toddler falls flat on their face they are more likely to push the tooth into the soft bone (intrusive luxation) than to fracture the jaw. Management of the intruded tooth depends on the direction and degree of intrusion as well as the presence or absence of an underlying alveolar fracture. Because the intruded teeth – most commonly the incisors – follow the line of the roots. i.e. in a labial direction – they are pushed away from the waiting secondary dentition. A watchful waiting approach, in a case series by Altun et al. found that 78% re-erupted, 15% partially erupted and only 7% remained impacted. The majority re-erupted within 6 months. If they intrude towards the underlying. No formal treatment is needed in the ED but the child should be seen urgently by a dentist because, if the tooth intrudes towards the underlying permanent teeth then they should be removed to avoid permanent disfigurement.
Intruded permanent teeth: no formal treatment is needed in the ED but dental follow-up within 24 hours is advised for repositioning and splinting, to assess for fractures and assessment of pulp necrosis.
Lateral luxations: the tooth is angulated sideways.
Reposition digitally if possible and place a temporary splint. The tooth can sometimes be lodged in a bony lock and as such will need forceps repositioning – one for our dental colleagues. If there is occlusal interference, whereby the displaced tooth impacts on the child’s ability to chew, discuss to on-call dental or maxillo-facial colleagues.
Parents may not be aware of the inciting trauma but become concerned when they notice a grey discolouration of the tooth. There may be underlying pulp necrosis but this may be asymptomatic. As the damage is only cosmetic no real treatment is needed, other than regular follow up to ensure that osteitis is detected early.
Avulsed deciduous teeth: avulsed deciduous teeth are not to be re-implanted. Doing so can cause damage to the development and eruption of permanent teeth. Determine the location of the avulsed tooth (particularly that it has not been aspirated), check for other injuries, and refer to a dentist for follow up. Check the child’s tetanus status. And don’t forget to give the tooth back to the child for the tooth fairy.
Avulsed permanent teeth: avulsion of a permanent tooth is a dental emergency and requires prompt action. Successful re-implantation is the goal and as such the tooth should be digitally reimplanted as soon as possible. Do not grasp the tooth by the root as this will disrupt periodontal cells, rather hold by the crown and irrigate with either milk or saline (a cannula attached to a syringe is a useful tool for this endeavour). Ensure the socket is clean of debris – irrigate the socket with saline to remove any blood clots (this allows revascularisation of the reimplanted tooth). Reposition the tooth by using adjacent dentition as a guide and hold in place by advising the patient to bite down gently on a soft medium such as handkerchief or rolled up gauze. Splint the tooth in place.
The ‘dry time’ of the tooth – the time outside of the socket – and the appropriate medium is one of the key indicators for successful re-implantation. The periodontal cells are no longer viable after 60 minutes so teeth that have not been reimplanted within an hour of avulsion are likely to fail.9 If a tooth cannot be immediately re-implanted, then it should be stored in either milk or normal saline. Storage in the mouth such as in the cheek or under the tongue is possible, however in a paediatric population the risk of swallowing is high, so a liquid external medium is preferable.
Reimplanting avulsed permanent teeth is one of the times antibiotics should be prescribed. Make sure you’ve checked the child is up to date with their tetanus vaccination; if they’re not, vaccinate in ED.
A temporary splint to secure a tooth until the child can get to a dentist can be made in the ED with skin glue and either steri-strips or the foil from a suture pack. But remember, don’t reimplant an avulsed deciduous tooth as you may damage the developing permanent tooth. Save this tooth for the tooth fairy! Only reimplant and splint avulsed permanent teeth or fragments of teeth that may be suitable for permanent splinting.
Image from: Academic Life in Emergency Medicine
All patients will need to see a dentist for definitive management and follow up, with the degree of urgency depending on the nature of injury. If in doubt do not hesitate to contact on-call services out of hours, particularly for avulsions. Patients should be advised to avoid contact sports or other high impact activities, only eat a soft diet, brush with a soft toothbrush and use a chlorhexidine (0.1%) mouth rinse twice daily for a week.
After giving Evie a sticker for being so brave, you solemnly wrap the fragment of her tooth in gauze and hand it to her. You tell Evie’s mum that as the fractured tooth is a deciduous tooth, and the fracture luckily doesn’t extend into the root, the fragment isn’t suitable for reimplantation. The tooth will need formal sealing though so you advise her to see her dentist as soon as possible. She phones and gets an appointment for later that afternoon. You advise her to keep Evie away from the toffees. That night, after receiving her second sticker from dentist, Evie carefully places the wrapped piece of tooth under her pillow. The following morning she’s delighted to find she’s had her first visit from the tooth fairy, who has left a shining Euro coin and a little note in beautiful, but tiny calligraphy that simply says, “Thank you”.
Andy Tagg has explored this issue before as it’s an incredibly important one for any clinician working with children to have insight into. As Andy says,
“The Tooth Fairy is not just an awful film starring Dwayne ‘The Rock” Johnson (it scored a grand 18% on Rotten Tomatoes) but a tall tale that has only been around for about 90 years. Before she (?he) flitted into our children’s bedrooms slipping shiny coins and more under pillows, parents told stories of La Petite Souris (in France) or Ratóncito Pérez (in Spain). This creature would sneak in like a rodent Indiana Jones swiping his shiny enamel treasure and replacing with a slightly weightier monetary equivalent.”
Andy ran a Twitter poll in 2017 to find out just how much La Petite Souris would have to leave behind. For children in Australia the almost unanimous vote came out in favour of a shiny two dollar coin (unless it was a first tooth then some recommended five dollars). For our international readers, at the time of first print, that worked out as £1.19 or US$1.52.
Altun C et al. Traumatic intrusion of primary teeth and its effects on the permanent successors: a clinical follow-up study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2009; 107(4): 493-8
Andersson L et al. International Association of Dental Traumatology guidelines for the management of traumatic dental injuries: 2. Avulsion of permanent teeth. Dent Traumato 2012; 28: 88-96
Andersson, L. Epidemiology of Traumatic Dental Injuries. Pediatric Dentistry, Volume 35, Number 2, March/April 2013, pp. 102-105(4)
Boffano P, Roccia F, Gallesio C, Karagozoglu K, Forouzanfar T. Inferior alveolar nerve injuries associated with mandibular fractures at risk: a two-center retrospective study. Craniomaxillofac Trauma Reconstr. 2014;7(4):280–283. doi:10.1055/s-0034-1375169
Brajdić D, Virag M, Uglešić V, Aljinović-Ratković N, Zajc I, Macan D. Evaluation of sensitivity of teeth after mandibular fractures. Int J Oral Maxillofac Surg. 2011;40(3):266–270
Colak I, Markovic D, Petrovic B, Peric T, Milenkovic A. A Retrospective Study of Intrusive Injuries in Primary Dentition. Dent Traumatol 2009;25: 605-10
DiAngelis A et al. International Association of Dental Traumatology guidelines for the management of traumatic dental injuries: 1. Fractures and luxations of permanent teeth. Dent Traumatol 2012; 28:2-12
Glendor U. Epidemiology of traumatic dental injuries – a 12 year review of the literature. Dent Traumatol 2008;24: 603–11.
Holan G, Ram D. Sequelae and prognosis of intruded primary incisors: a retrospective study. Pediatr Dent 1999;21:242–7.
Malmgren B et al. International Association of Dental Traumatology guidelines for the management of traumatic dental injuries: 3. Injuries in the primary dentition. Dent Traumatol 2012; 28: 174-182
Hermione is a 15-day old baby girl brought in for prolonged jaundice. She is breastfed and has no other risk factors. Her examination is normal other than being a bit on the yellow side. You ask the nurse to perform a blood gas to check her bilirubin, which is below 200. You notice the lactate on the gas is 4, but the nurse reports it was a “squeezed sample” which she suggests could explain the result?
This week sees the publication of a new paper in Pediatrics by the team at the Children’s Hospital of Pittsburgh and the University of Pittsburgh.
In 2016, the American Academy of Pediatrics published a guideline which renamed and redefined ALTEs (acute life-threatening event). The new term was BRUE (brief resolved unexplained event).
ALTE was initially coined in 1986 and the definition was:
an episode that is frightening to the observer and that is characterised by some combination of apnoea (central or occasionally obstructive), colour change…marked change in muscle tone (usually marked limpness), choking, or gagging. In some cases, the observer fears that the infant has died.
This was a broad definition and caused some difficulties for those of us assessing babies in hospitals. Although an ALTE could indicate a serious underlying problem – NAI, infection, seizure – commonly the infant was completely well. ALTEs by definition were subjective and this made the management of them tricky. Often these babies had overnight admissions to hospital for observation.
The new definition for BRUE is:
A BRUE has occurred if the observer reports a sudden, brief, and now resolved, unexplained episode of ≥1 of the following:
As well as the new definition, the guideline also stratifies patients and recommends management for those in the low-risk group.
Read our DFTB summary of the change in guidance here.
It has now been three years since the change from ALTE to BRUE. The aim of this study was to see whether the new guidance has affected rates of admission, investigations, or outcomes.
The objectives of the study were cleared stated and relevant to paediatric emergency medicine.
Patients were taken from the Pediatric Health Information System, which is a database with all information from presentations and admissions in hospitals across 26 states in the USA.
Patients were included if they were under 1 year old and had a diagnosis coded of either ALTE or BRUE between 2015 and 2017.
Exclusions were if patients had been transferred from another hospital, or had ambulatory surgery.
A control cohort was also used from all ED presentations of children under one year old during the inclusion period with no diagnosis of ALTE and BRUE (same exclusion criteria). The aim of the cohort group was to check whether there were any confounding trends in admissions/investigations during that time period.
This was an appropriate choice of patient group and the use of control cohort was beneficial. Sample size estimates were not stated explicitly but were alluded to.
The limitation here is the reliance on coding. However, additionally the authors were unable to determine if the diagnosis was correct, or if the patient could be classified as a low-risk BRUE as these assessments require a history and examination.
9,501 patients were used for the cohort analysis (5508 patients 0-60 days old, and 3993 who were 60 days to 1 year old). This group was split into a 2015 cohort (i.e. before the new guidelines) and a 2017 cohort (after the introduction of the new guidelines)
A second analysis was an interrupted time series analysis to look at trends in admissions over time. 13,977 patients were included in this group.
1.4 million patients were in the control cohort.
The cohort analysis looked at the rate of admissions as the primary outcome. Secondary outcomes included revisits and investigations performed. A comparison was also conducted by using the control cohort.
The interrupted time series analysis looked at whether admission rates changed over time following the introduction of the guideline. Admission rates were analysed in one-week batches throughout the three year time period.
The subjects were all accounted for and appropriate outcomes were considered.
Admissions: the proportion of admissions in the 61-365 day old group was 86.2% in the 2015 cohort and 68.2% in the 2017 cohort. The admissions were also significantly lower in the 0-60 days group – 89.9% in the 2015 group and 84.1% in the 2017 group.
Investigations: the 2017 group had significantly lower rates of EEG, MRI, CXR, FBC, U+Es, LFT, and urinalysis. Those in the 0-60 day old group (2017) had significantly lower rates of blood gas measurement, blood sugar testing, head CT, metabolic studies, and lumbar puncture.
Revisits: in the 0-60 day old group, revisits within 3 days were significantly lower in the 2017 group (3.7%) than in the 2015 group (5.2%). The rest of the revisit rates were similar.
Analysis of the control cohort here suggested that the decreased rates of these outcomes were independent of other trends over time.
Interrupted time series analysis: in the 0-60 day old group the introduction of the guideline did not affect trends in admissions rates. However, in the 61-365 day old group, the admission rates decreased each week after the guideline was published.
The authors were clear on what was measured and how it was measured. Follow up was for a 30 day period so should have picked up most complications. The measurements were reliable, valid, and the basic data was adequately described.
Between 2015 and 2017 there has been a significant reduction in the rates of admission and investigations for patients with ALTE/BRUE. This rate decreased steadily following the guideline publication.
The authors note that this reduction is seen in the 0-60 day old group, even though that age group would be stratified as higher risk in the new guidelines. The fact that BRUE is a diagnosis of exclusion, whereas ALTE was all-encompassing may mean that this diagnosis is being applied to a smaller, safer group over time, which might explain the findings. There were less patients diagnosed with ALTE/BRUE in 2017 compared to 2015.
The results are discussed in relation to existing knowledge and the discussion seems balanced and not biased. The conclusions are justified by the data.
Changing practice is challenging, changing a definition is a little easier.
This study is a great example of how to review the impact of guideline change and determine whether the outcomes have improved for patients without unintended consequences. At face value the BRUE approach has had beneficial clinical impact. We see an overall decline in admission and investigations with no obvious harm (returns don’t increase).
There are a few caveats that are important to consider though. This study was from a chain of hospitals likely working with similar cultures and convergent working practices. A random selection of children’s hospitals may have interpreted the AAP guideline with a greater degree of variance (and therefore application). With this in mind the relevance of quite a profound change in coding should be highlighted. In a similar timescale 25% of patients with a prior diagnosis of ALTE are no longer coded as such and it appears that these patients are not replaced with a BRUE code (as there was a 25% reduction overall in either code). This means that either the guidance has been successful in making staff think hard about about the underlying reason for the infant’s presentation or that perhaps initial coding was not as precise as it could have been (“I’m not sure what happening here so I’ll just call it an ALTE“). Of note the return rate isn’t supplied for those not coded as BRUE or ALTE so we don’t know if the cohort of patients now coded as something else have actually come to increased harm. It is also interesting to note the significant fall in admissions for those less than 60 days old. This wasn’t the intention of the initial guidance and while this group’s re-admission rates didn’t increase this study wasn’t powered (or designed) to look at whether the re-admission changes would be significant or not. The fact that it appears safer is a statistical construct, not a clinical one. This means a type II error is possible (there is actually a problem but we aren’t seeing it).
Ultimately, while these risks are real, and do need investigation in future study, it is likely that altering to using BRUE will effectively rationalize your investigation and management pathways without causing additional harm. The challenge for those outside the United States is whether national organizations are happy to formally endorse the BRUE concept as staff may feel uncomfortable applying new rules without official sanction. Locally certainly, we use the BRUE criteria in our risk assessment and this study only further endorses that approach.
This is a really wonderful summary and analysis of the study. The findings do suggest that patients in the low risk cohort identified by the AAP BRUE guidelines are being discharged safely without an increase in return visits. It is important to note that this narrower definition of BRUE has not excluded all high acuity conditions, as patients with high acuity co-diagnoses were identified in both age groups after the practice guideline publication.
Overall, I think our findings support continued clinical application of the BRUE definition and guidelines. While not within the scope of our study, the results did make us wonder about the impact of guidelines published by a national medical organization. How much of the change we saw in a three-year period were due to influence by the AAP and how much was because the medical community was ready for a change in ALTE management? Finally, we hope that our findings are able to support further research into management of both low-risk and high-risk BRUE and into understanding what has changed in the management of infants who are now excluded from the BRUE diagnosis.
Katie Noorbakhsh (author)
Here’s a printable A4 summary of the paper & our thoughts:
Okay, perhaps not perfect but we think these bite sized chunks of simulation from Children’s Health Queensland are pretty good! They are free to download and play with. You can find access to all current OPTIMUS resources here. Enjoy!
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Case, Nicky, “How to remember anything forever-ish.: Oct 2018. Available at: https://ncase.me/remember/ Cheng et al, “Resuscitation Education Science: Educational Strategies to Improve Outcomes from Cardiac Arrest; A Scientific Statement from the American Heart Association.”Circulation 2018; 138: e82-e122. Available at: https://www.ahajournals.org/doi/10.1161/CIR.0000000000000583 Cheng et al, “Highlights from the 2018 AHA Statement on Resuscitation.” June 2018. Available at: https://canadiem.org/aha-scientific-statement-on-resuscitation-education/ Dubner S.“Freakonomics Radio. How to become great at just about anything (Ep 244).” Apr 2016. Available at: https://freakonomics.com/podcast/peak/ Ericsson A,“Peak” Vintage 2017.
Case, Nicky, “How to remember anything forever-ish.: Oct 2018. Available at: https://ncase.me/remember/
Cheng et al, “Resuscitation Education Science: Educational Strategies to Improve Outcomes from Cardiac Arrest; A Scientific Statement from the American Heart Association.”Circulation 2018; 138: e82-e122. Available at: https://www.ahajournals.org/doi/10.1161/CIR.0000000000000583
Cheng et al, “Highlights from the 2018 AHA Statement on Resuscitation.” June 2018. Available at: https://canadiem.org/aha-scientific-statement-on-resuscitation-education/
Dubner S.“Freakonomics Radio. How to become great at just about anything (Ep 244).” Apr 2016. Available at: https://freakonomics.com/podcast/peak/
Ericsson A,“Peak” Vintage 2017.
A 10 year old boy presents to your emergency department following a high speed MVA – car vs tree. He was seated in the rear middle seat. On arrival he is noted to have significant bruising across his lower abdomen from the seat belt but otherwise appears well.
Otis is a 3yr old boy presenting to the emergency department with fever, and purulent discharge from his left ear. He otherwise looks well, however, his mother mentions this is his third ear infection since he was born, and he always seems to have a cough and a cold. She asks you if there could be a problem with his immune system?
Some children seem to have constant ear, nose or throat infections during childhood. We know that for a small, but important minority of children this may be the presenting feature of a primary immunodeficiency. Let’s look at how these may present, when to think of it, and what to do about it.
It’s worth stating from the outset, that the majority of children with recurrent ENT infections will not have a primary immunodeficiency. There is a relatively common phenomenon called “physiological immunodeficiency of infancy”, where-by there is a natural nadir in immunoglobulin levels as maternal immunoglobulin fades, and the child’s own immune system has only just become able to produce immunoglobulin for itself. This is at its lowest between 3-6 months and normally resolves by age 1. However, fully developed protection against encapsulated organisms doesn’t reach maturity until between 2-5 years, and IgA production doesn’t reach adult levels until adolescence. It can be completely normal for young children to suffer 4-11 respiratory infections a year (depending on exposure, e.g. siblings, nursery, etc.)
When considering the characteristics of infections that should trigger suspicion for immunodeficiency, we should be thinking about:
Combined immunodeficiency disorders (affecting both cellular and humoral immunity), such as severe combined immunodeficiency (SCID), present in the first 3-6 months with severe, life-threatening infection. Unusually aggressive infections should prompt further investigation
Infections with certain pathogens can point towards specific diagnoses, including respiratory infections with Pseudomonas aeruginosa (think cystic fibrosis or primary ciliary dyskinesia), oral/oesophageal candidiasis (think HIV or chronic granulomatous disease), upper respiratory infections with Pneumocystis carinii (think HIV or other T cell deficiencies) or recurrent otitis/sinusitis with Neisseria meningitidis (think complement deficiency).
Finally, to a lesser extent:
This is the least predictive of immunodeficiency, given the discussion above. Very frequent sinopulmonary infections in younger children with encapsulated bacteria can be the presenting feature of the rare condition X-linked agammaglobulinaemia (XLA: boys who produce no immunoglobulins). In late childhood and adolescence, the same presentation in a milder form may be a sign of combined, variable immunodeficiency (CVID), which is a heterogeneous group of disorders of antibody production.
Other, rare conditions include chronic granulomatous disease (CGD) which may present with deep abscesses of the outer ear or mastoid, or HIV presenting with recurrent otitis media (normally with other associated features)
Some general guidelines have been produced by the Jeffrey Modell foundation for when to consider referral for immunodeficiency workup:
Although having a low specificity, they provide a useful framework when thinking of children with more severe infections than usual.
If considering referral, there are definitely some basic tests are useful to do first (if the child is severely unwell, don’t wait for tests to refer).
Full blood count
This is useful for ANY suspected immunodeficiency. Persistent lymphopaenia in a child <2yrs should prompt screening for SCID.
NB: It can be normal to have transient lymphopaenia or neutropaenia in isolation in young children following a viral illness. Incidental neutropaenia does not need repeat testing if there are no concerns about underlying immunodeficiency.
IgG, IgM and IgA levels are useful to investigate children with recurrent ENT/airway infections.
It is also worth considering an HIV test if symptoms are consistent, but ensure you have a discussion with parents before testing.
If both FBC and immunoglobulins are normal in the setting of recurrent infections, it is perfectly acceptable to wait for 3 -6 months to see if the condition improves before referral.
Further reading: https://www.entmasterclass.com/ENT_Journal_2019_Interactive.pdf page 9
We see lots of children with suspected infections. Modern microbiology techniques have opened up a huge array of tests: some new and expensive, but we are often still reliant on good old fashion microscopy and culture.
With so many tests so readily available, we need to think hard about diagnostic stewardship. This means testing the right patients for the right reasons. We must be wary of over-diagnosis, preventing confusion, anxiety or unnecessary treatment, and making choices that represent good value. Many tests can be expensive and are often not necessary to make management decisions.
With that in mind, let’s take a look at some of the most common diagnostic tests for infections, and when we should (or shouldn’t!) be deploying them.
Urinary tract infections (UTIs) are the most common serious bacterial infection in high-income countries. There are many departments where it is routine to set up every febrile child to get a “clean catch” urine as soon as they arrive. This is unwise, because it is VERY EASY to contaminate a urine sample from a clean catch. We have all seen children or parents putting their hands/feet/face in the bowl, and let’s be honest – if the child is sitting on the container, it’s basically directly under the body’s primary waste pipe.
Accepting a decent risk of false positives, we must aim to test only those who need the test. So when should we do it?
This is the primary indication for doing a urine dip, and it is a sensible one. However, still not every child with fever and no source needs a urine dip. Older children can report urinary symptoms, and the absence of these makes a UTI much less likely. In addition, by school age, UTIs in males with normal renal tracts become very rare, so urine testing also becomes less useful.
As a framework, urine dips should be performed in the following groups with fever and no source (assuming they have no risk factors for UTIs and have no red flags):
Outside of these groups, use your clinical discretion to decide if the pre-test probability justifies the risk of a false positive – take into consideration the child’s age, gender, duration of symptoms, how unwell they appear, and obviously if they have known risk factors such as renal abnormalities or previous UTIs.
This seems obvious – but it’s worth stating that once urinary symptoms are present (increased frequency, dysuria) you should dip the urine to check for infection, and it may be worth sending samples for MC&S even if they are dip negative in this scenario (you can withhold treatment pending results).
It is worth taking more care for children with non-urinary symptoms, such as abdominal pain or vomiting (which is probably not predictive of UTI). Once at school age (particularly in boys) these symptoms are unlikely to be a symptom of a UTI so a higher threshold for testing should be adopted.
Some people say that all children with rigors require urine testing. Rigors are not evidenced to have any influence on the risk of UTI (or any significant risk of bacterial infection). If there is another source of the fever, urine dip is certainly not indicated on the basis of a rigor alone.
This becomes a slightly more controversial topic, and decisions require risk stratification based on the age of the child. For example, a febrile neonate with bronchiolitis might be lucky to escape the full shebang of a septic screen anyway – and a quick in/out catheter is unlikely to yield a false positive.
The literature on this topic is a bit confusing because of varying definitions of UTI and bronchiolitis (some studies including any child with RSV detected in their nose). The most recent meta-analysis with more stringent criteria for diagnosing UTI found a rate of concomitant UTI with bronchiolitis of 0.8% – low enough that testing is not advised.
Bottom line: if an infant has a fever and a clinical diagnosis of bronchiolitis, then urine dip is not necessary in most instances – however this should be given strong consideration in infants <60d and should be performed in neonates.
For a full myth busting exercise in blood cultures, please read the recent DFTB post on this topic. Some things to bear in mind if you’re thinking of taking a blood culture:
When it comes to swabbing for microscopy, culture and sensitivity (MC&S), there is a golden rule*:
Do not swab any non-sterile site that you have not already clinically diagnosed as being infected.
A skin swab, throat swab, eye swab etc. will grow bacteria 100% of the time, because these places are non-sterile. They will often grow pathogens, because many pathogens are quite happy just being colonisers a lot of the time, and actually some of them are more often found as bystanders than as trouble-makers (Pseudomonas aeruginosa is a prime example – it is very rarely pathogenic in non-sterile sites). A positive swab does not diagnose infection.
YOU have to diagnose infection; a swab will just tell you what bacteria is causing it.
I would like to give a special shout out to gastrostomies at this point – just because they are “mucky” is not a good reason to swab. If you do swab it, you will find good old Pseudomonas (it loves playing in wet stuff). Skin and soft tissue infections are red, hot and inflamed +/- a bit of pus. Yellowish clearish greenish stuff is normally just serous fluid, so don’t worry about it and don’t swab it!
The same goes for babies sticky eyes. If you swab it, it will grow bacteria, but this tells you nothing about whether they are infected. Look for inflammation, if you find it then diagnose infection, treat empirically and send a swab if you are concerned about resistant bacteria.
*there are some exceptions to the golden rule, including burns and chronic wounds in immunosuppressed patients.
Before starting – let’s remember that you cannot diagnose a bacterial throat infection with a swab alone. If you are considering swabbing a throat for MC&S, you must have already clinically diagnosed infection.
Guidelines vary quite widely in their recommendations to swab or not swab when diagnosing tonsillitis. It is worth considering that a throat swab has a reasonable sensitivity for group A Strep, if performed correctly. Sadly – we are all dreadful at performing throat swabs in children (who are usually very good at not wanting a throat swab), and often get a good dose of tongue and palate. Not good.
A further thing to consider is that approximately half of all throat swabs positive for group A Strep just indicate carriage – you’ve found the bug, but it’s just a bystander.
This means that if you swab and haven’t found the bacteria, it might be there but you’ve missed it, and if you have found it, there’s a 50% chance it’s not causing the illness anyway…
If it’s extremely important you detect the presence of group A Strep (for example in populations high risk for rheumatic fever) then I would definitely do a swab. If it’s not (and it usually is not), then make your decision to treat or not on clinical grounds alone.
Also, remember that in children <4yrs group A Strep tonsillitis is rare and almost never causes complications, so if you’re thinking of doing a throat swab for a child in this age group you need to have a very good reason.
Respiratory tract infections are extremely common in children. There is a fair amount of controversy and disagreement about the role for respiratory virus testing. It can have several roles:
A group of children you should not test for respiratory viruses is anyone with cough and coryza. They do not need a test – they can be safely diagnosed clinically, and the presence or absence of a virus on testing does not change anything.
What about in lower respiratory tract infections? We can imagine that the discovery of a virus would prevent unnecessary antibiotics. However, respiratory viruses are common (even among non-hospitalised populations) and co-infection with bacteria is also common in viral infections. The presence of a virus does not preclude a bacterial infection. As such, their use in this context is contentious, and they do not appear to reduce antibiotic use.
For a thorough look at the principles and evidence of respiratory virus testing in children, I would recommend this excellent review paper.