COVID-19 and children: what do you need to know?

Cite this article as:
Boast A, Munro A. COVID-19 and children: what do you need to know?, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.23868

In late 2019, a new infectious disease emerged and spread to almost every continent, called COVID-19. As of March 11th 2020 it was declared a global pandemic by the World Health Organisation, meaning that is was being spread among multiple different countries around the world at the same time. It has changed the way we live our lives.

What we understand about SARS-CoV2 and COVID-19 has increased dramatically, with research being done at an extraordinary rate. For those of us whose business is looking after children, what do we need to know?

 

Editor’s note: This post is based on what we know today, Wednesday 15th of April 2020, and will be updated as new information becomes available.

 

What is COVID-19?

  • COVID-19 is the name of the disease caused by a new coronavirus, which has been named SARS-CoV-2. COVID-19 is the disease, and SARS-CoV-2 is the virus.
  • A coronavirus is a type of virus named after its unique appearance – with a ‘crown’ of proteins – when viewed with high power microscopy.
  • Coronaviruses very commonly infects humans (and some animals).
  • In humans, coronaviruses are a frequent cause of the ‘common’ cold – resulting in an upper respiratory tract infection with cough and coryza. There are, however, three types which can cause severe, even life-threatening disease in humans (SARS, MERS, and COVID-19).

 

What is the difference between COVID-19, SARS, and MERS?

Whilst they are all severe illnesses caused by coronaviruses, there are some important differences. Some useful things to consider include the R0 (how many people, on average, one case of the disease will spread to in others) and the Case Fatality Rate (CFR), an estimate of how many people who contract the disease will die from it. Neither of these statistics is hard and fast (and are both highly context-specific), but they provide a rough yardstick with which to compare infectious diseases.

  • SARS: This is an acronym for Severe Acute Respiratory Syndrome, a disease caused by the virus SARS-CoV. In 2002-3 the spread of SARS-CoV resulted in around 8,000 cases, with a CFR of approximately 10%. Similar to COVID-19, SARS-CoV originated in China, before spreading around the world, predominantly Europe, North America, and South America. The R0 from SARS is thought to be 3.
  • MERS: This is an acronym for Middle East Respiratory Syndrome, caused by the virus MERS-CoV . As the name suggested, it originated in the middle east in 2012, transmitted initially from camels to humans. MERS causes the most lethal infection of the coronaviruses, with a CFR of around 35%. The R0 from MERS is thought to be <1.
  • COVID-19:This is an acronym for COronaVIrus Disease 2019, the disease caused by the virus SARS-CoV-2. It is a zoonotic disease (meaning it was transmitted to humans from animals) and although the intermediate host has not yet been identified, it’s thought to most likely have originated in bats. It was initially identified in December 2019 in China, before spreading around the world. The CFR is unclear, as it is still uncertain how many people actually have the virus, and how many who currently are unwell will die from the disease. The overall CFR is thought to be about 1.3%. This is highly dependent on the country (and available health resources) but another significant factor is age, with only a handful of deaths reported in children <12 years who have confirmed COVID-19. The R0 for COVID-19 is still unclear but is thought to be 2-3.

 

What are the symptoms?

  • The symptoms of COVID-19 are similar to other respiratory viral infections. Importantly, in children the symptoms of COVID19 are more likely to be mild, and a significant proportion may be asymptomatic.
  • Infected children who are symptomatic most commonly present with cough and fever.
  • A small proportion of children also present with gastrointestinal symptoms (vomiting or diarrhoea) (~10%)
  • Sore throat and runny nose do not appear to be uncommon features in children (as opposed to adults)

 

How does COVID-19 affect children?

Evidence from across the globe (namely China, Spain, Italy and America), has shown that children are significantly less affected by COVID19 than adults. There are both fewer cases in children, and less children who are severely unwell. Younger infants appear to be most likely to be hospitalised. Overall, there have been only a small number of deaths in children with confirmed COVID-19 reported. A number of epidemiological and clinical papers on COVID-19 in children have been published, summarised on DFTB.

The exact reason why there are so few children with confirmed COVID-19 is unknown. Initially it was thought that due to the high rate of asymptomatic infection children were simply less likely to be swabbed and have confirmed infection. However, recent evidence from Iceland, Japan and Korea shows that children may also be less likely to become infected with SARS-CoV-2 following exposure.

It is yet unknown whether asymptomatic children can pass the infection on to others. In epidemiological studies children have not been found to have a significant role in household transmission. It appears children may continue to excrete the virus through their faeces (poo) for several weeks after the symptoms of infection have passed, but the role of this excretion in viral transmission is not clear (there is some evidence to show it is only viral particles rather than active virus). Regardless, hand hygiene remains of paramount importance in reducing spread.

 

If my child is unwell, can I give them ibuprofen?

There has been considerable social media interest in the use of ibuprofen in suspected or confirmed COVID-19. In the UK, the MHRA has deemed there is no evidence of increased risk of using ibuprofen even in cases of COVID-19.

 

What about neonates?

Neonates without comorbidities do not appear to be at an increased risk. A large number of case series having been published of babies born to mothers with COVID-19. Although some neonates have swabbed positive for SARS-CoV-2, there have been no reports of this being associated significant illness. Evidence about the possibility of transmission from mother to baby in the womb is currently unclear.

In the UK, the RCPCH has published guidelines (with the Royal College of Obstetrics and Gynaecology) recommending pregnant women with COVID-19 who are in labour should deliver their baby in an obstetric unit, however there is no need to separate mother and baby after birth, and the benefits of breast feeding outweigh any theoretical risks. Of note, the American Academy of Pediatrics has released conflicting guidelines, suggesting separation of the mother and baby.

 

What about children with chronic conditions?

There is limited data to guide us currently on how COVID-19 might affect children with underlying health conditions. There are small case studies of children with suppressed immune systems who have not developed severe illness, including children treated for cancer and inflammatory bowel disease. There is some evidence that children with respiratory or cardiovascular comorbidities may be at higher risk of hospitalisation, but it is still unclear. For children currently being treated for cancer, the UK Children’s Cancer and Leukaemia Group have posted guidance for families including which groups are extremely vulnerable and should be “shielding”.

 

Is there any treatment?

There is no proven treatment for COVID-19, however, there are many clinical trials underway for many different therapies. The WHO has clearly stated that experimental therapies should only be used in the context of a clinical trial. Hydroxychloroquine and remdesivir have been studied most extensively, but there remains no clear evidence of benefit. Importantly, hydroxychloroquine has been associated with significant adverse effects, highlighting the importance of its prescription only in the context of a clinical trial.

Notably, there are only a handful of clinical trials for children registered, so it is unlikely that any therapeutics will be widely used in children with COVID-19. As the disease is generally mild in children, it is not likely to often be necessary to provide anything further than supportive care.

Vaccines will hopefully provide protection against future outbreaks of COVID-19, though these are still early in the drug development pipeline and unlikely to be available this year.

 

What can I do to minimize my risk?

Two words – hand hygiene. As with other viruses spread by droplet (e.g. influenza) hand hygiene, particularly when out in public, plays a critical role in preventing transmission. Washing hands with soap and water, for an adequate amount of time, covering all areas of the hands is most effective. Hand sanitizer is effective, but no more so than usual hand washing

It is important to avoid contact with others who are acutely unwell. Wearing surgical masks will not protect you from respiratory viruses. Wearing one if you are unwell may protect others from your respiratory secretions.

Physical distancing is becoming increasingly important, with many countries now mandating various ‘lock-downs’. You should follow advice from your public health authorities, and it would be wise to reduce non essential physical or close personal contact with other people to a minimum 

 

What should I do if someone in my family becomes unwell?

 

Resources for health professionals

Many journals have made their COVID-19 resources open access including NEJMThe LancetBMJ, and JAMA

National professional resources can be found at:

 

Literature

For a comprehensive review of all paediatric English language literature to date which has informed this article please see our separate page for COVID-19 Evidence

More questions than answers

Cite this article as:
Andrew Tagg. More questions than answers, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.24133

Given the rapidly changing climate for all things COVID19 the DFTB wanted more information. We know our strength is in our community so we hosted a series of webinars linking healthcare workers with a special interest in paediatrics. No one person is an expert but we are all in the same situation facing similar challenges. These are some of the questions that came out of the discussions. With the proviso that information is changing on a daily basis and resources in terms of staff, space and stuff is different, let’s dive in.

This data is correct as of 19th March 2020. Please let us know in the comments if you spot anything new.

Science

NSAIDs

There has been a suggestion that non-steroidal agents are unsafe for use in SARS-CoV2-19 patients. As we have already seen the evidence for anything in the paediatric realm is very slim.  However, as of the 17th of March 2020 the WHO has recommended against using ibuprofen in patients with symptoms suggestive of COVID19. What does this mean in real terms? We don’t know which children are asymptomatic carriers.

If you look at the source of the message it is even more striking – the French health minister suggested that anti-inflammatory drugs could exacerbate symptoms. He suggested that we should not prescribe NSAID’s or cortisone/steroids to patients with suspected COVID19. Given that one of the few drugs that work in one of our more prevalent respiratory diseases, croup, is a steroid then I think we need to look to more evidence of harm over benefit. If you want a great, easy read on the matter then check out fullfact.org.

ACE-I

Very little is known on the potential impact of ACE inhibitors on COVID19 in adults, let alone children. The Venn diagram of children with the disease and on perindopril (say) is represented by two separate and distinct circles at the moment. If you are curious as to how there may be an interaction then read this great Tweetorial from Jonny Wilkinson.

It is also worth taking a looking at this letter in the Lancet to better understand the theory.

Fang L, Karakiulakis G, Roth M. Are patients with hypertension and diabetes mellitus at increased risk for COVID-19 infection?. The Lancet Respiratory Medicine. 2020 Mar 11.

Vaccines and various treatments

To claim that there is a cure just around the corner or that a certain combination of vitamins and herbs will keep the virus away is pure quackery. Rather than tell you what research is going on then dashing your hopes when there is a negative outcome we’ll reserve our judgement at this stage.

 

Sorting and Streaming

A common challenge mentioned by all sites is just how do we triage? How do we sort patients so that we are not mixing potentially infected with non-infected patients? There cannot be a one size fits all approach as the needs of a single provider clinic are every different from those of a district general hospital and these are very different from a tertiary paediatric centre. Rural and remote populations have different resources to the big, shiny hospitals complete with fish tanks and meerkat enclosures.

Triage

A number of hospitals are using a concierge based approach. As a patient approaches the department they are met by a greeter (who is usually a member of the nursing staff), dressed in full PPE. They help determine the first decision point – possible COVID19 or unlikely COVID19. The latter group is pretty easy to spot. Determining what patient sub-types fall into the former is more of a challenge. In the initial phase of the disease, most hospitals have looked for the presence of respiratory symptoms PLUS a fever. If you look at the published and pre-print paediatric data around 2/3 of children with the disease have a fever and a large proportion appear to be asymptomatic. A number of patients also present with predominantly GI symptoms. Should they be treated as potential carriers? (And who should change their nappies given they can shed SARS-CoV2-19 for up to 40 days?)

An alternative triage approach utilizes a more 21sst century solution with carers/patients logging important information on a tablet-style device before their secondary medical triage. This would require the user to clean the interface after use – something that is already tough.

Children with special medical needs

There is insufficient data to make hard and fast rules about the management of children with complex healthcare needs. Adults with multiple comorbidities have increased mortality so it is biologically plausible that the same will hold true in the paediatric population. Pre-notification of attendance can help as these kids are brought in via a different entrance.

Many places are trying to replace standard outpatient visits with telehealth options on an ad hoc basis with little guidelines available on how to do this without just picking up your own mobile phone. This is not an ideal solution but is being offered to many children with diabetes, chronic respiratory conditions or children with rheumatological conditions requiring immunosuppressive agents.

The RCPCH recommends that children who have an exacerbation of their chronic respiratory illness and require admission should be considered to have COVID19 until proven otherwise.

Internal streaming

Once the children have been streamed into a respiratory disease cohort should we assume they all have COVID19 until proven otherwise? Should we treat the patient with clinical bronchiolitis or croup as a potential carrier? And what about those that are wheezy but don’t have a fever? Just what do we do then?

The number of critically ill children presenting to the ED is likely to be small but it has been suggested that these are rapidly assessed and transported to a negative pressure room in PICU for the full workup, whether they need intubation or not.

Testing

Children do not come into the hospital on their own. They often bring carers, parents, grandparents, aunts and uncles. Adjusting the policy on attendant carers is a tough sell to those that are looking after the potentially infected child. Most mixed EDs seem to be keeping the family unit together for testing. It would be interesting to know if any tertiary paediatric centres are testing the grown-ups that come with the children.

Just how accurate is the PCR test? And just how long does it take a result to come back? We are looking into the former question and can sense the frustration around the latter. Cohorting patients in negative pressure rooms just waiting five days for a swab result is not helping us clear the decks. We should be mindful, though, that there are things we can control and things we cannot. This is one of those things we have no control over at the moment.

Mixed departments

Most of us do not have the luxury of working in a tertiary paediatric centre where the only adults are dressed as clowns or doctors (or doctor-clowns). Some departments are making provisions by moving their paediatric space to allow for adult overflow. The RCPCH has also stated that paediatricians should be prepared to see patients up to the age of 25. That makes sense in a mixed environment but one wonders what happens in centres that do not routinely see any adults. With outpatients and elective surgery being cancelled across hospitals, there is a potential surfeit of doctors with markedly reduced day to day work.

There is also the question of what happens in adult hospitals when a COVID19 positive sole parent gets admitted. What happens to their swab-negative child? In some cases, the decision has been to treat them as a boarder but this can make many staff members feel uncomfortable.

Sicker children

At the time of writing this the mortality in children is exceedingly low. This is very reassuring but business will continue as usual. Treatment options may be limited dependent on restrictions with regard to aerosol-generating procedures. There have been mixed messages as to whether nebulization of medication. leads to increased healthcare worker risk. Some places are now controlling the use of nebulized treatment, as well as mandating consultant approval of high flow nasal cannula oxygenation. In centre without access to a PICU on-site how are these children being managed? What have measures have paediatric retrieval services put in place to deal with the potential increase in referrals?

Intubation teams are already being considered at a number of sites – teams of doctors, similar to a MET team, that are ready to provide critical care at the sound of a bleep, in the hope that this will reduce exposure to one of the highest risk aerosol-generating procedures – intubation. In mixed adult/paediatric hospitals it is also important to consider the implications of intubation in a resource replete setting. Some hospitals are starting to consider this and set up ethics committees to set rules early and consider just who should have access to that last ventilator. The decision is not as easy as you think.

 

Stuff

Personal protective equipment

There have been some mixed messages about what type of PPE should be worn in what scenario.  Public Health England has this handy table to guide you and, as always, be mindful of your local guidelines if they differ.

Some hospitals are requiring all healthcare providers to undergo mandatory, face-to-face training in donning and doffing PPE prior to deployment. It has been suggested that we should wear the highest standard of PPE for every encounter in order to present nosocomial transmission. Unfortunately, supplies are limited and so we should use the most appropriate PPE for the task in hand.

Aerosol generating procedures

There seems to be a lot of confusion about what an aerosol-generating procedure is. As always, it is important to follow your local clinical guidelines. But if you disagree with them, then let the evidence guide you, and seek to change the guidelines. Concerns have been raised about everything from just examining the throat, using nebulizers (a daily question), and whether we should be using HME filters on the Neopuff. Rest assured we are looking at this and a blog post will follow.

 

Staffing

Rosters

We are already overstretched – both on the floor and in the back office. Corona conditions are making this even more apparent as we are wondering whether we should stretch our elastic workforce just that little bit more before the wave hits so that we have a rested and well cohort, ready to go. Those of us that work in mixed EDs know that paediatric workforce planning is furthest from our minds as we read of the Italian situation.

Should (when?) the pandemic stretch on for months considerations need to be given to staff longevity. Will there be a burnt-out generation of ED physicians who have seen and been exposed to too much? What about those who have had much-needed leave cancelled? Perhaps some of the daily load can be taken up with doctors from those specialities who have a lower case burden? Orthopaedic registrars could oversea minor-injuries clinics in a remote location. Dermatology trainees could answer the question of “What on earth is that rash?” in a medical/non-COVID assessment area?

Healthcare workers that work across sites are already being asked to reduce cross-campus travel.

Though we go to work for our patients we also need to be mindful that we too may become patients. None of us is immune to catching the disease. In its mild form, it will be an inconvenience to us, our loved ones, and our colleagues. But healthcare workers will die. Healthcare workers have already died. How do we mitigate the risks for the more vulnerable? What should we do with the older, more at-risk, paediatrician, the immunosuppressed healthcare worker, the pregnant trainee? These are questions that have not yet been answered.

Everyday life

As we are being asked to work longer hours how many hospitals have made provision for routine, everyday tasks? How many have designated areas for staff to catch some sleep before driving home? How many are providing scrubs for staff to change into or are helping with the laundry? The last thing most of us feel like when we get home is loading up the washing machine (and then putting it out to dry. But how clean are your everyday clothes? Your stethoscope? Your phone?

How are workplaces supporting that other basic physiological need – food? With supermarkets reducing their opening hours how are healthcare workers being supported? McDonald’s in the UK is offering free drinks to those with NHS cards but you can only last so long on caffeinated brown water.

Information dissemination

The situation with SARS-CoV19-2 is a rapidly evolving one with advice changing on a daily basis. Most hospitals have set up incident management teams that meet at an executive level to discuss the changes that may impact our day to day – cancelling elective surgery, moving departments. Making sure that information trickles down from an operational level to a clinical level can be hard, especially with a workforce that might be relying on bank or agency staff. A lot of departments are trialling WhatsApp groups as a means of sharing the very latest information but it is still possible for a key piece of information to be lost in the stream.

Education

Most hospitals have now cancelled face-to-face education sessions. There are plenty of of resources available to help educators plan sessions remotely. This series from ALiEM is the standout.  The DFTB team hope to be adding more resources for you shortly (especially if we get put in isolation).

Students

A number of universities have pulled their students from clinical placements or placed restrictions on their interactions with patients e.g. not to see a respiratory patient. Many feel that they should be doing something and a number of great initiatives have been suggested. One group has launched a childcare service for healthcare providers. With schools in the UK due to close early for the Easter break this will come as a welcome relief to many who may usually rely on (at-risk) relatives. It has also been suggested that they would make excellent scribes to speed up the standard clerking process. Let us know what else is going on.

Morale

At the moment we are all nervous anticipation, stepping over wavelets or paddling our boards out ready to catch the big wave. This sense of nervous excitement is palpable in the emergency room. The feeling getting is getting stronger as regular hospital services wind down. How do we maintain our own morale in the face of hard shifts? How do we look after each other when a colleague gets ill? How do we make sure that strangers fro other services are welcome in the safe space we call work?

 

At this time of great uncertainty, it is important that we remain kind, that we show #PandemicKindness to those we meet. Everyone is working their hardest and to the best of their abilities. Take time to recognise that, whether it is the security officer that has to ask you for your ID to allow you into the building or the cleaners that we rely on. Take your time to thank them for their hard work, offer them a coffee (or a tea if they are in the Northern hemisphere. Remember that the ED is often overstretched so that serum rhubarb may not have been ordered. Be mindful that those of us who are dealing with adults as patients too and recognise that they need our kindness now, more than ever.

Please feel free to answer any of these questions in the comments section. Share your resources, your experiences, so that we may learn from each other. E-mail us at hello@dontforgetthebubbles.com with your ideas and suggestions. And be safe.

Communicating with children with additional needs: Liz Herrieven at DFTB19

Cite this article as:
Team DFTB. Communicating with children with additional needs: Liz Herrieven at DFTB19, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.21387

Communication is vitally important in so much we do as clinicians.  Without good communication we can’t hope to get a decent history, properly examine our patient, explain what we think is going on or ensure appropriate management.

Prematurity for the acute paediatrician: Camilla Kingdon at DFTB19

Cite this article as:
Team DFTB. Prematurity for the acute paediatrician: Camilla Kingdon at DFTB19, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.22288

Camilla Kingdon is the Vice President for Education and Development at the Royal College of Paediatrics and Child Health. Her day job is working as a neonatologist at Evelina London Children’s Hospital.

Whilst the core work of a neonatologist takes place behind closed doors in the safety and security of the NICU babies do not choose where or when they are born. Sometimes, just sometimes, they like to surprise us and pop out early, when we least expect it. What do we do then?

 
 
#doodlemedicine sketch by @char_durand 

 

This talk was recorded live at DFTB19 in London, England. With the theme of  “The Journey” we wanted to consider the journeys our patients and their families go on, both metaphorical and literal. DFTB20 will be held in Brisbane, Australia.

If you want our podcasts delivered straight to your listening device then subscribe to our iTunes feed or check out the RSS feed. If you are more a fan of the visual medium then subscribe to our YouTube channel. Please embrace the spirit of FOAMed and spread the word.

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Ankle sprains

Cite this article as:
Neil Thomspon. Ankle sprains, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.22248

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)

OR

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

OR

  • 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

OR

  • bone tenderness at the navicular

OR

  • 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:
https://doi.org/10.31440/DFTB.23718

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!

 

References

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

 

Taking your trauma team to the next level: Anna Dobbie at DFTB19

Cite this article as:
Team DFTB. Taking your trauma team to the next level: Anna Dobbie at DFTB19, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.22066

Anna Dobbie works in HEMS, PEM, and Adult ED and is a badass at all of them. She is the person you’d want leading your trauma team. Want to be just a little more like Anna? Then watch her talk and find out how to step up.

As we are so fond of saying, “You set the tone.” That first two minutes of any resus is critical – and not just because of the decisions you make. If you can appear calm and in control, your teams’ actions will reflect that. Running every trauma call the same allows for cognitive off-loading as some behaviours become automatic. Whether they are ‘real’ calls or not so serious ones the team is expected to act the same either way.

 

 
 
DoodleMedicine sketch by @char_durand 
 

This talk was recorded live at DFTB19 in London, England. With the theme of  “The Journey” we wanted to consider the journeys our patients and their families go on, both metaphorical and literal. DFTB20 will be held in Brisbane, Australia.

If you want our podcasts delivered straight to your listening device then subscribe to our iTunes feed or check out the RSS feed. If you are more a fan of the visual medium then subscribe to our YouTube channel. Please embrace the spirit of FOAMed and spread the word.

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Orbital fractures

Cite this article as:
Orla Kelly. Orbital fractures, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.21843

Epidemiology

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.

Anatomy

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 www.emj.bmj.com

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

Pearls

  • 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

Surviving Sepsis Campaign International Guidelines

Cite this article as:
Damian Roland. Surviving Sepsis Campaign International Guidelines, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.23460

The lens with which you view sepsis is dependent on the environment and emotion in which you associate the term. For a parent, this may be the spectrum from having never heard the term before “Your child is well enough to go home, we’ve ruled out sepsis and other serious conditions” to the anguish of being told, “I’m afraid your child died of sepsis“. This spectrum remains equally wide for health care professionals. A family doctor or general practitioner may never see a case of confirmed sepsis, and an emergency clinician can potentially go years between seeing a truly shocked child. An intensivist, however, may deal with the consequences on a weekly basis. Even in the last month, we have seen two papers from the same publishing group; one highlighting the global burden of sepsis and the other challenging the current hype surrounding its recognition and management.

Regardless of your viewpoint, the publication of the Surviving Sepsis campaign’s international guidance will have been of interest.

 

Weiss, S.L., Peters, M.J., Alhazzani, W. et al. Surviving sepsis campaign international guidelines for the management of septic shock and sepsis-associated organ dysfunction in children. Intensive Care Med 46, 10–67 (2020). https://doi.org/10.1007/s00134-019-05878-6

 

It is important to recognize two features of this publication which should carry an important health warning in its interpretation.

The first is that the authors are clear that they are focusing on severe sepsis or septic shock. While in adult practice definitions have changed, these have not been formalized or ratified for children:

 

“For the purposes of these guidelines, we define septic shock in children as severe infection leading to cardiovascular dysfunction (including hypotension, need for treatment with a vasoactive medication, or impaired perfusion) and “sepsis-associated organ dysfunction” in children as severe infection leading to cardiovascular and/or non-cardiovascular organ dysfunction.”

 

The authors clearly recognize that the absence of a clear definition of paediatric sepsis is challenging health care providers and organizations. The group has steered away from suggesting management options in the ‘pre-sepsis’ group i.e. those children with potential infections that may result in sepsis and have physiological instability but without organ dysfunction. They suggest that management practices for this group aren’t radically different, however:

 

Even though these guidelines are not intended to address the management of infection with or without SIRS when there is not associated acute organ dysfunction, we recognize that sepsis exists as a spectrum and some children without known acute organ dysfunction may still benefit from similar therapies as those with known organ dysfunction

 

The second is that this is a consensus document. It is neither a systematic review nor a clinical practice guideline (in a local hospital sense). It comprises the opinions of an expert group of clinicians (49 in fact) from a variety of international settings using the best available evidence. The publication is essentially a list of recommendations. This approach is valid in situations where evidence may be heterogeneous and that randomized controlled trials can not be performed for all possible permutations of clinical practice. As with all things in science, however robust the data is, it still needs interpreting and that interpretation is subject to all manner of explicit and implicit bias.

 

The panel supports that these guidelines should constitute a general scheme of “best practice,” but that translation to treatment algorithms or bundles and standards of care will need to account for variation in the availability of local healthcare resources.

 

Without becoming meta it’s important that this blog itself needs a health warning. It’s an interpretation of an interpretation of evidence.

So the big-ticket items

1. A child was defined as beyond 37 weeks gestation and up to 18 years old.

2. They apply to children with severe sepsis or septic shock as defined by the 2005 International Pediatric Sepsis Consensus Conference or inclusive of severe infection leading to life-threatening organ dysfunction.

2005 definition:

  • greater than or equal to two age-based systemic inflammatory response syndrome (SIRS) criteria
  • confirmed or suspected invasive infection, and cardiovascular dysfunction
  • acute respiratory distress syndrome (ARDS), or greater than or equal to two non-cardiovascular organ system dysfunctions

Septic shock was defined as the subset with cardiovascular dysfunction, which included hypotension, treatment with a vasoactive medication, or impaired perfusion.

3. Panel members were selected through recommendations from chairs and vice-chairs of the 12 worldwide member organizations. Each panel member was required to be a practicing healthcare professional with a focus on the acute and/or emergent care of critically ill children with septic shock or other sepsis-associated acute organ dysfunction. There was lay representation and the final membership was felt to be demographically diverse with regard to sex, race, and geography.

4. The panel was assisted by various methodological experts and split into six groups

  • recognition and management of infection
  • hemodynamics and resuscitation
  • ventilation
  • endocrine and metabolic therapies
  • adjunctive therapies
  • review research priorities in pediatric sepsis

5. A list of critical questions was developed in the PICO format (Population, Intervention, Control, and Outcome) which was then rigorously searched for by a specialist medical librarian and the resulting literature assessed according to GRADE criteria a well-recognized methodology for systemically presenting summaries of evidence.

6. Following discussion and debate recommendations would be made:

 

We classified recommendations as strong or weak using the language “We recommend…” or “We suggest…” respectively. We judged a strong recommendation in favor of an intervention to have desirable effects of adherence that will clearly outweigh the undesirable effects. We judged a weak recommendation in favor of an intervention to have desirable consequences of adherence that will probably outweigh the undesirable consequences, but confidence is diminished either because the quality of evidence was low or the benefits and risks were closely balanced.

 

The paper goes into considerable detail (which is why it is 55 pages long) into the rationale behind the recommendations. They are all summarised in the appendix (commencing page e102). It is beyond the scope of this blog to explore all the recommendations in detail, and it is important that health care providers read the paper itself. The following highlights some of the areas which may prompt debate or query.

 

‘Screening’ remains in

For those in emergency and acute care, this recommendation may have come as a surprise given a large amount of anecdotal feedback and experience suggesting that current screening mechanisms for the un-differentiated child are neither specific nor sensitive. It is worth nothing again the panel was looking at severe sepsis or shock and the evidence for ‘bundles’ of care i.e. targeted or mandated treatments once recognized is relatively robust. There is a further section on protocols/guidelines for treatment but it may have been useful to separate the afferent limb (recognition) from the efferent limb (response) in relation to collated evidence. This is important as the evidence for ‘bundles’ is cited under screening, with minimal evidence of screening approaches alone put forward (or to be fair to the panel perhaps of insufficient quality to make a judgment on).

Although subtle I think the panel recognized how important local buy-in is in relation to quality improvement. Of note, there is nothing on national guidance for recognizing sepsis. They also highlight how blindly integrating screening with any other scoring system may not be as beneficial as believed.

Ultimately no one particular screening system is recommended.

 

There is no target lactate

There appears to be a palpable sense of regret that the evidence didn’t support any particular threshold for lactate. Despite evidence of rising mortality with increasing lactate, the panel was not able to determine a specific level.

However, no RCTs have tested whether initial or serial measurement of blood lactate directly informs evaluation and/or management in children. Lactate levels should, therefore, be interpreted as a part of a more comprehensive assessment of clinical status and perfusion.

 

Take blood cultures but don’t delay treatment to obtain them

Appreciating this isn’t a particularly scientific response, but well, duh.

 

One hour time to treatment for those in shock but up to three hours without it. 

This is the potential game-changer from this body of work. While the evidence shows a temporal relationship between the administration of antibiotics and outcome in severe sepsis some pooled data demonstrated that it was unlikely the hour alone made the difference. Given the numerous papers showing a linear relationship between time to administration and outcome the ‘golden hour” was maintained. In the absence of shock, the panel felt, based on data showing a three-hour threshold effect, this would be a reasonable time point. This will be a welcome relief for those working in areas where there are associated penalties for not reaching the hour window and hopefully will remove some of the gaming associated with this target.

 

Broad spectrums antibiotics, but narrow when pathogens available

Little controversy here. The panel highlight that 48 hours should be the maximum time that is allowed to pass before re-evaluation in the absence of culture growth rather than a standard time to elapse.

If no pathogen is identified, we recommend narrowing or stopping empiric antimicrobial therapy according to clinical presentation, site of infection, host risk factors, and adequacy of clinical improvement in discussion with infectious disease and/or microbiological expert advice.

There are a number of recommendations on immunocompromised children and source control which appear pragmatic.

 

Bolus if intensive care available, if not then don’t unless documented hypotension

In units with access to intensive care, 40-60ml/kg bolus fluid (10-20ml/kg per bolus) over the first hour is recommended. With no intensive care, and in the absence of hypotension, then avoiding bolus and just commencing maintenance is recommended. It is not clear how long access to intensive care has to be to switch from fluid liberal to restrictive.

**Post-publication note (13/02/20): A more correct description of no intensive care would be “in health systems with no access to intensive care”. The guidance states, “For children with septic shock without signs of fluid overload in low-resource settings where advanced supportive and intensive care is not available, the panel recommends against bolus fluid administration,”. This question is raised in the comments section below as for units in without intensive care on site but it will resourced health systems then ‘access’ to intensive care should be assumed**

For purposes of this weak recommendation, hypotension can be defined as:

 

The panel suggests crystalloids, rather than albumin, and balanced/buffered crystalloids rather than 0.9% saline. They recommend against using starches or gelatin.

 

Use advanced haemodynamic variables, not bedside clinical signs in isolation

The evidence didn’t support a target mean arterial blood pressure but suggested avoiding using clinical signs to differentiate into cold and warm shock. No one monitoring approach was advised but included cardiac output, cardiac index, systemic vascular resistance, and central venous oxygen saturation.

 

Intensive care vasoactive and ventilation management is given but acknowledged as weak recommendations 

There is a list of suggestions regarding vasoactive infusion and ventilatory strategies that are very specific to intensive care management. While a number of recommendations are given (epinephrine rather than dopamine for septic shock for example) these are generally based on the panels summation of weak evidence.

There are further suggestions on corticosteroid management, nutrition, and blood products which will be of interest to those in intensive care and anaesthetic settings.

 

Summary

This is a very rich piece of work that is well structured and easy to read (even if you are not an expert on a particular field of practice). For most paediatricians there is unlikely to be an immediate change in practice but the softening of antibiotic time to delivery in the non-shocked child and emphasis of local review of sepsis incidence and performance will be welcome. How these filter into national guidance will be determined country by country but it is unlikely that radically different views can be drawn from the available evidence. What is still sorely needed is a working definition for the non-hypotensive child with sepsis (or an acknowledgment that perhaps this isn’t really a clinical entity…)

 

All Things Patella

Cite this article as:
Tadgh Moriarty. All Things Patella, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.22204

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.     

Incidence

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

 

Mechanism

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

 

Presentation

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.

 

Treatment

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.

 

Imaging

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.

 

Controversies

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.

 Incidence

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.

 

Mechanism

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.

 

Presentation

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.

 

Imaging

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.

 

Treatment

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.

 

Controversies

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….

Incidence

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.

 

Mechanism

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.

 

Presentation

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.

 

Imaging

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.

Treatment

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.

 

 

References

  • 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”, orthoinfo.aaos.org, 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

 

 

 

Back to School

Cite this article as:
Andrew Tagg. Back to School, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.23086

It’s the first day of school here in Australia and parents and carers are waving their young children off with a kiss for their first day.  When I first saw the size of school bags I was amazed. How can children carry so much? Surely they will just fall over and lie on their backs waving their little legs in the air like distressed turtles? What on earth are they carrying in there that needs the Bag of Holding?*

 

 

What’s the problem?

Barbosa J, Marques MC, Izquierdo M, Neiva HP, Barbosa TM, Ramírez-Vélez R, Alonso-Martínez AM, García-Hermoso A, Aguado-Jimenez R, Marinho DA. Schoolbag weight carriage in Portuguese children and adolescents: a cross-sectional study comparing possible influencing factors. BMC pediatrics. 2019 Dec;19(1):157.

With reduced access to lockers, it seems that children are taking the weight of the world on their shoulders. Surprisingly, this Portuguese group found that Grade 5 children carried more than Grade 9 kids. This trend has been replicated in New Zealand with Grade 3 kids carrying around 7kg (13.2% of their body weight) and Grade 6 leavers bearing only 6.3Kg (10.3% body weight). Most school items have a set weight, no matter what grade you are in, but one might have thought that as the educational load increases over the years so might the weight of the textbooks. Perhaps an increase in the use of personal electronic devices and e-books accounts for some of this difference.

Surely carrying those giant bags can’t be good for the growing body? Neck, back, and shoulder pain are prevalent in adolescents and are closely linked by carrying heavy school bags. These effects take place when the bag weighs more than 10% of their body weight. In nearly every study girls carry more than boys. This makes sense as although they may carry exactly the same things in their rucksacks girls are generally lighter and so the weight of their bag, as a percentage of their total body weight, is higher.

 

Mandrekar S, Chavhan D, Shyam AK, Sancheti PK. Effects of carrying school bags on cervical and shoulder posture in static and dynamic conditions in adolescent students. International journal of adolescent medicine and health. 2019 Oct 30.

This group looked at how they carry their bags. Trying to be cool and swinging your bag over just one shoulder changes one’s static biomechanics.  The head and neck move forward to compensate and the carrying shoulder rises. Then, because the centre of gravity is shifted the subject would tilt their torso away. Could this be the cause of the stereotypical teenage posture? It took just five minutes of bag wearing for any postural changes to become evident. It has also been suggested that a heavier bag weight is associated with an increased incidence of lower back pain in teens and this, in turn, is linked with an increased risk of lower back pain as an adult.

If they are not wearing their back slung over one shoulder they are wearing it slung low, rather than high and tight on their shoulders, and most of the biomechanic data suggests this puts a lower degree of stress on their lumbar spines than letting it ride high. The higher position also lends itself to more forward rotation of the pelvis and greater hip flexion. And, of course, wearing your bag on the front, instead of on the back, causes a whole new range of issues.

Harmless?

Whilst this post is focusing on just one potential downside of heavy school bags, Wierseema et al. found 247 children with injuries related to backpack use between 1999-2000. These were due to tripping over them (28%), getting hit by one (13%) or just trying to put them on (8%). Actually wearing the thing was associated with another 13% of complaints – specifically back pain.

There is also a condition called backpack palsy or, to be more accurate, backpack brachial plexus palsy. It is much more common in military recruits but can occur in children. Often unilateral, the paraesthesia, pain and sensory loss in addition to possible muscle wasting are due to neuropraxia of the brachial plexus.

Losing weight?

Does it make a difference if teenagers take some of the rubbish out of their bags?

Rodríguez-Oviedo P, Santiago-Pérez MI, Pérez-Ríos M, Gómez-Fernández D, Fernández-Alonso A, Carreira-Núñez I, García-Pacios P, Ruano-Ravina A. Backpack weight and back pain reduction: effect of an intervention in adolescents. Pediatric research. 2018 Jul;84(1):34.

This Spanish group targetted teenagers with an educational intervention. This comprised of a one-hour session on posture, the effects of backpack weight and some healthy lifestyle advice. They found that the intervention arm of the trial did indeed have (statistically significant) lighter bags moving forward in the younger cohorts but not in the older ones.

Strapping in?

Mathur H, Desai A, Khan SA. To determine the efficacy of addition of horizontal waist strap to the traditional double shoulder strap school backpack loading on cervical and shoulder posture in Indian school-going children. Int J Phys Med Rehabil. 2017;5(434):2.

If you want to reduce the usual bag-induced postural slump these authors, looking at 60 children, suggest that adding a waist strap to the usual two shoulder straps could make all the difference.

So what does this all mean?

As parents, we need to keep an eye on what our children are actually putting in their bags (compared to what they say they are putting in there). Perhaps we should weigh the bags as often as the children and limit the number of keyrings and Beanie Boos attached to the outside? Perhaps we need to further embrace technology and allow for the increased use of electronic devices coupled with a much, much older technology and let them use bags on wheels, similar to carry on luggage?

There have been a number of initiatives to make the wearing of school backpacks healthier. Sri Lanka introduced a National Healthy Schoolbag Campaign aimed at improving the lives of children. Large textbooks were split into smaller volumes to make it easier to carry just one small book around and a multidisciplinary schoolbag regulatory council was set up to liaise with industry partners to help regulate bags. In the US the “Pack it light, wear it right” initiative focussed on what the individual could do.

 

*If you really want to know what is in their bags you need to look inside. This wonderful paper from Archives suggests that the vast majority (96%) of parents had never checked the weight of their children’s bags and 34% had never even looked inside

Forjuoh SN, Little D, Schuchmann JA, Lane BL. Parental knowledge of school backpack weight and contents. Archives of disease in childhood. 2003 Jan 1;88(1):18-9.

 

Other Selected References:

American Academy of Pediatrics. How not to wear a school backpack. AAP Grand Rounds. 2008 Nov 1;20(5):58-9.

Brackley HM, Stevenson JM. Are children’s backpack weight limits enough?: A critical review of the relevant literature. Spine. 2004 Oct 1;29(19):2184-90.

Kim KE, Kim EJ. Incidence and risk factors for backpack palsy in young Korean soldiers. Journal of the Royal Army Medical Corps. 2016 Feb 1;162(1):35-8.

Goodgold S, Corcoran M, Gamache D, Gillis J, Guerin J, Coyle JQ. Backpack use in children. Pediatric physical therapy: the official publication of the Section on Pediatrics of the American Physical Therapy Association. 2002;14(3):122-31.

Jayaratne K, Jacobs K, Fernando D. Global healthy backpack initiatives. Work. 2012 Jan 1;41(Supplement 1):5553-7.

Maurya S, Singh M, Bhandari PS, Bhatti TS. Backpack brachial plexus palsy. Indian Journal of Neurotrauma. 2009 Dec;6(02):153-4.

Rose K, Davies A, Pitt M, Ratnasinghe D, D’Argenzio L. Backpack palsy: A rare complication of backpack use in children and young adults–A new case report. european journal of paediatric neurology. 2016 Sep 1;20(5):750-3.

Talbott NR, Bhattacharya A, Davis KG, Shukla R, Levin L. School backpacks: it’s more than just a weight problem. Work. 2009 Jan 1;34(4):481-94.

Weir E. Avoiding the back-to-school backache. CMAJ: Canadian Medical Association journal= journal de l’Association medicale canadienne. 2002 Sep;167(6):669-.

Wiersema BM, Wall EJ, Foad SL. Acute backpack injuries in children. Pediatrics. 2003 Jan 1;111(1):163-6.

Diabetic Ketoacidosis

Cite this article as:
Dani Hall. Diabetic Ketoacidosis, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.22689

Maisie is 2 years old. Apart from a few coughs and colds, she is usually a very well, happy little girl. She’s been a bit poorly for the last 48 hours – a bit off colour, off her food, lethargic and just not her usual cheeky self.

She’s been drinking though and has had good wet nappies. In triage she has a runny nose and slight cough. She is pretty tachycardic and tachypnoeic and doesn’t look well and so she’s moved to majors.

Maisie is put on a monitor and immediately you can see that her respiratory rate is elevated at 40 breaths per minute with saturations of 97% in air. Her heart rate is also elevated at 150 beats per minute with a normal blood pressure of 105/65. Her capillary refill time is 3 seconds peripherally and she is afebrile.

Her heart sounds are normal, her chest is clear and her abdomen is soft although mildly tender throughout.

The only objective thing you have is the tachypnoea with a bit of a runny nose. You wonder if she has viral induced wheeze and is just too tight for the wheeze to be audible so you prescribe salbutamol and review after 10 minutes. But that’s made no difference to her respiratory rate, and her chest is still completely clear.

Things just don’t add up. She’s holding her tummy – perhaps her tachypnoea and tachycardia are secondary to pain. Her abdomen remains soft with no guarding, but she doesn’t like you palpating it. Could this be appendicitis? Or even worse an intussusception? You speak to the paediatric surgeon who asks you to cannulate Maisie and send some blood. They’ll be down to review her shortly.

You cannulate Maisie and take a venous gas. The results seem to take an age. And your heart sinks when you see them…

She’s acidotic at 7.15 and it looks metabolic with a bicarbonate of 13.9 and base deficit of minus 8.7. Her lactate is 2.9 and her glucose is very high at 29.5. You run a drop of Maisie’s blood through the bedside ketone monitor. Her blood beta-hydroxybutyrate is. 5.1.

This is diabetic ketoacidosis.

 

DKA can be really difficult to diagnose in toddlers

Classically children with DKA present with polyuria and polydipsia with abdominal pain, nausea, and vomiting. This can progress to dehydration, weakness, and in severe cases, they may be lethargic. Blood tests show a raised white cell count as a physiological response to the raised stress hormones, cortisol and catecholamines, and so are not a reliable indicator of infection. But, and this is a big but, an infection can precipitate DKA so it is important it is considered.

Although ketoacidosis may result in a classic ‘pear drop/acetone’ smell to the breath, not everyone has the chemoreceptors to detect it.

Common misdiagnoses include dehydration secondary to infection or respiratory presentations. Ketoacids stimulate the respiratory centre resulting in rapid fast breathing – Kussmaul breathing – blowing off carbon dioxide to compensate for the metabolic acidosis. It may also present as an acute abdomen as abdominal pain and ileus can result from hypokalaemia, acidosis, and poor gut perfusion. If opioids are given for pain this can suppress the Kussmaul breathing leading to worsening acidosis

The BSPED (2020), and ISPAD definitions of DKA are:

acidotic with a bicarbonate of <15 mmol/l or a pH <7.3 and ketones of >3.0 mmol per litre

However… just when you starting thinking it was easy… children with known diabetes may develop DKA with normal glucose and so you must keep a high index of suspicion and check pH and ketones in an unwell child with diabetes.

Lack of insulin leads to rising blood glucose levels in the bloodstream. However, this glucose is not transported into the cells and so the body needs to produce an alternative energy source for cellular activity. Three processes occur:

  • muscle is broken down to mobilise amino acids which are then used to create glucose (catabolism)
  • fat is broken down to produce glycol and ketones (lipolysis)
  • the liver uses lactate, glycol and amino acids to create more glucose (gluconeogenesis)

High ketone levels lead to metabolic acidosis.

Hyperglycaemia leads to glucose spilling into the urine (glycosuria). These glucose molecules exert an osmotic pull, dragging water, cations, and anions such as phosphate, potassium, and sodium into the urine (osmotic diuresis). The child becomes dehydrated with physiologically low levels of potassium and phosphate. Ketones also spill into the urine (ketonuria) in preference to chloride, which is retained in the plasma, leading to a worsening chloride-driven acidosis.

Maisie is dehydrated because of the osmotic diuresis exerted by the glucose in her urine. And she’s acidotic because of the ketones circulating in her bloodstream. The question is, what are we going to do about this?

The complications of DKA have incredibly high mortality and morbidity, so we’re going to start here.

Cerebral oedema

Cerebral oedema occurs in approximately 1% of children with DKA. While relatively rare, it can have devastating consequences with mortality of approximately 25%. In fact, more than half of all diabetes-related deaths in children are caused by cerebral injury.

Cerebral oedema usually occurs within the first four to 12 hours of starting treatment for DKA, suggesting that it’s the treatment itself that precipitates cerebral oedema.

Risk factors for cerebral oedema in DKA can be split into two groups.

The first group is characterised by children who have a longer duration of symptoms and are therefore more severely dehydrated at presentation. Younger children, particularly toddlers, and children who present in DKA without a previous diagnosis of diabetes mellitus, fall into this group, most likely because they have been in DKA for a long period of time before the diagnosis is made.

The second group is children who develop cerebral oedema because of the treatment they have received. Giving insulin within the first hour of treatment increases the risk of cerebral oedema – the theory is that the usually inactive sodium-hydrogen ion exchange pump is activated by the double hit of high intracellular hydrogen ions early in treatment while children are more acidotic plus insulin crossing the leaky blood-brain-barrier. The exchange pump transports sodium into the intracellular fluid, which then drags water with it due to its osmotic effect, leading to cerebral oedema.

Giving bicarbonate also increases the risk of cerebral oedema. The physiological mechanism of this is unclear but there is some thought that giving bicarbonate to correct acidosis can worsen tissue hypoxia due to effects on 2,3-DPG in erythrocytes (remember acidosis shifts the oxygen dissociation curve to the right, increasing the affinity of haemoglobin and oxygen) or that giving bicarbonate may lead to preferential movement of carbon dioxide across the blood-brain barrier, both of which will promote acidosis and poor oxygen offload in the CSF. However, whatever the cause, it is clear from a systematic review published in 2011 by Chua et al that giving bicarbonate to children with DKA is linked with increased rates of cerebral oedema. The guidance, therefore, mandates that bicarbonate should not be used routinely to correct acidosis. Fluids and insulin will do that by improving skin perfusion and reducing ketosis. Only give bicarbonate if the acidosis is resulting in reduced cardiac function, and then give very carefully…

So, with that in mind, how are we going to treat Maisie?

ABC resuscitation

The initial management of a child with DKA follows the principles laid out in APLS: ABC resuscitation.

If a child is obtunded and not protecting their own airway then they should be intubated because of the risk of airway obstruction. However, intubation in DKA is risky… both sedation and the resultant hypercarbia can cause cerebral herniation. Central lines are also risky in these children because of the increased risk of thrombosis. Only use them if absolutely necessary and remove them as soon as possible.

Luckily, Maisie is maintaining her own airway, her GCS is 15 and she is not obtunded. The airway is not a problem for her.

After managing the airway and breathing we move onto circulation. So the question is: should we give Maisie a fluid bolus?

This is a big question.  We are taught that children with cardiovascular compromise should receive fluid boluses to support their circulation.  But assessing cardiovascular compromise in children with DKA can be very challenging. Clinical evaluation of hydration and shock is very difficult in children with DKA. Acidosis drives tachycardia and reduces peripheral skin perfusion.

Koves et al set out to look at this by studying a group of 37 children under 18 presenting with DKA.

Emergency Department doctors recorded heart rate, respiratory rate, blood pressure, cool peripheries, capillary refill time, skin turgor, the presence or absence of sunken eyes and dry mucous membranes to provide a clinical estimate of dehydration. A second emergency department doctor, blinded to the clinical interpretations of the primary doctor, was asked to review the patient before treatment and record their assessment of the same clinical variables. There was a good clinical correlation between the two assessments. Following admission, the children’s weights were measured daily until discharge and percentage dehydration was calculated from the weight gain from admission to discharge.

There was no agreement between assessed and measured dehydration. There was a tendency to overestimate dehydration in children with <6% measured dehydration and underestimate in children >6% dehydrated.

It’s a tricky business and these same parameters clearly won’t be of use in estimating shock in these children.

A true assessment of shock in DKA should rely on assessment on blood pressure measurements and peripheral pulse volume. So that doesn’t really help us. Maisie’s blood pressure and pulse volumes are normal so she’s not shocked. But she clearly is dehydrated. 

BSPED (2020) uses pH and bicarbonate to classify the severity of DKA:

  • pH 7.2–7.29 or bicarbonate <15 mmol/l is mild DKA with 5% dehydration
  • pH 7.1–7.19 or bicarbonate <10 mmol/l is moderate DKA with 7% dehydration
  • pH < 7.1 or bicarbonate <5 mmol/l is severe DKA with 10% dehydration

So, are we going to give her a fluid bolus?  Let’s turn to the guidelines…

BSPED 2020 states:

Any child in DKA presenting with shock (as per the APLS definition of tachycardia and prolonged capillary refill time) should receive a 20 ml/kg bolus of 0.9% saline over 15 minutes. Let’s call this a ‘resuscitation bolus’.

Further 10 ml/kg boluses may be given if required up to a total of 40 ml/kg. Then add inotropes if the child remains shocked.

Boluses given to treat shock should NOT be subtracted from the calculated fluid deficit.

All children with DKA, whether mild, moderate or severe, who require IV fluids should receive an initial 10 ml/kg bolus over 60 minutes. Let’s call this a ‘rehydration bolus’. This bolus SHOULD be subtracted from the calculated fluid deficit.

The American Academy of Pediatrics, agrees that all children with DKA should have a bolus of 10ml/kg over 30 minutes to an hour. If a child is critically unwell with hypovolaemic shock, then additional boluses of 20ml/kg of 0.9% saline should be given.

Australian guidelines vary depending on region – from no routine fluid boluses to 10-20 ml/kg 0.9% saline for the sickest. Some say subtract fluid boluses from rehydration calculations, others don’t. There is no clear consensus.

So why is there so much international variation?

Traditionally, we have been warned about the danger of causing cerebral oedema in children with DKA by giving them too much fluid, reducing serum osmolality and literally flooding the brain. This is based, on the most part, by an old paper that showed an association between large volume fluid resuscitation in DKA and cerebral oedema. Note the word association, not causation.

Fluid management in DKA

Dogma has been to restrict fluids in paediatric DKA. It is widely thought that the rapid administration of intravenous fluids reduces serum osmolality, resulting in cerebral oedema. Guidelines traditionally have, therefore, advised slow fluid replacement using isotonic fluids as using hypotonic fluids was thought to cause further drops in osmolality. 

And the evidence seemed to support this.  Retrospective reviews showed better outcomes in children with DKA who received less fluid.

But…

  • only an association had been demonstrated, not causality.
  • and it is reasonable to suspect a confounder in that those with more severe DKA could be expected to be both at higher risk of cerebral oedema and more likely to receive large volumes of fluid resuscitation based on their clinical presentation.

And then along came this paper by Kupperman et al published in the New England Journal of Medicine in 2018, which has shifted thinking a bit, as well as causing some controversy…

Lead authors Nate Kupperman and Nicole Glaser suggested the causal effect of fluid resuscitation and cerebral oedema was a myth in Glaser’s 2001 retrospective case-control study that gave us the list of risk factors for cerebral oedema in DKA.

Kupperman’s team wanted to look specifically at the relationship between fluids and cerebral oedema (defined in the study as a drop in GCS, or longer-term evidence of neurological injury defined as a drop in IQ or short-term memory difficulties 2-6 months later) in DKA in children. They looked at 1255 children with DKA presenting to 13 hospitals in the States over a 9 year period, which, because 101 children presented twice, equated to 1389 episodes of DKA. Children were excluded if their GCS was less than 12, or if they had already received significant DKA management prior to assessment. 289 were withdrawn by the treating physician. The mean age was 11. It’s important to think about all of this as these exclusion criteria mean that the very sick and the very young, two groups who are at significantly increased risk of cerebral oedema, were probably lost in this cohort.

Children were randomized into 4 groups. All patients in both groups received IV insulin at 0.1u/kg/hr. Dextrose was added to the saline solution when blood glucose dropped to 11.1 to 16.7 mmol/l.

Children were randomized into 4 groups:

  • FAST rehydration with 0.45% sodium chloride
  • FAST rehydration with 0.9% sodium chloride
  • SLOW rehydration with 0.45% sodium chloride
  • SLOW rehydration with 0.9% sodium chloride

In short, Kupperman’s team found no difference between the groups. There was no significant difference in GCS, or longer-term evidence of neurological injury. The endpoint that many of us are most concerned about, clinically apparent brain injury (deterioration in neurological status requiring hyperosmolar therapy or endotracheal intubation or resulting in death) was a secondary outcome, presumably due to its rarity and hence difficulty in showing statistically significant differences between groups. But again, there was no significant difference between groups.

There was a 0.9% rate of brain injury overall and it didn’t matter which type of fluids or how fast. Patients were more likely to get hyperchloraemic acidosis in the 0.9% NaCl group but this is of debatable clinical significance.

The evidence does not seem to support our traditionally cautious approach to DKA. The speed of IV fluids does not seem to be the cause of brain injury in DKA. But… and this is a big but… don’t forget the youngest and sickest patients weren’t included. All we can probably really conclude is that children who are not in the at-risk group for cerebral oedema are probably more resilient to higher volumes of fluids delivered at faster rates.

Ok… back to Maisie. How are we going to manage her fluids

Well, again it depends where in the world Maisie presents. 

BSPED 2020 advises to calculate maintenance fluids the same way as they’re normally calculated for children in the UK:

  • 100 ml/kg/day for the first 10kg
  • plus 50ml/kg/day for each kg between 10 and 20kg
  • plus 20ml/kg/day for each kg above 20kg

(A maximum weight of 80kg should be used for fluid calculations)

The International Society for Pediatric and Adolescent Diabetes guidance is as follows:

ISPAD says

  • Shock is rare in DKA but if present should be treated with 20ml/kg fluid boluses, repeated as necessary to achieve tissue perfusion.
  • Give all children a 10ml/kg bolus over an hour to rehydrate them.
  • Calculate maintenance fluids in the normal way using the simplified Holliday-Segar formula.
  • Replace rehydration fluids over 24-48 hours, using clinical signs of dehydration to estimate the degree of dehydration. 2 or 3 signs would constitute to 5% dehydration, more signs would equate to 7% dehydration and weak pulses, hypotension or oliguria would indicate the child is 10% dehydrated.

Managing electrolytes

Once you’ve navigated the quagmire of fluid management in DKA, you need to think about adding electrolytes. Remember, glucose molecules in the urine exert an osmotic pull, dragging water, cations, and anions such as phosphate, potassium, and sodium into the urine: the child becomes dehydrated with physiologically low levels of the electrolytes potassium and phosphate.

Always assume whole body potassium depletion in DKA. This is compounded by the treatment you give which causes potassium to move intracellularly. Replace potassium as soon as the patient has urine outpatient and labs confirm the child is not hyperkalaemic.

An ECG will give you clues about clinically significant hypokalaemia:

  • Prominent U waves (an extra positive deflection at the end of the T wave)
  • Flat or biphasic T waves
  • ST-segment depression
  • Prolonged PR interval

Although phosphate is lost in the urine as part of the osmotic diuresis in DKA, prospective studies involving relatively small numbers of subjects and with limited statistical power have not shown clinical benefit from phosphate replacement. Administrating phosphate can be dangerous, by causing calcium levels to drop. However, symptomatic severe hypophosphataemia, when serum phosphate levels drop below 1 mg/dL with an ensuing metabolic encephalopathy or depressed cardiorespiratory function, can be dangerous, albeit very rare. A sensible approach is to monitor phosphate levels alongside regular potassium level checks and, if a child is hypophosphataemic and symptomatic, replace phosphate whilst carefully monitoring serum calcium levels.

Back to Maisie. We’ve managed her fluids according to our local guidelines. But how can we tell if we’ve got the balance right?

We can’t monitor urine output as Maisie is going to be polyuric anyway because of the osmotic effect of glycosuria. Her capillary refill time will be prolonged because she’s acidotic and therefore skin perfusion will be reduced.

And her serum sodium and osmolality won’t be reliable indicators of fluid balance because of the effect of plasma glucose on her electrolytes. On top of this, her kidneys will preferentially excrete chloride from any saline and potassium chloride over ketones so there’s limited value to monitoring the anion gap because it doesn’t differentiate between hyperchloraemia or ketones. Instead, we should measure Maisie’s corrected sodium.

Because of its osmotic effect, glucose drags water with it into the intravascular compartment diluting the other osmols – 1mmol rise in glucose will drop sodium and chloride by 1mmol/L.  If Maisie’s glucose goes up by 1 the other osmols will go down by 1.  If glucose goes down by 1 the other osmols will go up by 1.

The corrected sodium must rise with therapy at a rate of 0.5-1 mmol/h

  • Falling corrected sodium means too much water gain: we’ve been overzealous the fluids.
  • A rapidly rising corrected sodium means too much water loss: we’ve been too fluid restrictive.

The Evelina London South Thames Retrieval Service has a great corrected sodium calculator on their website. You plug in her numbers – her initial sodium was 148 with glucose of 29.5, giving her a corrected sodium of 157.6. A couple of hours have passed and her latest gas shows that her glucose has come down to 24.5 – great – and her sodium has improved slightly to 144. You press calculate…

… and your heart sinks as you see her second corrected sodium has fallen by 6 points to 151.6 as you know that the corrected sodium must rise with treatment.

You go back to Maisie’s bedside to review her.

Maisie has dropped her GCS to 12 (E3, V4, M5).  This is incredibly worrying – her GCS was 15 when you last checked on her.  You move her round to resus and ask your nurse to grab some hypertonic saline.

Clinical features of cerebral oedema

  • Headache
  • Slowing heart rate
  • Rising blood pressure
  • Focal neurology such as cranial nerve palsies
  • Falling oxygen saturations
  • Change in neurological status including restlessness, irritability, drowsiness, confusion, incontinence

Treat cerebral oedema with either hypertonic saline or mannitol.

Calculate your dose of hypertonic saline or mannitol before you need it and know where it’s kept. If a child has an acute deterioration, treat it.

Mannitol is an osmotic diuretic and can be given at 0.5 – 1 g/kg over 10-15 minutes. The effects should be apparent after 15 minutes. Mannitol lasts about 2 hours and can be repeated at this point if needed.

Hypertonic saline is a good alternative to mannitol or can be used after mannitol if a second agent is needed.

Don’t forget other neuroprotective measures like elevating the head of the bed to 30 degrees and intubation if concern regarding airway protection.

If there’s no improvement in GCS, do a CT, but not until the child is stable. CT is used to identify any potential lesion that would warrant neurosurgery – intracranial haemorrhage, or a lesion that would warrant anticoagulation such as thrombosis.

Hypertonic saline or mannitol?

DeCourcey et al (2013) conducted a retrospective cohort study over a 10 year period to see whether the increase in the use of hypertonic saline had had any effect on mortality in DKA. They looked at over 43,000 children under the age of 19 with DKA presenting to 41 children’s hospitals in America and found that the use of hypertonic saline replaced mannitol as the most commonly used agent in many of the participating hospitals. Controversially, their data suggested that hypertonic saline may not have benefits over mannitol and may be associated with a higher mortality rate.

However, this does remain controversial, with a counter-argument published as a letter to the editor a few months later arguing that (1) the fact that mortality from cerebral oedema in DKA had decreased by 83% over the same time period that use of hypertonic saline had increased, along with (2) the fact that DeCourcey’s paper only found a statistically significant difference in mortality between hypertonic saline and mannitol once age and race were removed from analyses (two factors that, themselves, have a significant influence on mortality in DKA-related cerebral oedema), meant that we shouldn’t be rushing to conclude that hypertonic saline is less safe than mannitol in the treatment of cerebral oedema.

No guidelines are yet to recommend mannitol over hypertonic saline. This seems to be one of those situations where a prospective study is needed to really answer the question of whether mannitol is superior, or at least non-inferior to hypertonic saline.

Back to Maisie. You give Maisie 3ml / kg 3% saline over 15 minutes and are relieved to see her wake up.  You decrease her fluid prescription and thankfully from that point on her corrected sodium starts to slowly rise.

Insulin

Finally, you’re ready to give Maisie some insulin. Insulin will control Maisie’s glucose and switch off ketosis, therefore improving her acidosis.  Some departments use 0.1 units/kg/hr and some use 0.05 units/kg/hr.  The question is, what is the optimal dose? 

Nasllasamy’s team set out to compare the efficacy and safety of low-dose and standard-dose insulin infusions. They randomized 50 children under the age of 13 with DKA presenting over a 12 month period to receive insulin infused at either 0.05 units/kg/hr or 0.1 units/kg/h. They found that the rate of decrease in blood glucose and time to resolution of acidosis were similar in each group. There was no statistical difference in complication rates of hypokalaemia, hypoglycaemia or cerebral oedema.

This study suggests that low dose insulin is non-inferior to standard-dose insulin in managing children with DKA.  It’s important to note that this was a non-inferiority trial and a larger study, powered to show superiority would be helpful. However, many units have been using lower doses of insulin at 0.05 units/kg/hr safely for some time and this study supports the use of lower dose insulin.

BSPED 2020 states:

Insulin can be given at 0.05units/kg/hr or 0.1 units/kg/hr, although ‘0.05 units/kg/hr would probably be sufficient in most cases except perhaps severe DKA’.

Children under 5 years should be given 0.05 units/kg/hr.

And so, as Maisie is young and therefore in the higher risk group of children with DKA, you opt to start her on insulin at 0.05 units/kg/hr.

In children who are already on long-acting insulin, BSPED 2020 states that it should be continued, or if they are newly diagnosed, they advise to consider starting long-acting subcutaneous insulin alongside intravenous insulin.<

 

Manage high-risk children in PICU

  • pH <7.1
  • young (under 2s or under 5s depending which guideline you read)
  • cardiovascular shock
  • corrected sodium >150 or <130
  • hyper or hypokalaemia
  • altered conscious state
  • glucose >50

Maisie has multiple risk factors: she’s young and she developed clinically apparent cerebral oedema.  You admit her to PICU where she makes stable progress and is discharged home 4 days later on a subcutaneous insulin regime.

Selected references

Take a read of Chris Gray’s take for St Emlyns here

Lawrence SE, Cummings EA, Gaboury I, Daneman D. Population-based study of incidence and risk factors for cerebral edema in pediatric diabetic ketoacidosis. J Pediatr 2005; 146:688

Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. N Engl J Med 2001; 344:264

Edge JA, Jakes RW, Roy Y, et al. The UK case-control study of cerebral oedema complicating diabetic ketoacidosis in children. Diabetologia 2006; 49:2002

Marcin JP, Glaser N, Barnett P, et al. Factors associated with adverse outcomes in children with diabetic ketoacidosis-related cerebral edema. J Pediatr 2002; 141:793

Scibilia J, Finegold D, Dorman J, et al. Why do children with diabetes die? Acta Endocrinol Suppl (Copenh) 1986; 279:326

Edge JA, Hawkins MM, Winter DL, Dunger DB. The risk and outcome of cerebral oedema developing during diabetic ketoacidosis. Arch Dis Child 2001; 85:16

Chua HR, Schneider A and Bellomo R. Bicarbonate in diabetic ketoacidosis – a systematic review. Ann Intensive Care. 2011; 1:23

Koves IH et al. The Accuracy of Clinical Assessment of Dehydration During Diabetic Ketoacidosis in Childhood. Diabetes Care 2004:27(10);2485-2487

Kuppermann N et al. Clinical Trial of Fluid Infusion Rates  for Pediatric Diabetic Ketoacidosis. N Engl J Med. 2018;378:2275-87

DeCourcey et al. Increasing use of hypertonic saline over mannitol in the treatment of symptomatic cerebral edema in pediatric diabetic ketoacidosis: an 11-year retrospective analysis of mortality. Pediatr Crit Care Med. 2013; 14(7):694-700

Tasker RC, Burns J. Hypertonic saline therapy for cerebral edema in diabetic ketoacidosis: no change yet, please. Pediatr Crit Care Med. 2014;15(3):284-285

Nallasamy K et al. Low-Dose vs Standard-Dose Insulin in Pediatric Diabetic Ketoacidosis. A Randomized Clinical Trial. JAMA Pediatr. 2014; 168(11): 999 – 1005

ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic ketoacidodis and the hyperglycaemic hyperosmlar state. Pediatric Diabetes 2018; 19 (Suppl. 27): 155–177