The child with a limp

Cite this article as:
Andrew Tagg. The child with a limp, Don't Forget the Bubbles, 2020. Available at:

This post is based on the talk Andrew Tagg was invited to give at BadEMFest20 in Capetown. Unfortunately, world events made that a little challenging.

Humans evolved from Homo erectus to Homo sapiens around 500,000 years ago. Fossils dug up from by the Leakeys in Olduvai Gorge, Tanzania, revealed how we moved from shuffling knucklewalkers to the upright hominids we recognize today. Walking on two legs allowed us the freedom to use our hands – to communicate, to use tools, and to keep ourselves safe.


How do we walk?

The normal human gait is comprised of three distinct phases:

  • The contact phase – from heel strike to flat foot
  • The stance phase – from flat foot to heel off the ground
  • The swing phase – the propulsion phase as weight transfers from the toes

The swing phase normally comprises 40% of the gait cycle.



Like Sherlock Holmes or his progenitor, Joseph Bell, if you watch your patient walk you can get a lot of clues as to the potential underlying pathology before you even exchange a word with them or their parents.

Antalgic gait

This hobbling gait has a normal contact phase and normal propulsion with a decreased stance phase. In essence, the patient is trying to decrease the amount of time spent bearing weight through the hip joint itself.

Trendelenburg gait

In this gait disturbance, the hip muscles are too weak and so the unaffected side drops towards the floor. It suggests a biomechanical issue such as ass avascular necrosis, or a slipped capital femoral epiphysis.

Circumduction gait

The patient swings their leg out and around to clear the floor. This is often due to a leg-length discrepancy in the delayed diagnosis of developmental dysplasia of the hip (DDH).

Equinus gait

Toe walking, though normal up to the age of three may suggest that the child is unwilling or uncomfortable engaging their gastrocnemius muscles in walking. This can occur in many conditions.


The rate of presentation to the emergency department with an atraumatic limp is approximately 1.4 per 1000 in children under the age of 14. It occurs more often in boys than in girls (1.7:1) and the median age is 4.4 years. When we consider the potential causes the list is massive. In this post, we are going to concentrate on both the more common conditions and those diagnoses that we really shouldn’t miss. Whilst any part of the limb might be the cause (from the toes to the hip) this post is going to focus on causes centred around the hip joint. They account for about 60% of cases of limp. That doesn’t mean you shouldn’t look in their shoes for pebbles or look at their toes though!

Let’s break it down to some age-specific diagnoses and those that can occur at any age

Late presentation of developmental dysplasia of the hip (DDH)

It is just possible that routine screening with Ortolani’s and Barlows test might have missed a case of hip dysplasia. The limb resultant limb shortening can be hard to detect if it is bilateral but this is one time to get out the tape measure and look for a leg length discrepancy as you measure from anterior superior iliac spine (ASIS) to medial malleolus.

If you don’t have a tape measure to hand then look for a positive Galeazzi sign, suggesting a shorter hip segment on the affected side.

Original by Walt Shumway


Transient synovitis

This diagnosis accounts for the majority of cases of atraumatic limp and may follow an upper respiratory tract infection though the evidence for causation is poor. It is most common in young boys, aged 4 to 8 years of age and is self-limiting in nature. It’s a diagnosis of exclusion rather than anything else made easier by the well-appearing, afebrile child. It should respond to simple NSAIDs though is recurrent in 20% of cases.

Dr. Sathya Subramaniam, Pediatric EM Fellow – Kings County/SUNY Downstate and The POCUS Atlas

According to Viera and Levy, bedside sonography has a sensitivity of 90% and specificity of 100% to detect an effusion. Unfortunately, it doesn’t help with determining the cause.

Occult trauma

It’s beyond the scope of this post to talk about NAI and long bone injuries in children (especially as Nikki Abela did such a great job at DFTB18) so instead, it’s worth thinking about toddlers’ fractures. These occur due to torsional force on the tibia, accompanied by a fall, and may only be picked up as tenderness over the distal third of the tibia. That first set of x-rays performed in the emergency room may not show any obvious pathology with signs only becoming obvious after a couple of weeks. This is one of those occasions where ultrasound may be much more helpful though if clinical suspicion remains it should be treated with immobilization and close follow-up. Repeat imaging may then show the beginnings of some callus formation or a radionuclide bone scan may be needed. If they are not toddling and waddling it is not going to be a toddler’s fracture.


Case courtesy of Dr. Jeremy Jones, From the case rID: 9317


Although unlikely to present as an isolated limp, cerebrovascular events may present as hemiparesis; It’s beyond the scope of this post to go into them in more detail. Watch this space.


Perthes disease

This is idiopathic avascular necrosis of the growing femoral head and typically presents in boys at the younger end of the scale (4 to 8 years old). Because of this, these children are often shorter than their peers and there is a possible association with hyperactivity. The classical findings on a plain AP x-ray of the pelvis include sclerosis leading to destruction and the eventual collapse and flattening of the femoral head.  As this is a biomechanical problem, they might present with a slow onset antalgic gait with pain on internal rotation and ABduction. Around 20% of cases are bilateral.

Case courtesy of Assoc Prof Frank Gaillard, From the case rID: 7980


Both MRI and bone scan are equally sensitive if the plain films are equivocal. Treatment may be surgical or conservative depending on the degree of bone destruction and the age of the child. Left unchecked neovascularization occurs with the destruction of the femoral head.

Though first described in 1897, it was not until 1910 that it was found to be unrelated to tuberculosis. Arthur Legg, Jacques Calvé and Georg Perthes are guilty of its eponymous name.

Transient synovitis

I think we’ve said enough about transient synovitis already.


As well as a stroke a limp might be the initial feature of an ascending paralysis in Guillain-Barré. We’ll talk about that and ADEM another time.


Slipped Capital Femoral Epiphysis

A slipped capital femoral epiphysis or slipped upper femoral epiphysis is more common on older, overweight boys, over the age of 10 years of age. There is often a structural weakness of the physis itself so it is more common in cases of endocrine dysregulation (such as hypothyroidism) and metabolic conditions (such as renal osteodystrophy). The proximal epiphysis displaces anteriorly and laterally relative the metaphysis. Involvement of the medial obturator nerve may mean that they present as knee pain rather than hip pain. Early fixation and we mean in less than 24 hours in unstable cases, can ward off the threat of life-long pain and deformity. Plain AP films may not be enough in the case of subtle slippage. So if you are suspicious then you should go ahead and order a lateral film as well.  A lot of other hip pathology is made easier to spot in a frog-leg lateral. Don’t do this if you are suspicious of a SCFE, you might make things much, much worse.

Look for Klein’s line. A line along the superior aspect of the femoral neck should intercept with the epiphysis. Imagine it as an ice cream slipping off the cone on a hot summer day.

Adapted from case courtesy of Assoc Prof Frank Gaillard, From the case rID: 2715

Case courtesy of Dr. Hani Salam, From the case rID: 9298



Some things need to be in our differential no matter the age of the child.

Septic arthritis

The hip is the most commonly infected joint with the haemategenous spread of organisms grown dependent on the local flora. Young children (under the age of 2), those who are immunosuppressed or asplenic are at higher risk. In Australia, for instance, the commonest organisms grown are Staphylococcus aureus and Group B Streptococcus (especially now that Haemophilus influenzae b infections have been almost wiped out by immunization). In the youngest, patients consider the weirder organisms like Kingella kingae and Salmonella (in patients with sickle cell disease).

The juvenile physis does not prevent the spread from a remote source from entering the epiphysis and so haematogenous spread (rather than direct local invasion) is often the culprit. The hip is classically held in a position of external rotation, ABduction and, flexion, perhaps in an effort to maximize the joint space and minimize the pain.

It would be great if there was a way we could differentiate the serious diagnosis of septic arthritis from something less serious, such as transient synovitis. Step forward Meninder Kocher et al. and their seminal paper.

Kocher MS, Zurakowski D, Kasser JR. Differentiating between septic arthritis and transient synovitis of the hip in children: an evidence-based clinical prediction algorithm. JBJS. 1999 Dec 1;81(12):1662-70.

They looked at 17 years of data for patients that presented to a single tertiary hospital with an acutely irritable hip. This amounted to 282 cases in all of which only 168 had their hip joint aspirated.  Of this 168,  only 26 had true septic arthritis as confirmed by a positive culture of joint aspirate or 50,000 WCC in the aspirate with a positive culture, 9 had a positive joint culture and negative blood cultures and 3 had only positive blood cultures.  By performing a multivariate analysis they then looked for key indicators that differentiated cases of septic arthritis from the more benign irritable hip. Four key factors cropped up. They were a history of fever, inability to bear weight, a WBC greater than 12 x 109/l and an ESR ≥ 40mm/hr. If you had none of these then the probability of having septic arthritis is 0.1%. But if you have all four it jumps to 99.8%.

Of course, this is all the primary literature that most people read but when Kocher tried to validate the study having all four markers gave the chance of having septic arthritis as 93% and when Luhmann et al. tried to externally validate the criteria it dropped to 59%. Caird et al. must have realized that not many of us use ESR any more and so appended the more common C-reactive protein (CRP). Having all 5 gave a 97.5% positive predictive value though there were only 14 cases of transient synovitis, and 5 of septic arthritis.




An indolent course and a non-specific physical examination make this a difficult diagnosis to pick up at first glance. Around 1.5-2% of all children presenting with an atraumatic limp will have osteomyelitis.  Plain films may be unremarkable early in the course of the illness and only show periosteal changes after a week to 10 days. An MRI scan is more sensitive and if the diagnosis is still a challenge then radionuclide scanning might pinpoint the infection. The hip is one of the more common joints affected (25%) followed by the tibia/fibula (25%) then the humerus (13%). Osteomyelitis and septic arthritis can coexist as infection from the bone spreads to the joint capsule.


One case series suggests that 40% of cases are due to transient synovitis, chronic muscle sprain or trauma accounted for 16% and no diagnosis was made in 30%. All those diagnoses we have to learn for exams are much less common (Perthes’ disease 2%, osteomyelitis 1.5%, toddlers’ fractures 1%, and SCFE 1%). What has not been mentioned, as the incidence is incredibly low is the thing that many parents worry about – cancer.



Whilst parents may not have heard of a slipped capital femoral epiphysis or Kocher’s criteria but they have heard of cancer and so we need to address it. Primary benign tumours (unicameral bone cysts, for example, as well as malignant ones can present as bony hip pain.  Hip pain can also be a presenting feature in haematological malignancies such as acute lymphoblastic leukaemia. The most common malignant bone tumours in infants are osteogenic sarcoma and Ewing’s sarcoma. Both of these are most common in the second decade of life.

Persistent pain, coupled with constitutional symptoms such as night sweats, weight loss and night pain are highly suspicious and should prompt imaging and blood tests.




Selected references

Please, Just STOP LIMPING from Tim Horeczko and the PEM Playbook

Septic arthritis from PEM Morsels


Adamson J, Waterfield T. Fifteen-minute consultation: The limping child. Archives of Disease in Childhood-Education and Practice. 2019 Jun 29:edpract-2018.

Caird MS, Flynn JM, Leung YL, Millman JE, Joann GD, Dormans JP. Factors distinguishing septic arthritis from transient synovitis of the hip in children: a prospective study. JBJS. 2006 Jun 1;88(6):1251-7.

Fischer SU, Beattie TF. The limping child: epidemiology, assessment and outcome. The Journal of bone and joint surgery. British volume. 1999 Nov;81(6):1029-34.

Flynn JM, Widmann RF. The limping child: evaluation and diagnosis. JAAOS-Journal of the American Academy of Orthopaedic Surgeons. 2001 Mar 1;9(2):89-98.

Herman MJ, Martinek M. The limping child. Pediatrics in review. 2015 May;36(5):184-95.

Hill D, Whiteside J. Limp in children: Differentiating benign from dire causes. Journal of Family Practice. 2011 Apr 1;60(4):193.

Hussain M, Gholipour B, Owen N. A pictorial review of the radiological presentations of the child presenting with an acute limp in the emergency department. Clinical Radiology. 2019 Oct 1;74:e14.

Kocher MS et al. Differentiating between septic arthritis and transient synovitis of the hip in children: an evidence-based clinical prediction algorithm. J Bone Joint Surg Am. 1999 Dec;81(12):1662-70.

Leet AI, Skaggs DL. Evaluation of the acutely limping child. American Family Physician. 2000 Feb 15;61(4):1011-8.

Lewis D, Logan P. Sonographic diagnosis of toddler’s fracture in the emergency department. Journal of Clinical Ultrasound. 2006 May;34(4):190-4.

Long B, Koyfman A, Gottlieb M. Evaluation and Management of Septic Arthritis and its Mimics in the Emergency Department. Western Journal of Emergency Medicine. 2019 Mar;20(2):331.

McCarville MB. The child with bone pain: malignancies and mimickers. Cancer Imaging. 2009;9(Special issue A):S115.

Mooney III JF, Murphy RF. Septic arthritis of the pediatric hip: update on diagnosis and treatment. Current opinion in pediatrics. 2019 Feb 1;31(1):79-85.

Perry DC, Bruce C. Evaluating the child who presents with an acute limp. BMJ. 2010 Aug 20;341:c4250.

Ryan DD. Differentiating Transient Synovitis of the Hip from More Urgent Conditions. Pediatric annals. 2016 Jun 15;45(6):e209-13.

Sawyer JR, Kapoor M. The limping child: a systematic approach to diagnosis. American family physician. 2009 Feb 1;79(3):215.

Singhal R, Perry DC, Khan FN, Cohen D, Stevenson HL, James LA, Sampath JS, Bruce CE. The use of CRP within a clinical prediction algorithm for the differentiation of septic arthritis and transient synovitis in children. The Journal of bone and joint surgery. British volume. 2011 Nov;93(11):1556-61.

Vieira RL, Levy JA. Bedside ultrasonography to identify hip effusions in pediatric patients. Ann Emerg Med. 2010;55(3) :284-9

Wainwright, AM; Catterall, A (2010). “Chapter 27: Legg–Calvé–Perthes disease: Its name”. In Benson, M; Fixsen, J; MacNicol, M; Parsch, K (eds.). Children’s orthopaedics and fractures (3rd ed.). London: Springer. p. 465

Ankle sprains

Cite this article as:
Neil Thomspon. Ankle sprains, Don't Forget the Bubbles, 2020. Available at:

David, 11, intends to play football in the Premier League when he is older.  Before then, he must serve his time with the school team.  During training, he ships a heavy tackle and rolls over his ankle. He limps over to the sideline and calls for help. Taking no risks with his future star, the coach insists mum takes him to ED. You are waiting with your game face on.

Having seen one or two sore ankles before, you are aware of the Ottawa ankle rules, but what are they? And are they applicable in kids?


Ottawa ankle rules

The Ottawa ankle rules are an evidence-based decision tool to advise indication for x-ray in an ankle injury.

An ankle x-ray series is required if:

There is any pain in the malleolar zones and…

  • bony tenderness over the posterior aspect of distal 6cm of tibia (i.e. medial malleolus)


  • bony tenderness over the posterior aspect of distal 6cm of fibula (i.e lateral malleolus)


  • inability to weight bear (>4 steps) both immediately after the injury and in the ED


A foot x-ray series is required if:

There is any pain in the midfoot zone and…

  • bone tenderness at the base of the 5th metatarsal


  • bone tenderness at the navicular


  • inability to weight bear (>4 steps) both immediately after the injury and in the ED


Practice common sense – these rules are not applicable if your patient is: unable to give a reliable answer; has other distracting injuries; has diminished sensation in legs; is too swollen to establish bony tenderness; unable to walk prior to the injury.  Remember that a patient who walks with a limp is able to weight bear.

The rules were designed with adults in mind, however, they have been shown to be reliable in the assessment on children. They are sensitive but not specific for detecting fractures, therefore, they are most useful in ruling out fractures (and the need for imaging).  For every 1000 patients that exhibit negative Ottawa ankle rules, 14 will actually have fractures.


David does not meet the criteria for imaging.  He does have a swollen ankle with tenderness over the anterior aspect of his lateral malleolus.  You suspect an ankle sprain.


What is an ankle sprain?

A sprain occurs when you stretch or tear a ligament.

Symptoms include pain, swelling, bruising, tenderness, impaired function and joint instability (if severe).

Classification of a sprain:

  • Grade 1 is stretching of the ligament, minimal swelling or bruising, no joint instability
  • Grade 2 is a partial rupture of the ligament, moderate swelling or bruising, no joint instability
  • Grade 3 is total rupture of the ligament, severe swelling or bruising, with joint instability

There are three main sets of ligaments in the ankle

  • Lateral – Anterior Talo-Fibular Ligament (ATFL), Calcaneo-Fibular Ligament (CFL), Posterior Talo-Fibular Ligament (PTFL)
  • Medial – Deltoid ligament
  • Interosseous (tibiofibular) ligament

There are two tests for instability, which should be compared between the good and bad ankles:

  1. Anterior drawer test – stabilize the leg with one hand, use the other hand to cup the heel and draw the foot anteriorly. If there is excessive movement then the test is positive.
  2. Talar tilt test – stabilize the leg with one hand, use the other hand to cup the heel and rock the foot in an inversion movement. If there is excessive movement then the test is positive.


How should I manage an ankle sprain?

A simple PRICE approach, along with analgesia, is the first line of management:

Protection. For example, with a supportive boot.

Rest. Usually for 72 hours.

Ice. Cover ice in a tea-towel and apply to the ankle for 10-15minutes every 2-3 hours.

Compression. An elasticated bandage will help with swelling and provide some support (but should be removed at night).

Elevation. Elevate the ankle until the swelling goes down.

Early mobilization as tolerated will facilitate faster recovery, however more severe sprains may require a period of immobilization. (7-10 days).

Supervised physiotherapy has been shown to benefit in early follow-up but does not make a difference in the long term.

What is the prognosis?

The recovery period depends on the severity of the sprain. A grade 1 sprain may return to play in 1-2 weeks; whilst a more severe sprain may return to walking in 1-2 weeks, running in 6-8 weeks and return to regular sporting activity in 8-12 weeks.


David’s ankle was strapped up in a Tubigrip and he limped home, eager to get back on the pitch and continue his journey to stardom.

Procedural sedation

Cite this article as:
Tadgh Moriarty. Procedural sedation, Don't Forget the Bubbles, 2020. Available at:

Sometimes we have to do things that children don’t like. These procedures may be scary, or potentially painful. In this post, we’ll cover a few of the more common techniques.


Case one: Kayla

Earlier this month, the UK Royal College of Emergency Medicine, RCEM, published new guidance on the use of ketamine for procedural sedation in children in the emergency department, superseding their 2016 guidelines. Follow Kayla through her ED visit as she helps us explore the changes RCEM recommends.


It’s 3 pm on a busy Friday afternoon on your PEM shift. You have just seen Kayla, a 20-month-old girl who fell from onto a concrete step and sustained a nasty L-shaped laceration to her thigh. You have satisfied yourself that her joints are not involved, and an x-ray reveals no underlying fracture. You can see a large amount of debris within the wound. Her vaccines are up to date and she has no significant medical history. She is, however, eating a large ice cream cone that her parents had purchased to pacify her. You wonder how best to proceed as you have a nasty wound that needs thorough irrigation and closure. A toddler is unlikely to tolerate local anaesthetic infiltration as the primary means of anaesthetising the wound.


Does Kayla need procedural sedation?

Paediatric Procedural Sedation (PPS) aims to alleviate the distress around painful procedures but should not be viewed as a substitute for good pain relief. Maximize analgesia and recruit any distraction devices to hand (iPads / parents / play specialists – these are a particularly excellent resource and should be utilized wherever possible).

Is the wound suitable for ‘LAT gel’? This revolutionary gel which combines lignocaine, adrenaline and tetracaine can prevent many sedations when used correctly. It takes 30-60minutes to be fully effective after application so be sure to allow sufficient time. Even if the patient is progressing to procedural sedation this gel will help with local anaesthesia and analgesia.

The ability to perform PPS will be based on current acuity within the department, available resources, and appropriate staffing skill mix. The three main agents used for procedural sedation in paediatrics are midazolam, nitrous oxide, and ketamine.


Kayla’s LAT gel has been in situ for half an hour. You return to the cubicle armed with a play specialist and nurse, along with your irrigation and suturing materials. Despite a stellar sock puppet show by your play specialist, loud sing-along songs, and Peppa Pig showing on the iPad, your attempt at irrigation is futile; Kayla remains upset. You decide PPS is needed to ensure effective irrigation, neat wound closure, and avoiding further trauma to an upset child (and mother!)


Which agent is best suited?

You need to consider what you hope to achieve with sedation and what level of experience and resources are available currently in the department to aid in answering this question. The spectrum of use varies from diagnostic imaging, through minimally painful procedures (e.g. foreign body removal, vascular access), to painful procedures (e.g. fracture reduction, wound washout and closure). The choice of agent, therefore, will reflect the individual patient (anxiety, co-operative, parental preference), and the staff available at the time.


Kayla requires a short painful procedure to be carried out and nitrous oxide or ketamine would be suitable. As you start showing her the face mask for nitrous, Kayla freaks out – Kayla had a slightly traumatic experience with a bronchodilator and spacer, her mother explains. There’s no way you’re going to get Kayla to cooperate with the nitrous mask. So ketamine is selected as the agent of choice.

Just as you are about to begin the pre-procedure assessment one of the student nurses who will be observing the procedure tells you that she has seen a lot on Twitter about the new RCEM ketamine PPS guideline recently but is unclear as to exactly what ketamine is and why it’s useful in paediatrics.


Ketamine is an NMDA receptor antagonist. It is a dissociative anaesthetic and potent analgesic and amnesic. Rather than the typical ‘sleep‘ which results after administration of other anaesthetic agents, ketamine induces a trance-like state, oftentimes with the patient’s eyes open but ‘nobody home‘ (it is important to warn parents beforehand about this as it can be quite scary if unexpected). Some of the many benefits of ketamine are that airway reflexes are maintained, while is augmented heart rate and blood pressure (for the most part – in the compromised circulation bradycardia and hypotension can occur).


The pre-sedation assessment

You begin Kayla’s pre-sedation assessment. Your assessment includes a focussed history: has Kayla undergone any previous anaesthesia or PPS? If so, did she have any reactions or adverse events? Does she suffer from any chronic medical conditions, take any regular medications or have any drug allergies? Does Kayla have any concurrent medical conditions – especially active asthma, respiratory tract infection or tonsillitis?

You then examine Kayla, ensuring you conduct as cardiorespiratory exam and an assessment of her airway anatomy, including ASA grade. You need to assure yourself that no contraindications exist.


RCEM’s 2020 guidance is very specific about the need for conducting a thorough pre-sedation assessment, including assessing ASA grade, all of which should be thoroughly documented for clinical auditing and safety purposes. An example proforma template is provided at the end of their guideline. This contrasts with the 2016 guideline, which included a list of contraindications, but did not require documentation of ASA grade.


It’s time to consent Kayla and her mum for the procedure. You remember that ketamine is considered safer than other hypnotic drugs such as Propofol but need to remind yourself of the specifics, and the side-effect profile prior to consenting.


How safe is ketamine?

Does ketamine have side effects? Yes, but of all sedation agents studied by Bhatt et al in 2017 (6,760 patients across 5 sites in Canada), ketamine came out on top. This looked at ketamine/propofol, ketamine/fentanyl, propofol alone and ketamine alone. There were 831 adverse events across all agents (11.7%) – these included oxygen desaturation (5.6%) and vomiting (5.2%). There were 69 (1.1% of cases) serious adverse events (SAE). Ketamine as single-agent had the lowest SAEs at just 0.4%.

Pre-procedural opioids and laceration repair were associated with increased risk of emesis. Bhatt et al noted that prophylactic antiemetics reduce the risk of vomiting by half, but these were not needed in those under 5 years of age due to the low overall risk of emesis.

This endorsed previous data from a large case series by Green et al (2009) which demonstrated low rates of adverse events with ketamine PPS; most notably, noisy breathing (not requiring any intervention other than airway repositioning) occurred in 1%, laryngospasm in 0.3% and of these only 0.02% required intubation.

Both of these large studies demonstrate ketamine’s excellent safety profile when used with the appropriate preparation and patient selection.


Does Kayla need to have fasted?

Let’s have a look at the current guidelines and evidence. Several large studies have looked at this controversial issue: one study in a US PED in 2001/2002 where only 44% of patients met traditional fasting guidelines demonstrated no statistically nor clinically significant increase in adverse events in the unfasted population.

A series of over 30,000 children undergoing PPS by Cravero et al (2006) reported only 1 episode of aspiration – and this was in a fasted patient!

In 2016, Beach et al published a report based on 140,000 procedural sedation events, noting that aspiration was a rare event. Furthermore, they concluded that non-fasted patients were at no greater risk of major complications or aspiration than fasted patients.

In 2014 the American College of Emergency Physicians (ACEP) altered their national guidance stating that procedural sedation “should not be delayed for children in the ED who have not been fasted.” This was based on a systematic review including 3,000 sedation events showing that pre-procedural fasting failed to reduce the risk of emesis, aspiration, or other adverse events. They acknowledged that the current evidence does not support the rationale put forth in the non-emergency medicine guidelines that adherence to minimum fasting times decreased adverse events in ED procedural sedation.


This is reflected in RCEM’s 2020 guidance, which states that there is no evidence that complications are reduced if the child has fasted. They advised that the fasting state should be considered in relation to the urgency of the procedure, but recent food intake should not be considered as a contraindication to ketamine use.*


*We cheered when we read this in the 2020 guideline. No more fasting – we’ve been saying this for years! But, a quick look back at the 2016 guideline shows that this was actually the recommendation back then too. Really careful scrutiny shows that a single word, “however”, has been removed from the start of the sentence, “traditional anaesthetic practice favours a period of fasting”, altering the tone of the recommendation to a much less dogmatic mandate about nil by mouth status.


Satisfied that the evidence does not suggest any advantage to fasting children before PPS (who, let’s face it, tend to be less cooperative when hungry anyway), you prepare the room, staff, and equipment for the procedure.


Where will Kayla’s procedure be carried out, how many staff do you require, and what equipment should get ready?


RCEM recommends at least three operators: the proceduralist (the clinician performing the procedure), the sedationist (clinician responsible purely for managing sedation) and a sedation assistant*. They specifically acknowledge that the clinician responsible for the sedation and the patient’s airway should be experienced in the use of ketamine, and capable of managing its complications. The 2020 guideline has elaborated further on this, coming with a recommendation for a need for suitable training, a minimum of six months’ experience in anaesthesia or intensive care medicine and an up-to-date APLS course.

*RCEM says ‘nurse’ for the third member of staff but really, it’s anyone who is experienced in monitoring children and supporting the sedationist – doctors can take on this role too.

ACEP’s 2014 position statement concurs with the need for three operators.

The recommendation is that the procedure should be carried out in a resuscitation bay or high dependency area with immediate access to full resuscitation facilities.

Monitoring (every five minutes) of heart rate, blood pressure, respiratory rate, and oxygen saturation is mandated. The American Academy of Pediatrics advised the use of capnography as an adjunct in order to detect hypoventilation and apnoea earlier than pulse oximetry or clinical assessment alone. While no evidence currently shows capnography reduces the incidence of serious adverse events, available studies show a decreased incidence of hypoxia and respiratory events.


The use of capnography during sedation has been affirmed by RCEM who have made it a mandatory minimal requirement in their most recent guideline iteration, in parallel with their previously recommended monitoring of respiratory rate, heart rate, oxygen saturations, ECG and BP.
The 2020 RCEM guideline also includes ‘degree of dissociative sedation’ as part of its recommended monitoring during the procedure, which is a new addition to their guidance. Ketamine is unique in that it does not conform to the ‘sedation continuum’ – the patient is either dissociated or not. This recommendation is perhaps aimed at prompting the sedation clinician and nursing colleague as to whether dissociation has occurred, and as to whether a top-up dose is required (more on that later).
The updated RCEM document specifically advises having key resuscitation drug dose calculations performed prior to the procedure and ready access to these, another new addition to their guidance, although no specific drugs are recommended.


Some doses you may find useful are:

As you’re checking the ketamine and emergency drug doses with your nursing colleague she asks whether you want her to draw up atropine and midazolam? She is a recent addition to the ED team and mentions that when she worked in theatre some years ago they frequently gave these medications together with ketamine.


Should any adjunctive agents be used with ketamine?

There was a previous vogue to co-administer a benzodiazepine to reduce the incidence of emergence. A 2018 BestBets review looked at this very question by studying 6 relevant studies (including 2 RCTs: Sherwin et al 2000, and Walthen et al 2000). These failed to demonstrate a significant difference in emergence between ketamine alone and ketamine with midazolam. In fact, the only difference demonstrated was increased rates of adverse advents when a benzo was co-administered. So, no prophylactic benzodiazepine required.

Having said this, if a child suffers severe emergence (older children, in particular, have increased risk of recovery agitation), then it is worth considering midazolam (aliquots of IV 0.05-0.1mg/kg) to treat (but not routinely or for minor / moderate emergence).

Another previous trend involved the co-administration of atropine to reduce the risk of aspiration. But the evidence does not support this practice, Green et al concluded “There is no evidence to support routine use of anticholinergic medication such as atropine to prevent laryngospasm or other adverse airway events.” Concurrent anticholinergics may actually increase the rate of airway and respiratory adverse events. There is a small increased risk of laryngospasm with oropharyngeal manipulation (including suctioning) so atropine (20 micrograms/kg IV) may be considered as rescue therapy if PPS is being used for intraoral laceration repair (although RCEM would recommend not using ketamine for these procedures for this precise reason).

A common side-effect of ketamine is vomiting. RCEM’s 2020 guidance recommends the use of IV ondansetron at 0.1mg/kg (max dose 4mg) to treat intractable vomiting.

Given ketamine’s emetogenic properties, is it worth giving an antiemetic prophylactically? It is worth considering ondansetron (0.1mg/kg IV) as prophylaxis in high risk groups: those with previous nausea/vomiting during sedation/anaesthesia, older children, or IM administration. The NNT depending on age of the patient will lie between Var7 and 9. This was further endorsed by a BestBets review published in the EMJ in 2018 which concluded that ondansetron should be considered when using ketamine for PPS, especially in older children or for those receiving preprocedural opioids. As with any drug, however, you’ll need to balance the risk-benefit ratio in your mind. Some would prefer not to use ondansetron prophylactically because of the risk of arrhythmias in children with undiagnosed long QT. But, again, long QT is rare…


A resus bay is prepped. Kayla and her mother are ready. Roles have been allocated; your nursing colleague is ready and is just removing the Ametop from Kayla’s hands which had been applied when PPS was considered; one of the ANPs will be the procedural clinician and your consultant will supervise you as the sedation clinician. You cannulate first go, while Kayla is distracted by Peppa Pig on screen. It’s time to dissociate.


But what dose will you give Kayla?

Various opinions exists regarding the exact or perfect dose; the most commonly accepted dosing schedule is 1-1.5mg/kg for intravenous (IV) administration.


RCEM’s guideline recommends a starting dose of 1mg/kg over 60 seconds (to reduce adverse events such as laryngospasm). This can be supplemented with top-up doses of 0.5mg/kg. This has not changed from their previous guidance.


You should notice onset of action within a minute. It is easy to spot as the child will develop horizontal nystagmus coupled with a loss of response to verbal stimuli. The heart rate, blood pressure and respiration rate may all increase slightly. Sedation will start to wear off after 20 minutes, with full recovery should occur by about 60 to 120 minutes.

Many departments are still using intramuscular (IM) ketamine. This can be particularly helpful in certain situations such as where IV access is difficult.


Due to its variable onset and offset time, longer time to recovery and increased risk of emesis, however, RCEM have now advised against IM except where senior decision-makers deem it necessary. The advice is that “clinicians should be mindful of the perceived safety benefits of having intravenous access from the start of the procedure to mitigate a rare adverse event.” This is the biggest change in their new guidance; the 2016 guideline included dosing and top-up recommendations for IM ketamine.


There are still some children who would benefit from IM ketamine, so if choosing the IM option, consider a dose of 2-4mg/kg, with senior clinical support. Ideally IV access could be achieved once the child is dissociated and the IV top-up dose can be administered if required. However if IV access is impossible or not obtained the IM top-up dose is 1-2mg/kg. You can expect a slightly slower onset at about 3-5 minutes with its duration extended from 15-30minutes. Recovery is variable occurring anywhere between 60-120 minutes.


As you walk over to the drug cupboard to collect your syringes with carefully calculated doses, your consultant asks, “Are you confident in managing any potential airway complications?”


Airway complications with ketamine PPS

Thankfully complications with ketamine are rare. Most events such as noisy breathing or stridor, and minor desaturation will respond to simple airway manoeuvres to ensure the airway is open, plus the use of high-flow oxygen via a mask with a reservoir bag. The most feared complication, laryngospasm, is extremely rare and most often will respond to simple airway manoeuvres. But sedationists must be competent in managing this prior to administering the first dose of ketamine. If laryngospasm is suspected, stop the procedure and call for help. Ensure 100% oxygen is administered if not already in situ. Gently suction any visible secretions. If this fails to improve the situation begin manual ventilation with ventilation via a bag-valve-mask or, if you are comfortable using an anaesthetic circuit, apply PEEP. Some guidelines (and anaesthetists) suggest applying pressure to Larson’s point, very similar to performing a strong jaw thrust. If there is no response at this point, with critical airway compromise, then RSI is required. Administer the pre-calculated dose of paralytic and intubate. Remember, Green’s reported incidence of intubation secondary to laryngospasm was only 0.02%.

The flowchart below may be of benefit – it formed part of my quality improvement project on PPS and was used as a wall chart in the sedation cubicle and included in each sedation proforma booklet. When emergencies occur, being able to cognitively offload by following step by step aide memoires and having pre-calculated doses to hand can be immensely comforting and helpful.



Kayla’s procedure is completed without difficulty and the nurse enquires as to how long Kayla needs to remain monitored for?


Children should remain monitored until their conscious state, level of verbalization and ambulation is back at pre sedation levels. They should be able to tolerate oral fluids. Prior to discharge, a final set of observations should be within normal limits for their age. Consider the need for a prescription (antibiotics or analgesia) prior to discharge.


Kayla successfully underwent ketamine PPS, allowing a thorough wash out of her wound and suturing which provided a tidy end result. She was later discharged with an antibiotic prescription and a teddy which the play specialist had found in the toy room for her. Delighted with your chance to use “Special K”, you quickly took out your phone to tweet about the latest changes in RCEM guidance in ketamine for procedural sedation in children in the ED (along with the endless uses of ketamine!)


The new RCEM guidance has come at an interesting time – how might it change our practice in PPS in the ED? PERUKI are soon to launch a two-level paediatric procedural sedation survey (name PoPSiCLE – we all know that a good study needs a catchy name) to inform the current status and variations in the practice of PPS in PERUKI , to provide baseline information for developing a network-wide training resource and patient registry. Watch this space…


Case two: Ronan


It’s a sunny Saturday afternoon. The smell of BBQ and summer is wafting through some open windows in the department. On your way to work, you noticed plenty of bouncy castles and trampolines in use. It’s not surprising your first patient is an 8-year-old boy who has fallen awkwardly while trying to impress some other kids at his birthday party. After examining him and his xray you see he has a midshaft radius and ulnar fracture with some angulation. Thankfully his DRUJ (distal radio-ulnar joint) appears intact, and his radial head is in joint. He needs manipulation of the fractures and application of a backslab. He’s in a lot of pain, despite the paracetamol and ibuprofen he had at triage. He tells you his favourite birthday cake is at home waiting for him and he wants to get home to blow out all the candles. You wonder if you can avoid him a trip to the operating room for a general anaesthetic. Would PPS perhaps be a safe alternative?


Nitrous oxide provides anaesthesia, anxiolysis, and also some mild amnesia. However, it offers limited analgesia and so co-administration of an analgesic is recommended. Several key papers, including the FAN study (2017) and Seith et al (2012) have demonstrated the safety and efficacy of co-administrating intranasal fentanyl (INF) with nitrous oxide.

Once you’re ready to go, move the child into the dedicated resus bay or sedation room. If using piped nitrous oxide with a variable concentration flow meter (ensuring the scavenging system is switched on) titrate the dose from 30-70% according to clinical response. The alternative is Entonox (a 50/50 mix of nitrous and oxygen) which usually comes in portable canisters but requires the child to be able to take a deep breath to overcome a demand valve circuit, usually tricky for the under-fives. You should notice the onset of effect in 30-60 seconds, but its peak effect will be 2-5 minutes so best to wait for this before commencing the procedure. Once the intervention or procedure is completed it is important to administer 100% oxygen for 3-5minutes post-procedure to avoid diffusion hypoxia. The offset of effects should occur within 2-5 minutes.

Does nitrous oxide have any side effects? While well tolerated by most children, transient minor side effects such as nausea, dizziness and occasionally nightmares can occur. It can cause vomiting in 6-10% of children receiving 50% nitrous dose. This rate increases with higher concentration and can increase up to 25% if an opioid is co-administered. Be sure to warn parents about this relative frequency of vomiting when using nitrous oxide, both during and after sedation. The risk of vomiting also increases with a longer duration of nitrous administration. Consider a prophylactic antiemetic if the child has a history of nausea or vomiting.

Nitrous oxide diffuses through tissues more rapidly than nitrogen alone and can expand in air-containing spaces within the body. This makes it contraindicated for use in patients with gastrointestinal obstruction, pneumocephalus, pneumothorax and after diving.

Nitrous oxide inactivates the vitamin B12-dependent enzyme, methionine synthase, and so can deplete vitamin B12 stores. Because of this, caution is advised in those at risk of vitamin B12 deficiency such as vegetarians, patients with gastrointestinal disorders and those taking regular H2 receptor blockers and proton pump inhibitors. Nitrous should also be avoided in those with metabolic diseases especially methionine synthase deficiency, methymalonic acidaemia, and homocysinuria (because inactivation of methionine synthase can affect homocysteine metabolism). There’s a theoretical risk to pregnancies in the first trimester and so guidance often suggests avoiding nitrous oxide exposure in early pregnancy.

During administration monitor heart rate, respiratory rate and oxygen saturations. At least two staff members are required; a sedationist and a proceduralist.


Ronan and his mum are happy for you to use nitrous oxide and eagerly his mum signs the consent form. While setting up the sedation room and recruiting a nursing colleague to assist, you administer intranasal fentanyl. Ronan successfully undergoes manipulation of his fractures and an above elbow backslab is applied. His post-reduction x-ray shows you performed a pretty awesome reduction and, in consultation with your orthopaedic colleagues, you are happy for Ronan to be discharged to return to their fracture clinic in a few days’ time. This delights Ronan, as he gets to return home to his birthday party (with strict instructions to remain off the trampoline) and he promises to bring you back some of his birthday cake later!



Case three: Chantelle

Your junior colleague has come to you for advice. She has just seen a 4-year-old girl who was hard at work in her playroom creating unicorn pictures. Her mum had given her lots of colourful supplies including some glittery sequins and beads. Chantelle became adventurous and decided to decorate herself rather than the unicorns. Unfortunately, one of the beads has become lodged in her ear and despite an attempt by your colleague using both parents, and a play specialist, the removal of the foreign body was unsuccessful. You believe the use of PPS will be required and begin pondering which agent to use.


Midazolam is a hypnotic agent providing anxiolysis and amnesia. It does not have analgesic properties, which is why it is important to co-administer with analgesia for any painful procedure. It can be administered by many routes, the two commonest for PPS being intranasal (IN) and orally. If used intranasally, a dose of 0.3-0.5mg/kg is suggested. You should notice its onset within 10-15 minutes, lasting about 60 minutes. This route of administration can cause some nasal irritation and burning, so some clinicians prefer to use it orally. With an oral dose of 0.5mg/kg you should notice onset at 15-30 minutes with a duration of effect for 60-90 minutes. Midazolam tastes bitter – so give it with some juice or squash to make it more palatable. Midazolam can be given intramuscularly (IM) and intravenously (IV), but it is less likely to be used in this fashion for PPS.

Does midazolam have any side effects? Yes! It can cause hypoventilation and apnoea – be aware that this risk is increased if co-administered with an opioid such as fentanyl or diamorphine. A reversal agent does exist: flumazenil (0.01mg/kg, max dose 1mg) but this is rarely required, and oftentimes using basic airway manoeuvres is sufficient. Paradoxical excitatory or agitation reactions can occur in up to 15% of children. Do warn parents of this possibility prior to administration. The best course of action if it does occur is to let the child “ride it out”. Because of this, many ED clinicians will choose ketamine or nitrous oxide as their PPS agent of choice over midazolam.

With these side effects in mind, it is prudent to ensure basic monitoring includes heart rate, respiratory rate, and oxygen saturation monitoring. At least two staff are required; proceduralist and sedationist.


Having obtained informed consent from Chantelle’s mother, you decide to give her intranasal midazolam. 45 minutes later you remove the mischievous bead from her left ear. Her parents are thrilled, but before you leave the room you remember the mantra of “always check the other ear”. So before packing up your tools and leaving her with your sedation nurse, you decide to check her other ear. Interesting you find two glittery sequins hiding in her right ear canal. Phew, that saved a second sedation event!



Ketamine Procedural sedation for children in the emergency department. The Royal College of Emergency Medicine. Best Practice Guideline. February 2020.

Bhatt M, Johnson DW, Chan J et al. Risk factors for adverse events in emergency department procedural sedation in children. JAMA paediatrics 2017 Oct 1;171(10):957-964

Bhatt M, Johnson DW, Chan J et al. Risk factors for adverse events in emergency department procedural sedation in children. JAMA paediatrics 2017 Oct 1;171(10):957-964

Green SM, Roback MG, Krauss B, et al. Predictors of airway and respiratory adverse events with ketamine sedation in the emergency department: an individual-patient data meta-analysis of 8,282 children. Ann Emerg Med. 2009; 54(2):158-168.e1-4

Agrawal D, Manzi S, Gupta R, Krauss B. Pre-procedural fasting state and adverse events in children undergoing procedural sedation and analgesia in a paediatric ED. Annals of Emergency Medicine. 2003; 42(5): 636-646

Cravero JP, Blike GT, Beach M, et al. Incidence and nature of adverse events during pediatric sedation/ anesthesia for procedures outside the operating room: report from the Pediatric Sedation Research Consortium. Pediatrics. 2006; 118(3):1087-1096

Beach ML, Cohen DM, Gallagher SM, Cravero JP. Major Adverse Events and Relationship to Nil per Os Status in Pediatric Sedation/Anesthesia Outside the Operating Room: A Report of the Pediatric Sedation Research Consortium. Anesthesiology 2016;124(1):80-8

Godwin SA, Burton JH, Gerardo CJ, et al. Clinical policy: procedural sedation and analgesia in the emergency department. Annals of Emergency Medicine 2014;63(2):247-58.e18

Sherwin TS, Green SM, Khan A, et al.Does adjuctive midazolam reduce recovery agitation after ketamine sedation for pediatric procedures? A randomised, double-blind, placebo-controlled trial. Ann Emerg Med 2000;35:229–38.

Walthen J, Roback M, Mackenzie T et al. Does midazolam alter the clinical effects of intravenous ketamine sedation in Children? A double-blind, randomized, controlled, emergency department trial. Annals of emergency medicine 2000;36(6): 579-587

Green SM, Roback M, Kennedy R et al. Clinical practice guideline for emergency department ketamine dissociative sedation: 2011 update. Annals of emergency medicine 2011; 57(5): 449-461

Dunlop L, Hall D. Antiemetic use in paediatric sedation with ketamine. Emerg Med J 2018; 35:524-525

Krauss B, Green SM. Procedural sedation and analgesia in children. Lancet 2006;367(9512):766-80

Nickson C. Paediatric Procedural sedation with Ketamine. Life in the Fast Lane. March 2019

Zier ZL, Liu M. Safety of high concentration nitrous oxide by nasal mask for pediatric procedural sedation: experience with 7802 cases. Pediatr Emerg Care. 2011 Dec;27(12):1107-12

Gamis AS, Knapp JF, Glenski JA. Nitrous oxide analgesia in a pediatric emergency department. Ann Emerg Med. 1989; 18:177-181

Comfort Kids Programme. Royal Children’s Hospital Melbourne. 2016

Peyton PJ, Wu CY. Nitrous oxide-related postoperative nausea and vomiting depends on duration of exposure. Anesthesiology. 2014;120(5):1137–1145

Baum VC. When nitrous oxide is no laughing matter: nitrous oxide and pediatric anesthesia. Paediatric Anaesthesia 2007;17(9):824-30

Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine. Acute Pain Management: Scientific Evidence.: Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine, 2005

Axelsson G, Ahlborg G, Jr., Bodin L. Shift work, nitrous oxide exposure, and spontaneous abortion among Swedish midwives. Occupational & Environmental Medicine 1996;53(6):374-8

Hoeffe J et al. Intranasal fentanyl and inhaled nitrous oxide for fracture reduction: The FAN observational study. Am J Emerg Med. 2017;35(5):710-715.

Seith RW, Theophilos T, Bable FE. Intranasal fentanyl and high-concentration inhaled nitrous oxide for procedural sedation: a prospective observational pilot study of adverse events and depth of sedation. Acad Emerg Med. 2012;19(1):31-6

Kennedy RM, Porter FL, Miller JP, Jaffe DM. Comparison of fentanyl/midazolam with ketamine/midazolam for pediatric orthopedic emergencies. Pediatrics. 1998;102:956–63

Pena, B.M. and Krauss, B. Adverse events of procedural sedation and analgesia in a pediatric emergency department. Ann Emerg Med. 1999; 34: 483–491

Wright, S.W., Chudnofsky, C.R., Dronen, S.C. et al. Midazolam use in the emergency department. Am J Emerg Med. 1990; 8: 97–100

Davies FC, Waters M. Oral midazolam for conscious sedation of children during minor procedures. J Accid Emerg Med. 1998;15(4):244–248. doi:10.1136/emj.15.4.244

Graff, K.J., Kennedy, R.M., and Jaffe, D.M. Conscious sedation for pediatric orthopaedic emergencies. Pediatric Emerg Care. 1996; 12: 31–35

Bailey, P.L., Pace, N.L., Ashburn, M.A. et al. Frequent hypoxemia and apnea after sedation with midazolam and fentanyl. Anesthesiology. 1990; 73: 826–830

Gregory GA. Pediatric Anesthesia. 4th ed. Philadelphia, PA: Churchill Living- stone; 2002


Orbital fractures

Cite this article as:
Orla Kelly. Orbital fractures, Don't Forget the Bubbles, 2020. Available at:


Facial fractures in children accounted for just 4.6% of paediatric trauma admissions on review of the American National Trauma Databank. However, even though they are less prevalent than in an adult population, they are associated with other severe injuries and higher mortality compared with adults. The pattern of injury descends the face as the patient ages – the under 5s are more likely to sustain frontal bone and orbital roof fractures, while the 6-16-year-olds are more likely to have midface and mandibular fractures. Orbital fractures as a subset comprise between 5 to 25% of facial fractures.


Bones of the orbit
  • The orbit is comprised of 7 bones – maxilla, zygomatic, frontal, ethmoid, lacrimal, sphenoid and palatine.
  • The rim is formed by the frontal bone, maxilla, and zygoma.
  • The orbits are pyramidal structures, with a wide base opening on the face, with its apex extending posteromedially.
  • They lie anterior to the middle cranial fossa and inferior to the anterior cranial fossa.
  • Their close proximity to the sinuses coupled with the ophthalmic veins communicating with the cavernous sinus creates a possible introduction of infection into the intracranial cavity.
Location of the facial sinuses
  • The infra-orbital nerve exits through the inferior orbital foramen inferior to the orbital rim and innervates lateral aspect of the external nose, inferior eyelid and cheek and upper lip and related oral mucosa.
  • Paediatric anatomy and development confer different injuries depending on age, with orbital floor fractures becoming more common than roof fractures at approximately age 7 due to the development of the maxillary sinus.

History and Examination

Mechanism of injury is always important to elicit in trauma as well as careful and thorough (and documented) examination. Initial assessment as always in trauma is by the ATLS ABC approach followed by a careful secondary survey.

Children are prone to a pronounced oculocardiac reflex which may become apparent in the initial ABC assessment; this is caused by compression of the globe or traction on the extra-ocular muscles. Connections between the sensory afferent fibres of the ophthalmic division of the trigeminal nerve and visceral motor nucleus of the vagus nerve cause bradycardia and hypotension often with headache, nausea, and vomiting.

Have a systematic approach to examination so as to ensure all important aspects are covered. Always examine and document:

  • General inspection – oedema, laceration, and bruising
  • Enophthalmos/proptosis
  • Subconjunctival haemorrhage
  • Periorbital emphysema
  • Pupillary response including RAPD
  • Eye movements in all directions
  • Visual acuity
  • Diplopia
  • Palpation of the orbital rim for tenderness or step
  • Abnormalities of the nasal bridge (saddle nose deformity) and widening of the midface (telecanthus)
  • Disruption to the infraorbital nerve: numbness of the ipsilateral cheek, lip, and upper gum
Sensory distribution of infra-orbital nerve

Investigation and Management

Investigation of orbital fractures is by x-ray and CT, with CT being the modality of choice, though it can be unreliable in children with blowout fractures. A CT may already be appropriate due to a mechanism of injury or red flags for a head injury.

The aim of initial management in the ED is to prevent further damage to the globe.

Patients should be advised to not blow their nose and to sneeze with their mouths open. A cold compress and raising the head of the bed can help alleviate periorbital oedema. Ensure the eyelids can close fully and lubricate the cornea. Provide a protective patch if necessary.


Types of Injuries

 Orbital Floor and Medial Orbital Wall Fractures

The term ‘blow out fracture’ has historically meant a fracture of the orbital floor secondary to a direct blow to the globe, causing an increase in pressure that results in the thin orbital floor fracturing. Children presenting with floor or medial wall fractures are at high risk of entrapment, as paediatric bones are more prone to greenstick fracture, which then creates a ‘trapdoor’ effect ensnaring the inferior oblique and inferior rectus muscles or other orbital contents. Clinically, the child will be unable to complete upwards gaze. Entrapment is a surgical emergency, as ischaemia of the involved musculature can cause permanent damage. The infraorbital nerve is commonly damaged in these injuries.

Orbital blow out fracture

Children with orbital floor fractures may not have any facial bruising, classically presenting with a ‘white-eyed’ fracture with the only sign being limitation of eye movement secondary to entrapment.

(A) Restriction of upgaze in the right eye with no evidence of periocular trauma. (B) CT scan of the orbits demonstrating inferior rectus muscle entrapped within inferior orbital wall fracture (arrow). Reproduced with permission from

Orbital Roof Fractures

Orbital roof fractures are more common in childhood as the frontal sinus has not yet pneumatised, therefore all posterior force to the superior orbital rim is transferred to the anterior cranial base. Another mechanism of injury is a ‘blow-in’ fracture, where there is an inferiorly directed supraorbital force.

NOE (nasal-orbital-ethmoidal) Fractures

Nasal bone injuries are common in older children and adults and must always be assessed for an underlying NOE fracture. When direct force is applied to the nasal bone, it can cause a collapse of the paired nasal, lacrimal, and ethmoidal bones. If this fracture is missed in a child, significant midface deformities can result.

Midfacial fractures

Although children are more likely than adults to suffer isolated orbital rim fractures, orbital fractures are often involved in midfacial fractures of the maxilla and zygoma: the orbit is involved in Le Fort II and III; zygoma fractures are often accompanied by orbital floor or medial wall fractures.

Globe Injuries

Orbital fractures can often result in globe injuries ranging from corneal abrasion to rupture. If there are any signs of globe rupture (360 degrees conjunctival haemorrhage, misshapen pupil or a flat anterior chamber) a gross visual examination should be completed, vaulted eye protection applied, and immediate ophthalmology consult sought. Do not apply pressure to a possibly ruptured globe.

Retrobulbar haemorrhage

A rare but sight-threatening complication is a retrobulbar haemorrhage which causes increased pressure, stretching of the optic nerve and can result in permanent blindness. If optic pressure is low, medical management with mannitol, steroids, and acetazolamide can be used after expert involvement. However, if there is an indication that the pressure is high, a lateral canthotomy should be performed as a matter of urgency. The procedure should ideally be performed by an ophthalmologist, but when ophthalmology are delayed or unavailable, the procedure must be performed by an emergency clinician in the ED. Do not delay a lateral canthotomy for imaging if sight is threatened.

Indications for lateral canthotomy include:

  • Retrobulbar haematoma
  • Decreased visual acuity
  • Afferent pupillary defect
  • Proptosis


  • Repeat a child’s eye examination while they are in the emergency – repeated examination can drastically change disposition from maxillofacial non-urgent transfer to a blue light ophthalmological review
  • Oculo-cardiac reflex can cause bradycardia and hypotension
  • Children are more likely to have other and significant injuries: the secondary and tertiary survey is imperative.
  • Children are more likely to suffer ‘trapdoor’ floor fractures causing entrapment that can present as a ‘white eye’ fracture– this is a surgical emergency, act fast.
  • Patients should avoid nose blowing and should sneeze with their mouth open following injury.
  • Ophthalmological assessment should be sought in all patients with orbital trauma.

Selected references

Imahara SD, Hopper RA, Wang J, Rivara FP, Klein MB. Patterns and outcomes of pediatric facial fractures in the United States: a survey of the National Trauma Data Bank. J Am Coll Surg. 2008;207:710–716

Oppenheimer AJ, Monson LA, Buchman SR. Pediatric orbital fractures. Craniomaxillofac Trauma Reconstr. 2013;6(1):9–20.

Koltai PJ, Amjad I, Meyer D, Feustel PJ. Orbital fractures in children. Arch Otolaryngol Head Neck Surg. 1995;121:1375–1379

Cohen SM, Garrett CG. Pediatric orbital floor fractures: nausea/ vomiting as signs of entrapment. Otolaryngol Head Neck Surg. 2003;129:43–47

Grant JH III, Patrinely JR, Weiss AH, Kierney PC, Gruss JS. Trapdoor fracture of the orbit in a pediatric population. Plast Reconstr Surg. 2002;109:482–489; discussion 490–495

Boyette, J. R., Pemberton, J. D., & Bonilla-Velez, J. (2015). Management of orbital fractures: challenges and solutions. Clinical ophthalmology. 2015;9:2127–2137.

Cobb ARM, Jeelani NO, Ayliffe PR. Orbital fractures in children. British Journal of Oral and Maxillofacial Surgery. 2013;41–46

Kassam K, Rahim I, Mills C. Paediatric orbital fractures: the importance of regular thorough eye assessment and appropriate referral. Case Rep Emerg Med. 2013:376564. doi:10.1155/2013/376564

All Things Patella

Cite this article as:
Tadgh Moriarty. All Things Patella, Don't Forget the Bubbles, 2020. Available at:

Patella dislocation

Robert is a 14-year-old boy who has just arrived by ambulance having been playing a rugby match. He was running just short of the try line when he tried to make a dastardly last-minute course correction, however, while rapidly altering course his body went one way, while his foot remained planted on the ground and he felt his left knee suddenly give way. A sudden surge of pain followed and he dropped to the ground. On the ambulance stretcher, you see his knee is hugely swollen with an obvious deformity out laterally. He is in obvious pain and distress. The triage nurse thinks his patella is dislocated and wants you to prescribe some analgesia.     


Patella dislocation is a common knee injury, particularly associated with sports (61-72% Steiner 2010) and physical activity among teenagers.



The two most common mechanisms for a patellar dislocation are:

  • Non-contact twisting injury (66-82% Khormaee 2015) – this is where foot remains planted on the ground, usually externally rotated, while the knee is extended and internal rotation about the hip causes a dislocation.
  • Direct contact (less common) – e.g. knee to knee strike during basketball or a helmet/head to knee in rugby.


Risk factors

Some children are more prone to patellar dislocation than others. It is worth noting that those with underlying anatomical abnormality may not present with as much obvious swelling and deformity as those with normal anatomy. Look out for the following:

  • Connective tissue disorders e.g. Ehlers-Danlos
  • Lateral patellar tilt
  • Trochlear dysplasia
  • Genu valgum (‘knock-knee’)
  • Patella alta (high-riding patella)
  • Increased femoral anteversion
  • Vastus medialis muscle hypoplasia



A child will usually present following a sudden ‘pop’ or sensation of instability and severe anterior knee pain. Acute dislocation is usually associated with a moderate haemarthrosis, however, those with underlying risk factors (especially ligament hyperlaxity) may not.

A detailed ligamentous exam is important to assess for integrity and damage to cruciate and collateral ligaments. Medial tenderness is common as the MPFL (medial patella-femoral ligament) is ruptured in over 94% of dislocations. Providing over half of the restraining force for the patella, it extends to its medial border from the femur.

The patellar apprehension test is described for those whose dislocations have reduced pre-hospital (according to Willis et al. most spontaneously reduce). With the knee flexed to 30 degrees, apply some lateral pressure; with medial instability, the patient will feel apprehensive about the kneecap “popping” again.



This is a painful injury so ensure adequate analgesia has been provided. Next question – has the dislocation been reduced yet? If yes – jump to post-reduction management, if not read on…

The use of procedural sedation with nitrous oxide is ideal for this short painful procedure. Flex the hip on the affected side, thereby relaxing the quads muscle. Apply pressure to the lateral border of the patella in a medial direction while extending the knee. A satisfying ‘clunk’ should be felt as the patella slides back into its home in the trochlear groove of the distal femur.


Post-reduction management:

There is no evidence-based consensus to guide ongoing treatment, especially in first-time dislocations (see controversies below). Once reduced, the application of a knee immobilizer will help reduce ongoing analgesia requirements. Studies have failed to demonstrate a benefit of one type of immobilization device over another – therefore follow local guidance; knee brace in full extension, cylinder cast or above knee back-slab are all acceptable.

Ensure ongoing analgesia requirements post-discharge are met, and consider crutches until seen back in the orthopaedic clinic.



This is not always necessarily required pre-reduction. A post-reduction x-ray (AP and lateral) is important to assess associated osteochondral fractures and to check the patella location. An MRI scan can be particularly useful to assess for associated ligamentous integrity and rupture, VMO sprain, and osteochondral fractures. In fact, MRI is more sensitive than arthroscopy to assess for MPFL tear. However, this can be organized from orthopaedic follow-up clinic.


What to tell the patient

Will it happen again?

The younger the patient the higher the rate of re-dislocation: 60% for those 11-14 years, and 33% 15-18 years.

Is everything fixed now that the kneecap is back in place?

It can be difficult to tell is there are associated ligamentous injuries on the day of presentation which can lengthen recovery to baseline. Not all osteochondral fractures will be apparent on the plain film radiograph. Repeat examination in the orthopaedic clinic +/- MRI will often provide a more detailed assessment of prognosis.

What happens next?

Traditionally first-time dislocations were treated with immobilization for 3-6 weeks followed by intensive physio to strengthen the quads. There is now a move towards earlier motion and rehab (despite a lack of RCTs). Surgery has usually been reserved for those requiring loose body (within the joint) removal, fixation of osteochondral fractures and for those with recurrent instability and dislocation.

When can I go back to playing sports?

As a general rule of thumb 8-12 weeks.



There has been a recent trend towards surgical fixation (usually of the MPFL) in recent times. Whereas this was usually reserved for recurrent dislocations, a systematic review by Nwachukwu et al in 2015 showed reduced re-dislocation with surgical treatment of first time patellar dislocation (31% Vs 21%, p=0.04). However, there was no difference between surgery versus conservative management in subjective or objective knee function.

Why is this important? Ultimately it will depend on local orthopaedic preference but it’s important to know that not all first-time dislocations will be treated conservatively so we don’t inadvertently give parents and patients misinformation.


Case Resolution

You correctly identify this as a patellar dislocation and organize a nitrous oxide procedural sedation and successfully reduce the dislocation. Post-procedure you place his knee in an above-knee backslab and organize a fracture clinic follow up. Before leaving you to ensure his parents have appropriate dosed analgesia at home.


Patellar tendon rupture

Rachel is a 13-year-old girl who is a keen runner and has recently discovered a passion for hurdling. She was attending training, on her third lap, while jumping over the hurdle felt a sudden pop followed by immense pain causing her to drop to the ground. She was unable to walk, the pain being too intense. An ambulance was called and the triage nurse asks you to see her next as she is crying in pain.


This is a relatively rare condition with the peak age of occurrence being 40. That being said, the rate of patella tendon rupture (PTR) is increasing in frequency. This is often a sports-related injury (e.g. hurdling, basketball) with the mean age for children being 13 years.



The patellar tendon is part of the very important extensor mechanism of the knee, connecting the patella to the tibial tuberosity. This is crucial to help us overcome the forces of gravity. The entire mechanism includes the quads femoris muscles, the quads tendon, the patellar tendon, the patella itself and the tibial tubercle.

The most common ways to injure the PTR is through a direct blow (e.g. fall), or through forceful contraction of the quads muscle (usually while the foot is planted and knee flexed) – e.g. missing a step while climbing stairs, or in jumping sports.

The force required to rupture the tendon is 17 times that of the average body weight

There are three main patterns of injury which can result

  • Avulsion from the inferior pole of the patella (there is an increased risk of concurrent bony avulsion with children’s growth plates)
  • Mid-tendon
  • Distal avulsion from the tibial tuberosity


Risk factors

Conditions that cause microscopic damage to the tendon blood supply such as repeated microtrauma (e.g. athletes), chronic renal failure, collagen vascular disease, diabetes, osteogenesis imperfecta, and steroid use.



There will usually be some history of a popping sensation, knee pain, swelling and difficulty or inability to weight bear. On exam, the knee usually has a moderately large haemarthrosis. A high riding patella (patella alta) may be noted when compared to the contralateral side.  Localized tenderness and a palpable gap below the inferior pole of the patella may be present in complete tears. The pain will limit the range of movement of the knee. The inability to actively straight leg raise is indicative of serious extensor mechanism pathology and should be assumed to be a complete tear until proven otherwise. Pain may limit the range of movement examination of the knee (ensure adequate analgesia) so an alternative is to have the patient maintain a passively extended knee.



X-rays – AP and lateral. While not conclusive, certain features may suggest the diagnosis. A joint effusion is likely, the presence of a high riding patella (patella alta) is highly suggestive of a complete tear.


Want to really impress your orthopod service – measure the Insall-Salvati ratio and if >1.2 – this is diagnostic of patella alta. This is measured by A/B, where A= patellar tendon length (posterior surface of the tendon from the lower pole of the patella to tibial insertion) and B = patellar length (longest pole -> pole length).

Ultrasound – while this modality is user and operator dependent, its availability aids its usefulness. It can be effective at detecting and localizing disruption to the tendon. Differentiating between partial and complete tears can be more challenging.


MRI – the favoured imaging modality, but access can limit its usefulness. It will aid accuracy in delineating partial from complete tears and reveal any associated bony avulsion or soft tissue injuries.



Consider the diagnosis. While a rare event among the paediatric population, delayed diagnosis causes increased morbidity. 7% of those who sustain acute trauma to the knee will have a PTR. These are painful injuries, and so judicious use of analgesia is paramount.


Conservative management may be considered for those children with only partial tears and an intact extensor mechanism. Immobilization with a removable knee splint in full extension followed by graduated weight-bearing and rehab program.


Surgical repair is indicated for complete tears. A comparison of different techniques is difficult due to the small numbers of patients. Two main options exist depending on the level of the tear, associated injuries and surgeons choice:

  • Primary repair – using end to end repair, trans-osseous repair or suture anchor tendon repair.
  • Tendon reconstruction is usually reserved for severely disrupted tendons and involves the use of an autograft.



Traditional management post-surgery involved applying a cylinder cast for six weeks allowing the child to weight bear as tolerated. A newer school of thought involved early controlled movement at the joint. This involves applying a knee brace which allows up to 90 degrees of flexion for four weeks followed by graduated controlled increases in flexion until 12 weeks. This early mobilization aids quicker knee function return and prevents muscle atrophy.


What to tell the patient

Will I need an operation?

If there is complete tendon rupture or a compromised extensor mechanism, then surgical repair is needed.

When can I return to sports?

Full return to sports usually takes six months (range of 13-30 weeks depending on exact injury).


Case Resolution

On examination, you note she Rachel is unable to straight leg raise. An x-ray shows a large haemarthrosis. You refer her to the on-call orthopaedic service and the next day she undergoes an MRI confirming your suspicions of a patellar tendon rupture. This is operatively repaired and she has now commenced her rehab, looking forward to returning to running soon.


Patella fracture

The next card you pick up is a 14-year-old boy (Brian) who is a ‘return’ patient. He attended two days ago with right knee trauma and has represented with ‘ongoing pain’. He was playing rugby at the time and made a sudden twisting movement while avoiding a tackle. He felt searing hot pain in his knee and dropped to the ground. He wasn’t able to walk and had to be stretchered off the pitch. He had intranasal fentanyl pre-hospital and a top-up dose in triage two days ago. Being a keen sports player and with the rugby final coming up he was determined to return to play and was documented in the notes as being able to ‘tentatively weight bear’. On exam, you note a tense, swollen right knee. Being stoic he denies any focal tenderness but you notice a grimace when you examine his inferior patella. He is unable to straight leg raise and when he attempts to weight bear fully he is clearly in pain. You wonder whether his patellar tendon might be injured as surely a fracture would have been noted on his XR from two days ago….


Patellar fractures are relatively rare, with an incidence of 0.5-1.5% of all skeletal injuries. They are most common between 8-16 years with a mean age of 12.4 years. Unsurprisingly they are mainly caused during sporting and leisure activities.



There are two main types of patellar fractures in paediatrics. The first is a ‘typical’ bony fracture, which is caused by a direct impact on the patella, similar to adults. The second is almost exclusive to paediatrics; patellar sleeve fracture. These are caused by indirect trauma to the knee and are the result of a forceful quads muscle contraction in a skeletally immature individual. Patellar sleeve fractures are three times more common in males than in females. They account for over 50% of all patellar fractures in children. Inferior pole sleeve fractures are most common.



There may be a history of either a direct blow to the knee or a non-contact twisting injury with the foot planted. A knee effusion is likely to be present, with point tenderness at the affected site. Inability to extend the knee fully and inability to fully weight bear are red flags and underlying pathology must be assumed. Patella alta or patella baja may be present with patellar sleeve fractures with disruption of the inferior (alta) or superior (baja) tendon. A palpable gap may be present inferior/superior to the patella with complete disruption of the corresponding tendon.



X-ray: AP and lateral radiographs. A haemarthrosis may be visible. Bony fractures of the patella are most likely to be transverse or vertical. The patellar sleeve fractures require a high index of suspicion and can easily be missed as often only a tiny sliver of avulsed bone can be seen on plain film. Don’t be misled by this seemingly innocuous x-ray finding, a significant cartilaginous component will be involved.

Image from Orthobullets: Patellar sleeve fracture

Up to 8% of the population have bipartite patella – don’t confuse this for a patella fracture. Contralateral imaging is not always useful as 50% of those affected will have bilateral patella affected. Characteristically it will be present supero-laterally and will have smooth edges around the cortex.

Courtesy of Orthobullets: X-Ray showing bipartite patella

Ultrasound: can be helpful in confirming injury to the tendon. Soft tissue oedema and fluid hyperemia are other indirect signs that may be seen suggestive of tendon disruption.


MRI: this remains the imaging modality of choice if the diagnosis is in doubt. This will allow displaying the extent of the chondral injury and any concomitant extensor mechanism injury.


Non-operative: this may be considered in those with a nondisplaced (<2mm) fracture and an intact extensor mechanism. A cylinder cast will be applied for six weeks and then intensive rehab following its removal.


Operative: Any displaced fracture (>2mm) usually require open reduction and internal fixation (as the extensor mechanism needs to be restored).

Patella sleeve fractures will require ORIF with suturing of the tendon; superior sleeve fracture necessitating quads tendon repair, and inferior sleeve fracture requiring patellar tendon repair.

Post-operatively these patients are usually placed in an extension brace or cast until the wound is healed and then active flexion and extension exercises are commenced to restore normal knee function as soon as possible.


What to tell the patient?

Is there a fracture there?

If no fracture can be seen but the child has a large swollen knee, cannot weight bear or cannot fully extend the knee – have a low threshold to immobilize the knee even in the absence of a fracture on plain film. Patellar sleeve fractures are easily missed and lead to increased morbidity for the patient. If ready access to ultrasound or MRI this will confirm or refute the diagnosis, otherwise immobilize the knee and arrange confirmatory imaging as soon as possible or via local orthopaedic outpatients.

When can I return to sport?

Depending on the fracture and associated tendon injury – usually 3-6 months.


Case resolution

On review of his x-ray from two days previously you notice a tiny sliver of bone inferior to the patella and you organize an ultrasound which confirms your suspicions of a patellar sleeve fracture, involving his patella tendon. You apologize to his parents for the delayed diagnosis and refer him to the on-call orthopaedic service for an ORIF.




  • Panni AS, Vasso M, Cerciello S. Acute patellar dislocation. What to do?Knee Surg Sports Traumatol Arthrosc. 2013 Feb;21(2):275-8
  • Krause E1, Lin CW, Ortega HW, Reid SR. Pediatric lateral patellar dislocation: is there a role for plain radiography in the emergency department?J Emerg Med. 2013 Jun;44(6):1126-31
  • Seeley M, Bowman KF, Walsh C, Sabb BJ, Vanderhave KL. Magnetic resonance imaging of acute patellar dislocation in children: patterns of injury and risk factors for recurrence.J Pediatr Orthop. 2012 Mar;32(2):145-55
  • Sillanpää PJ, Mattila VM, Mäenpää H, Kiuru M, Visuri T, Pihlajamäki H. Treatment with and without initial stabilizing surgery for primary traumatic patellar dislocation. A prospective randomized study.J Bone Joint Surg Am. 2009 Feb;91(2):263-73
  • Lu, D. Wang, E. Self, W. & Kharasch, M. (2010). Patellar Dislocation Reduction. Academic Emergency Medicine. 226
  • Jaquith BP, Parikh SN. Predictors of Recurrent Patellar Instability in Children and Adolescents After First-time Dislocation. J Pediatr Orthop. 2015
  • Khormaee S, Kramer DE, Yen Y-M, Heyworth BE. Evaluation and Management of Patellar Instability in Pediatric and Adolescent Athletes. Sport Heal A Multidiscip Approach. 2015;7(2):115-123
  • Palmu S, Kallio PE, Donell ST, Helenius I, Nietosvaara Y. Acute patellar dislocation in children and adolescents: a randomized clinical trial. J Bone Joint Surg Am. 2008;90(3):463-470
  • Putney SA, Smith CS, Neal KM. The location of medial patellofemoral ligament injury in adolescents and children. J Pediatr Orthop. 2012;32(3):241-244
  • Seeley M, Bowman KF, Walsh C, Sabb BJ, Vanderhave KL. Magnetic Resonance Imaging of Acute Patellar Dislocation in Children. J Pediatr Orthop. 2012;32(2):145-155
  • Steiner T, Parker RD. Patellofemoral Instability: Acute Dislocation of the Patella. In: DeLee, Jesse C; Drez, David Jr.; Miller MD, ed. DeLee & Drez’s Orthopaedic Sports Medicine. 3rd ed. Philadelphia: Saunders Elsevier; 2010:1534-1547
  • Nwachukwu BU, Conan S, Schairer WW, Green DW, Dodwell ER. Surgical versus conservative management of acute patellar dislocation in children and adults : a systematic review. Knee Surg Sports Traumatol Arthrosc (2016) 24:760-767
  • Stefancin JJ, Parker PD. First-time traumatic patellar dislocation: a systematic review. Clin Orthop Relat Res. 2007 Feb; 455:93-101
  • Sillanpaa P, Mattila VM, Iivonen T, et al: Incidence and risk factors of acute traumatic primary patellar dislocation. Med Sci Sports Exerc 40: 606-611, 2008
  • Bicos J, Fulkerson JP, Amis A: Current concepts review: The medial patellofemoral ligament. Am J Sports Med 35:484-492, 2007
  • Nikku R, Nietosvaara Y, Aalto K, et al: Operative treatment of primary patellar dislocation does not improve medium-term outcome. Acta Orthop 76:699-704, 2005
  • Buchner M, Baudendistel B, Sabo D, et al: Acute traumatic primary patellar dislocation: Long-term results comparing conservative and surgical treatment. Clin J Sport Med 15:62-66, 2005
  • Maenpaa H, Sillanpää P, Paakkala A: A prospective, randomized trial following conservative treatment in acute primary patellar dislocation with special reference to patellar bracesKnee Surg Sports Traumatol Arthrosc (2010) 18 (Suppl 1):S119
  • Sillanpaa PJ, Mattila VM, Maenpaa H, et al: Treatment with and without initial stabilizing surgery for primary traumatic patellar dislocation. A prospective randomized study. J Bone Joint Surg Am91:263-273, 2009
  • Wilkerson and S. J. Fischer, “Patellar Tendon Tear”,, February 2016. [Online]
  • Hsu H, Siwiec RM. Patellar Tendon Rupture. [Updated 2019 Jun 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan
  • Miyamoto S, Otsuka M, Hasue F, et al., “Acute Traumatic Patellar Tendon Rupture at the Tibial Tuberosity Attachment without Avulsion Fracture,” Case Reports in Orthopedics, vol. 2017, Article ID 2537028, 5 pages, 2017
  • Dupuis CS, Westra SJ, Makris J, Wallace EC. Injuries and conditions of the extensor mechanism of the pediatric knee. 2009 May-Jun;29(3):877-86
  • Yousef M. Combined avulsion fracture of the tibial tubercle and patellar tendon rupture in pediatric population: case series and review of literature.Eur J Orthop Surg Traumatol. 2018 Feb;28(2):317-323
  • Ali Yousef M, Rosenfeld S. Acute traumatic rupture of the patellar tendon in pediatric population: Case series and review of the literature. 2017 Nov;48(11):2515-2521
  • Gettys FK, Morgan RJ, Fleischli JE. Superior Pole Sleeve Fracture of the Patella. Am J Sports Med 38(11):2331-2336, 2010
  • Hunt DM, Somashekar N. A review of sleeve fractures of the patella in children. The Knee 12:3-7, 2005
  • Grogen DP, Carey TP, Leffers D, Ogden JA. Avulsion Fractures of the Patella. J Pediatr Orthoped 10: 721-730, 1990
  • Schmal H, Strohm P, Niemeyer P, Reising K, Kuminack K, Sudkamp N. Fractures of the patella in children and adolescents. Acta Orthop. Belg. 2010 Oct;76(5): 644-650




Monteggia fracture dislocations

Cite this article as:
Rie Yoshida. Monteggia fracture dislocations, Don't Forget the Bubbles, 2019. Available at:

Emiko is an 8-year-old girl who presents to the ED with a swollen and painful left arm. She is a keen mixed martial arts enthusiast and has suffered a direct blow to the arm whilst practising earlier today. On examination, her left proximal forearm and elbow joint are swollen and tender. She has limited movement of her elbow joint. The arm is neurovascularly intact.

Wrist torus and greenstick fractures

Cite this article as:
Emily Cadman. Wrist torus and greenstick fractures, Don't Forget the Bubbles, 2019. Available at:

Forearm fractures (torus and greenstick fractures combined) are very common in children and happen in about 1 in 100 children. Wrist and forearm fractures account for half of all paediatric fractures.

They are often discussed alongside each other as they have several things in common. They are both almost exclusively seen in children due to the cartilaginous, compressible, soft nature of young bones. Which means you will often hear people say “they are the same thing” (in fact, if you google “buckle fractures” they often offer up beautiful examples of…greenstick fractures!) . But that just isn’t true; while they have things in common, they also have significant differences. Read on to find out…

Pelvic avulsion injuries

Cite this article as:
Owen Keane. Pelvic avulsion injuries, Don't Forget the Bubbles, 2019. Available at:

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.


Case courtesy of Dr Mark Holland , From the case rID: 16820


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.


Anatomy and Mechanics

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:

  • Ligaments, tendons and muscles are stronger than their bony apophyseal outgrowths.
  • Pubescent bone is subject to transient deficiencies in minerals during periods of rapid growth. The resulting porous bone is weaker and more susceptible to injury.
  • Chronic repetitive physical loading and tensile stresses across the musculotendinous attachment to an apophysis can predispose to acute avulsion type injuries.

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:

Radiographic Examples

Left AIIS avulsion. Results from strong eccentric contraction of long head of rec femoris while hip is extending, and knee flexed. Classically associated with kicking a ball.


Left ASIS avulsion – “Hip pointer”. Caused by sudden and forceful contraction of sartorius and tensor fascia lata. Occurs during hip extension (sprinting, swinging a bat). Image from Orthobullets.


Left ischial tuberosity avulsion. Caused by sudden forceful contraction of the hamstrings. Case courtesy of Dr Andrew Dixon, From the case rID: 30012


Left lesser trochanter avulsion. Caused by sudden forceful contraction of iliopsoas during sprinting.


Management, Prognosis and Recovery

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:

  • Protected weightbearing with crutches for 2-4 weeks until painless normal gait is achieved.
  • Gentle ROM and strengthening exercises from weeks 4-8 with physiotherapy.
  • Consider return to sport at 8-10 weeks if pain is minimal with squatting and jumping.
  • Return to full sporting activity should only be considered once the patient is pain free doing sports-specific movements.

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.–pediatric

Supracondylar Fractures

Cite this article as:
Lisa Dunlop. Supracondylar Fractures, Don't Forget the Bubbles, 2019. Available at:

Malcolm is 9 years old. He jumped off the swing at the play park but tripped and fell onto his outstretched hands. His left arm took the brunt and had severe pain and swelling in his left elbow after the injury. He attends the local Emergency Department and is informed that he has a supracondylar fracture of his humerus.

Scaphoid Fractures

Cite this article as:
Sarah Perkin. Scaphoid Fractures, Don't Forget the Bubbles, 2019. Available at:

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.


What is the scaphoid?

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.


How common is scaphoid fracture in children?

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.


Mechanism of Injury:

 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.


Examination Findings:

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.


Fracture Patterns in Children:

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.


Case Resolution

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.


Selected references

Abbasi D. Scaphoid Fracture. Orthobullets. Website. Available from:[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: [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.

Dental trauma

Cite this article as:
Orla Kelly. Dental trauma, Don't Forget the Bubbles, 2019. Available at:

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.

Which tooth is which?

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.

deciduous versus permanent tooth characteristics

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.

Tips and tricks in the ED: investigations you might consider

  • Chest x-ray: to check a lost tooth hasn’t been aspirated if the history is suggestive of an inhaled foreign body
  • Soft tissue x-ray: to check the soft tissue of the cheek and lips to find a lost toothy fragment if there is soft tissue swelling or a palpable embedded fragment.
  • Orthopantomogram: useful when there’s doubt as to whether a traumatised tooth is deciduous or permanent or whether a tooth that only has a very small portion visible in the mouth has intruded or is fractured.

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.

Tips and tricks in the ED: splinting teeth

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

  1. Hold the tooth by the crown (not the root) and lightly rinse the tooth with saline.
  2. Rinse the socket with 20-40 mL of saline solution and then pat dry with gauze.
  3. Gently reimplant tooth into a satisfactory anatomic position.
  4. Pat the tooth dry and apply skin glue to the edges of the tooth to adhere it to the adjacent teeth.
  5. Use either layers of steristrips or foil from a suture pack as a splint. NB if using foil, cut it to the appropriate size and round the edges to avoid injury.
  6. Secure the replanted tooth by applying skin glue to the inner aspect of the splint and outer surface of the target and one/both adjacent teeth.
  7. Hold the splint under pressure for about 1 minute.
  8. Confirm stability.

Dental follow-up

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”.

Pearls of wisdom

  • The emergency management of dental trauma in the ED is limited, however can have drastic positive implications if done correctly.
  • Avulsed primary teeth are for the tooth fairy, even if their sacrifice was premature.
  • Avulsed permanent teeth should be resuscitated within 60 minutes – store in milk, hold by crown, wash root and socket with saline and replace and splint ASAP
  • Things that look like they’re not in the right place – attempt replacement (permanent teeth only!)
  • Check and document sensation of the lower lip and chin – disruption of the mental nerve suggests mandibular trauma
  • Antibiotic cover when reimplanting avulsed teeth or in immunocompromised children
  • Tetanus tetanus tetanus
  • Head injury head injury head injury


How much does the tooth fairy leave?

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