All paediatricians are complicit in delivering a racist healthcare service

Cite this article as:
Zeshan Qureshi and Anna Rose. All paediatricians are complicit in delivering a racist healthcare service, Don't Forget the Bubbles, 2021. Available at:

We’re supposed to be the nice ones. The friendly, fun, caring and supportive speciality – right? We’re the ones who have teddies on our stethoscopes and know all the words to Disney songs. In the hospital, we’d like to think we’re the Good Guys – but maybe we’re not when it comes to race. 

The COVID-19 pandemic has been a monumental challenge to the NHS and has, undoubtedly, showcased the everyday heroism of our staff. It has also thrown a sharp light onto the ongoing racial inequalities in our society and healthcare systems. Racial disparities in the pandemic have been widely documented – and make for sobering reading. Analysis of national hospital data suggests that people of black and other minority backgrounds are up to twice as likely to die from the virus, as compared to white Britons – with some groups, such as black African-born men living in Britain, having an even higher risk [1]. Despite this, we have little doubt that the major impetus for the unprecedented emergency measures, national lockdowns, and political obsession was not the deaths of the poor, the ethnic minorities, or those in low and middle-income countries – but the perceived threat to wealthy, predominantly white, Westerners.

In an eerie parallel to the racial inequalities highlighted by the pandemic, the past year has also seen racial tensions in the USA reach boiling point. Following several high-profile incidents of police brutality, there was an eruption of social unrest and protest in America and around the world. The systemic disregard of black lives is not just written in blood on American pavements. It is written into the systems that surround us in our everyday working lives. As a speciality, and in the NHS as a whole, we must confront these engrained systemic inequalities, if we are to provide truly equitable care to all of our patients. 

In this blog series, we will examine how clinical outcomes for common paediatric conditions are worse for children from minority ethnic backgrounds. Stillbirth, low birth weight and preterm birth are all more common in minority groups as compared to white northern European populations [2,3,4 ]. Outcomes for common chronic conditions, such as asthma and type 2 diabetes, are also worse for children within minority groups [5,6]. This could be because care received by children with chronic conditions is worse. Non-white children with renal failure are less likely to pre-emptively receive a renal transplant, for example [7]. There are also complex social and environmental roots to these adverse health outcomes – such as increased poverty in non-White groups [8] — and we will try to investigate these issues in more detail. 

We will also explore how paediatrics has normalized white Northern European genetics, physiology and behaviour, leading to biased clinical decision making. Normalization of one ethnic group has lead to the classification of other normal values (in both the laboratory and social sense) as pathological or inappropriate. In other words – you are only normal if you are white and normal. Neutrophil counts are often lower in black babies [9]. Rather than reporting ethnically normal ranges babies often end up having multiple blood tests due to a lack of awareness of the variation. Parents get told that their neutrophil count is low, but it’s acceptable for a black baby (rather than categorically stating that their count is normal). Worst still, it might be classified as a disease – benign ethnic neutropenia – despite not being associated with increased morbidity or mortality.

Within medical education, we are guilty of peddling irrelevant and outdated racial and religious stereotypes. These hold little educational value, but risk enforcing dangerous bias within our future doctors. Any paediatrician would be able to tell you about the association between Tay-Sachs disease and Ashkenazi heritage, or sickle cell disease and sub-Saharan Black Africans. Such associations are often over-simplified and over-emphasized, to the point of creating a disease-ridden caricature, particularly in exam questions. Most of these stereotyped conditions are very rare, and over-emphasis during medical school risks blinkering us to more common diagnoses. We’ll explore how racial bias is ingrained in medical education in the UK, and try to come up with some ideas on how we can improve MedEd to be more diverse and inclusive in the future. 

There also seems to be a disproportionate concern that those from Muslim backgrounds might be consanguineous, and that we need to ask about this even when it is not relevant to the presenting complaint. Conversely, when genetic testing is being sent off, a detailed family tree needs to be drawn. It should include details of any consanguinity – yet it seems that a white family is less likely to be asked. As first or second cousin marriages are no longer a social norm in the UK, they have become defined by pathological associations with genetic conditions, such as inborn errors of metabolism. And whilst there are, of course, differences in the prevalence of disease alleles in different populations, and an increased risk of recessive disorders in families with intergenerational consanguinity, it does not automatically follow that a child from a Muslim background has a recessive disorder, or that a white British child does not. The same considerations need to be given to other cultural practices that might be different to the social norms of Northern and Western Europe. Putting children on a vegetarian diet is often classed as a ‘restrictive diet’ – despite the fact that it is only restrictive based on traditional Western standards – and might, in fact, hold health benefits [10]. 

Finally, in our series, we will examine how systemic racism within the health service tolerates – and sometimes even facilitates –  the unacceptable behaviours demonstrated by some parents. One thing that sets paediatrics apart from adult medicine is that patients are almost never seen alone, and a parent is often required to deliver care. This can present a dilemma to staff when confronted with a racist parent. Any punishment directed towards the parents might directly harm their child. We will explore how guidelines should be developed to help clinicians handle racist parents, whilst minimizing the effect on the clinical care of our patients. 

It can be painful for us – as individuals and as a speciality – to consider that we might be complicit in a racist system that ultimately leads to poorer health outcomes for some children. Just because something is painful, does not mean we shouldn’t do it. We hope that you’ll join us for this series of short articles, as we try to explore how we can begin to move from a white-centric healthcare system to a child-centred one.

James Baldwin quote on racism

Selected references

1) The IFS Deaton Review. Are some ethnic groups more vulnerable to COVID-19 than others? 

2) Gardosi J, et al. (2013). Maternal and fetal risk factors for stillbirth: population-based study. BMJ 346:f108.

3) Kelly Y, et al. (2008). Why does birthweight vary among ethnic groups in the UK? Findings from the Millenium Cohort Study. Journal of Public Health, 31:131–137.

4) Aveyard P, et al (2002). The risk of preterm delivery in women of different ethnic groups. British Journal of Obstetrics and Gynaecology 109:894-899.

5) Asthma UK (2018) On the Edge: How inequality affects people with asthma. Available at

6) RCPCH (2020) State of Child Health: Diabetes. Available at

7) Plumb LA et al. (2021) Associations between Deprivation, Geographic Location, and Access to Pediatric Kidney Care in the United Kingdom. CJASN. 16:194-203.

8) Office for National Statistics (2020) Child poverty and education outcomes by ethnicity. Available at

9) Haddy TB, Rana SR, Castro O. (1999) Benign ethnic neutropenia: what is a normal absolute neutrophil count? J Lab Clin Med. 133:15-22.

10) Kalhoff H. et al (2021) Vegetarian Diets in Children—Some Thoughts on Restricted Diets and Allergy. International Journal of Clinical Medicine. 12:43-60.

An Evidence-Based Cookbook for the Treatment of Adolescent Acne Vulgaris

Cite this article as:
Kate Hensley. An Evidence-Based Cookbook for the Treatment of Adolescent Acne Vulgaris, Don't Forget the Bubbles, 2021. Available at:

A 14-year-old patient named Shannon presents to their primary care physician for a sports clearance physical. During the visit, the patient’s parent mentions that they are concerned about Shannon’s acne. Shannon is being teased by other students at school. They make comments like, “why don’t you wash your face? You look disgusting.” Shannon appears embarrassed and admits that these comments are very upsetting. The parent reports that they have “tried everything” and when asked for specifics, they cannot name ingredients or brands, but they have tried numerous over-the-counter washes and topical preparations. Shannon reports they have never used any one product for more than about a week because “nothing works”. On physical exam, the patient is noted to have significant comedonal acne over the forehead, nose and chin with a pustular and nodular lesions on their cheeks. There is some mild scarring on the cheeks as well.

Acne vulgaris is extremely common, affecting about 85% of adolescent patients across ethnicities and nationalities.  Some 36% of adolescents experience moderate to severe acne. Adolescents with acne have increased social impairment and mental health problems. Those with severe acne are up to twice as likely to experience suicidal ideation compared to their clear-skinned counterparts.

Many effective treatment options are available over-the-counter, but patients, and their parents, may lack knowledge around which agents will work best for them. It is also important to educate them both about just how long treatment takes.  Most patients can expect to see a difference in their acne after 2-3 weeks of persistent use. Often, patients will cease using effective products too soon because they do not have realistic expectations of the treatment.


  • Increased androgen levels in adolescence lead to sebaceous hyperplasia.
  • Alterations in follicular growth and differentiation affected by genetic factors.
  • Colonisation by Propionibacterium acnes (P. acnes).
  • Individual immune system response and inflammation.
  • NOT poor personal hygiene or too much junk food (education about this is important!).
Aetiology of adolescent acne

Types of Acne

Comedonal Acne

This results from increased cell division and cohesiveness of cells within the follicular lumen. These cells mix with sebum (production is increased in response to increasing androgens) and obstruct the follicular opening.

If the follicular opening is closed, comedones appear as whiteheads. If the follicular opening is larger, the keratin build-up is exposed to the air and will thus oxidize and darken. These lesions appear as blackheads.

Acne vulgaris

It is a common misconception among laypersons that the dark colour of blackheads is caused by dirt, reinforcing the myth that adolescents with acne are unclean.

Inflammatory Acne

This is caused by colonization by P. acnes. and leads to inflammation and formation of pus collections within the follicles. These then coalesce to form nodules or pseudocysts.

They may cause scarring and permanent disfigurement.

The type of acne and the presence of scarring determines the severity. It may be classified as mild, moderate, or severe. The severity does not necessarily correlate with the level of distress for the patient. Adolescents may be significantly affected by even mild acne.


Choice of treatment should be tailored to the underlying etiology and level of severity.

Different active ingredients address different underlying problems. Ingredients all fall into one of four major categories:

  • antibiotic agents.
  • agents that reduce production of sebum.
  • agents that reduce desquamation of the follicular epithelium.
  • chemical exfoliants (i.e. keratinolytics).

Benzoyl peroxide

  • Acts as an antibiotic and eradicates P. acnes.
  • Advantageous over other topical antibiotics as there is no development of resistance.
  • Useful as a spot treatment for inflammatory lesions. Continued generalised use prevents their formation.`
  • May be used in combination with topical clindamycin to increase efficacy. It is important to note that topical clindamycin ALONE has not been shown to be effective for most inflammatory acne. 
  • Adverse effects – may cause irritation in some patients but this can be mitigated with use of a moisturiser, may cause bleaching of clothing and towels – recommend that patients wash hands after application. May cause a temporary orange discoloration of the skin when used in combination with topical dapsone.

Salicylic acid

  • Topical antibiotic, also has some mild exfoliant effects.
  • Can be used as spot treatment for inflammatory lesions.
  • When tested head-to-head, less efficacious than benzoyl peroxide.

Tea Tree Oil

  • Topical antibiotic.
  • Spot treatment.
  • Less efficacious than benzoyl peroxide.
  • May have estrogenic effects in males.
  • Strong and distinctive odour.


  • Systemic antibiotic, effective for moderate to severe inflammatory acne that is NOT predominantly nodular.
  • Dosing is 50-100mg given once or twice daily (i.e. 50-200mg per day total).
  • Can cause GI upset, sun-sensitivity.
  • Very rarely can cause Stephens-Johnson syndrome.
  • Should not be used in children under 8 years.
  • Most effective when used in combination with a topical antibiotic.
  • Should be discontinued 1-2 months after new lesions have stopped emerging. After cessation, plan to maintain control with a combination of topical antibiotic and retinoid.

Topical Dapsone

  • Effective for combination type acne.
  • Most effective when used in combination with a topical retinoid or BP.
  • Can cause skin dryness, mitigate with daily moisturiser use.

Topical Retinoids

  • Work by normalising desquamation of the follicular epithelium.
  • Most effective for comedonal acne.
  • Also have some anti-inflammatory activity.
  • Can cause dryness, irritation, and sun sensitivity. Patients should be advised to apply a pea-size amount all over the face (i.e. do not spot treat) at bedtime and use a moisturiser with SPF during the day.

Chemical exfoliants (hyaluronic acid, glycolic acid, uric acid)

  • Decrease build-up of keratin.
  • Can be an effective adjunct agent for comedonal acne but not very effective on its own.


  • Decreases oil production.
  • Adjunct treatment for comedonal acne.

Oral Isotretinoin

  • Effective for very severe nodular inflammatory acne.
  • Can cause severe dry skin and myalgias.
  • Requires special licensing to prescribe because of teratogenicity. Patients who can become pregnant must also use hormonal contraception and have regular pregnancy tests.
  • Generally prescribed only by dermatologists.

Hormone therapy (oral contraceptives)

  • Combination oestrogen/progestin with spironolactone are most effective as they block the production of androgens as well as block the effects of androgens on sebaceous glands.
  • Using a lower dose of oestrogen can decrease risk of thromboembolism.
  • Should not be used in patients who smoke due to increased risk of blood clots.
  • Only an option in patients who have achieved menarche and who have no other complicating factors that would make contraindicate use of oestrogen.
  • Can be advantageous over oral isotretinoin due to fewer unpleasant side effects and no requirement for monthly follow-up visits.
  • Also of note, if a patient has significant acne with other signs or symptoms of hormone access dysfunction (oligomenorrhea, obesity, hirsutism), they should be screened for polycystic ovarian syndrome and congenital adrenal hyperplasia.

Shannon was prescribed a 30-day course of minocycline, along with low-potency topical tretinoin. The paediatrician recommended an over-the-counter benzoyl peroxide preparation to be used as a spot treatment for the inflammatory lesions. She also recommended her favourite moisturiser – an oil-free lotion containing niacinamide with an SPF of 30. The paediatrician also recommended using an alarm app on Shannon’s smartphone to help her remember to use all treatments daily. At follow-up, four weeks after the initial visit, Shannon’s acne had improved. Thus, minocycline was discontinued but the topical retinoid and benzoyl peroxide were continued. Both patient and parent were happy and grateful.

Emergency ambulance transport in those with Autistic Spectrum Condition

Cite this article as:
Vicki Marchant. Emergency ambulance transport in those with Autistic Spectrum Condition, Don't Forget the Bubbles, 2021. Available at:

A small bit of knowledge about Autistic Spectrum Condition (ASC) can make a huge difference in how an emergency situation evolves. ASC is also referred to as ASD – Autistic Spectrum Disorder – but there is a move away from using the term “disorder”, driven by autistic people themselves. Many see their autism as part of their character and identity, hence “autistic people” rather than “people with autism”, and prefer to think in terms of a condition rather than a disorder due to the negative connotations this carries.

Unlike the UK, Ireland does not have official clinical guidance for transporting those with ASC or communication difficulties to the ED. There are two ambulance services in Ireland: the Dublin Fire Brigade (DFB), who run 12 ambulances in the greater Dublin area, and the National Ambulance Service (NAS) who run the remainder of the ambulances in Dublin and the rest of the country. Neither has any formal training in the management of those with ASC. Although some personnel have knowledge of the intricacies of the condition this is mostly due to personal experience with friends or family members.

A call to a situation where the patient has ASC is usually a last resort. Family members don’t want to make the situation worse by calling in strangers and will have tried their best to de-escalate the situation themselves. If the call has been made, the situation has gone past their control and they are admitting they need help. The parents may feel they have failed their child and the attitude of the staff coming into the house can make a huge difference to all involved.

Sam is 15, he’s 5ft 10 and 20 stone. He trips going out the front door and twists his ankle. He starts screaming and tries to get up. He puts weight on his foot and it goes from under him, further aggravating the injury. Due to his size and his injury, he is unable to get up. His dad tries to help him but is unable to lift him. He is screaming very loudly and a crowd is gathering. His family call an ambulance which arrives after 15 minutes. You can hear his screams as you pull up. There is a large crowd gathered, watching and offering ‘helpful’ suggestions to his father who is sitting behind Sam gripping him very tightly. Sam is trying to headbutt his dad and writhing around in apparent agony. You can see his ankle is injured but you can’t get near enough to assess him without getting kicked. You have to shout loudly to make yourself heard and the crowd are enjoying the entertainment.

You feel you need a few more bodies here to help and escalate the call to a behavioural emergency scenario which warrants the police being called. Within a few minutes you have two police officers with you shouting at the dad, trying to get him to stop assaulting the boy. The dad tries to explain but can’t be heard over the noise Sam is making, which has somehow gotten louder. You, your colleague and the two police are standing over Sam trying to hold him down with the dad telling you to get away. The crowd are filming everything. Every time Sam kicks out, he injures his ankle more. The situation is completely out of control.

From a Different Perspective…..

Sam is 15, he’s 5ft 10 and 20 stone. He is autistic and non-verbal. He trips going out the front door and twists his ankle. He starts screaming and tries to get up. He puts weight on his foot and it goes from under him, further aggravating the injury. Due to his size and his injury, he is unable to get up. His dad tries to help him but is unable to lift him. He is screaming very loudly due to pain and frustration and a crowd is gathering. His family call an ambulance which arrives after 15 minutes. You can hear his screams as you pull up. There is a large crowd gathered, watching and offering ‘helpful’ suggestions to his father who is sitting behind Sam bear-hugging him very tightly. One of Sam’s coping mechanisms to deal with unusual situations is to headbutt whatever is around him, in this case the ground, so his dad is sitting behind him to try and stop this but also giving deep pressure to Sam which helps comfort him. You can see Sam’s ankle is injured and a quick survey of the situation shows you that Sam is aggravated by the noise in the crowd also.

You ask your partner to quietly move the crowd on and you slowly approach Sam and his dad but stay out of kicking distance. You introduce yourself to Sam and his dad in a calm, quiet voice and ask what you can do to help.  By asking this way you are acknowledging that the parent knows this child the best. You may be asked to go into the house and get an object to help calm the child: a blanket, a tablet or a favourite toy. In this case Sam’s dad asks you to go in and get his sleeping bag which he immediately puts over Sam’s head. Sam continues to sob but immediately stops kicking out. You are able to chat with Sam’s visibly shaken dad about what happened, and you can look at Sam’s injured ankle. You say what you are going to do and Sam’s dad says it in words Sam may understand. Although he protests a bit, you are able to assess his ankle and determine he needs ED assessment as it may be broken.

You are able to splint his ankle and, between the 3 of you, help Sam onto the chair and get him into the ambulance. His father asks if you can dim the lights and he runs back into the house and grabs a few bits including a tablet which he gives to Sam who is now trying to undo the seat belts. Sam calms immediately and even lets you do some obs when he’s distracted although he thoroughly dislikes the BP monitor and rips the cuff off. You pre-alert the hospital to ask if they can find a quiet space for Sam to wait to be seen and give them chance to review Sam’s care pathway, if he has one.

If you have no knowledge of ASC you will approach this scenario as an ordinary call and walk into chaos. You will see the father essentially holding this child down for no reason and you will act accordingly and put the safety of the child first.

The Autistic Spectrum

People with ASC vary from having very mild symptoms and being able to manage very well to someone like Sam who is completely non-verbal and also has an intellectual disability. The autistic spectrum isn’t a linear thing, with “high functioning” at one end and “low functioning” at the other. Think of it as a pie, made up of variable-sized slices – the social communication difficulties slice may be quite big, whilst the slices for inflexible thinking and anxiety may be fairly small. The whole pie is different for every autistic person. “Slices” vary, depending on the source used, but commonly also include sensory issues, routine, repetitive movements and intense focus or interests.

Autistic Symptoms and Coping Mechanisms

One of the most common symptoms of ASC is a dislike of change in routine, leading to use of personal coping mechanisms which can be seen as self-harm: head-butting walls, picking at skin etc. In this case, Sam was trying to headbutt the ground which would have caused him more injuries than just his ankle. As with some with ASC, Sam does not understand the consequences of doing this so could hurt himself badly before stopping.

Some autistic people have sensory processing difficulties. This can mean that the body misinterprets certain sensations – light touch may be uncomfortable, deep pressure may be comforting, loud or sudden noise may be very distressing. This is why Sam’s dad had a very tight hold on his upper arms. Other coping mechanisms in those with ASC may include talking about one subject, loudly and constantly, perhaps to distract themselves from something distressing, or sometimes if they feel they are not being engaged with. Some may not understand you may be talking to someone else about something more important, the situation is scary to them and this is their way to cope. Further symptoms may include a dislike of loud noises, bright lights, strangers or crowds.

You will be seeing these patients on an already bad day. Something unexpected has happened which has put them out of their comfort zone already, but it has happened to the extent that someone else has been called to their side. This can often be in a noisy environment with lots of people trying to help. Their senses are overloaded and they will need to employ all their coping mechanisms to try and manage.

You will not always know immediately that a person has ASC. They may tell you if they are able, or a family member/carer may say. If you feel the person’s reactions are out of proportion given the situation, consider whether they may be autistic.

Tips to Remember

Unfortunately, parents are used to getting unsolicited advice about how to best manage their children and a large number of people feel the symptoms of ASC are just a child being naughty with poor parenting. Parents may appear defensive at first but asking how you can help may calm them as they realise you are there to help rather than criticise.

Speak quietly and don’t crowd the patient. Don’t touch them without asking. Ask what you can do to help: do they have a toy/blanket/comforter with them that you can get? Is there anything that usually helps to make them feel more comfortable? If they are in the ambulance, can you turn the lights down and travel without the siren?

First and foremost, go into every situation with an open mind and ask what you can do to help. Not everything is as it looks and by being aware of this you can turn chaos into, well, less chaos.

PEM adventures chapter 4

Cite this article as:
Team PEM Adventures. PEM adventures chapter 4, Don't Forget the Bubbles, 2021. Available at:
Miserable child with asthma

Meet Jasmine, a 23-month-old girl with a background of recurrent viral-induced wheeze. Today, she’s come in with a three-day history of coryzal symptoms and has been struggling with her breathing since this morning. Her mum had been giving 10 puffs of salbutamol at home but it didn’t seem to be making much difference so she’s brought her into your Paediatric ED.

On examination, Jasmine looks pale. There’s a scattered wheeze and a few basal crepitations. She has moderate abdominal breathing with some associated tracheal tug.

Her observations are up:

Ouch, you don’t like the look of those oxygen saturations. She’s not that wheezy, but you wonder if she will open up with a bronchodilator and is currently too tight for you to hear much wheeze.  

You pop on high flow oxygen at 15 L/min but what do you prescribe?

The oxygen brings Jasmine’s sats up to 95%, her colour improves a little but she continues to work hard with her breathing.

BTS 2019 asthma guidelines

You know the BTS/Sign guideline suggests children over 1 year may benefit from asthma medications and she has responded before. Looking at her observations, you decide Jasmine fits a picture of Acute Severe wheeze and decide to try a single dose of salbutamol then reassess for a response.

The oxygen brings Jasmine’s sats up to 95%, her colour improves a little but she continues to work hard with her breathing.

BTS asthma severity

Looking at her observations, you decide Jasmine fits a picture of Acute Severe wheeze as per the BTS/SIGN guidance and prescribe a burst of 3 back-to-back salbutamol nebulisers with ipratropium added to the first. She is quite young, but you know she’s been wheezy with coughs and colds before.

While these are running through you pick up an ankle injury that you can see quickly and ask Jasmine’s nurse to repeat her observations when she has completed treatment.

The oxygen brings Jasmine’s sats up to 95%, her colour improves a little but she continues to work hard with her breathing.

BTS asthma severity

Looking at her observations, you decide Jasmine fits a picture of Acute Severe wheeze as per the BTS/SIGN guidance and this is the most likely diagnosis since she has been wheezy with cough and colds before.

However, she’s still young and you don’t want to overdo the beta-agonists, so you decide to prescribe a single salbutamol nebuliser and review her response 15 minutes later.

As you are about to pick up the next card, some of the medical students you’ve worked with before ask if they can follow the case with you. “We’ve barely seen any wheezy kids in our whole placement,” they say. “Of course,” you reply, “but we’ve barely seen any during the pandemic either… I might need your help remembering how to treat her!”

You recap the case for them and explain what treatment you have decided to give first.

“Wouldn’t you ever use nebulised magnesium in a case like this?” one of the students asks. “I am sure I read that the BTS/Sign guideline suggests it for all children with sats of less than 92% at presentation?”

You pull the guideline up on your phone.

They’re right. However, you’ve never done this in practice. As far as you remember the evidence around nebulised magnesium is mixed.

In 2013 the Lancet published the results of the MAGNETIC trial.

This, you explain, was an RCT designed to compare standard acute asthma treatment with standard treatment plus nebulised magnesium sulphate. 500 children aged 2-16 years with acute severe asthma were randomised to receive either nebulised magnesium sulphate in addition to salbutamol or placebo plus salbutamol. They found no difference in the asthma severity score at 60 minutes post randomisation. However, they did note, that magnesium made more difference to those with more severe symptoms at presentation and a short duration of wheeze.

Following this there was some enthusiasm for giving magnesium to children with short duration of severe wheeze, but, you continue, it’s never really caught on. Last year, a large study of over 800 2 to 17 year olds with acute wheeze, showed absolutely no benefit of magnesium sulphate over placebo: there was no difference in hospitalisation within 24 hours or change in asthma severity score at four hours. “So, in answer to your question,” you tell the students, “it’s probably not going to make much difference here.”  

As you finish explaining, Jasmine’s nurse comes in to find you. ”Can you come and review Jasmine please?” she asks. “She’s not looking too great.”

And she’s right, in fact Jasmine barely looks any better than when she arrived. She is more tachycardic and feels cool at her hands and feet. She is still recessing, a bit less wheezy, and the oxygen saturations, in 15L, are sitting at 96%.

Observations forchild with asthma

Hmmm… you think to yourself… she needs another neb and if she doesn’t improve after that we’ll have to escalate things…

While Jasmine’s nurse gets the next nebuliser ready, you wonder whether a dose of steroids wouldn’t go amiss. At almost two years old, with a history of similar episodes, this sounds like a case of viral induced wheeze to you.

You know from Foster’s 2018 trial, that in children with pre-school wheeze, steroids made no difference to acute change in respiratory score or time to ED discharge. The key benefit they showed was reduction of length of hospital stay amongst children who were admitted.

This could be Jasmine. But you’re not sure which way she’s going yet… So what do you prescribe?

You prescribe a dose of oral prednisolone – which Jasmine promptly vomits.

If only your hospital was using dexamethasone these days.

You know that the original trial by Cronin and colleagues showed no significant difference in day 4 respiratory score or unscheduled reattendance when they compared dexamethasone to prednisolone for wheezing children aged 2-16. And there seems to be a growing evidence base to support these findings. Unfortunately, the most recent systematic review you’ve read was underpowered to draw strong conclusions. Although one thing was pretty clear – children with wheeze are far less likely to vomit after dexamethasone compared to prednisolone.

You go back and select again…

You’ve read up a bit on the evidence around this, and know that the original trial by Cronin and colleagues showed no significant difference in day 4 respiratory score or unscheduled reattendance when they compared dexamethasone to prednisolone for wheezing children aged 2-16. This finding has been replicated in many subsequent trials as Wei and colleagues summarise in their recent systematic review. Although the review was underpowered to draw strong conclusions, there was one thing they were pretty clear on – kids are hands down less likely to vomit after dexamethasone compared to prednisolone. Jasmine tolerates the dex just fine.

You’d rather not start the steroids just yet.

Jasmine is only 23 months old. You know she’s been wheezy before but this could still be bronchiolitis.

As far as you remember, the greatest benefit of prednisolone for pre-schoolers is supposed to be amongst those admitted to hospital, when oral prednisolone will reduce time to hospital discharge. So, you hold off for now thinking that you can always give a dose later.

It’s time for a clinical review. But Jasmine looks worse. She is still tachycardic, a bit mottled, wheeze is unchanged and she’s more tachypnoeic.

Observations for child with asthma

“She’s not responding,” you say. “We’re going to need an IV bronchodilator after all.”

You insert a line for IV treatment and take a gas and a few other bloods while you are at it. You decide to make your consultant aware that Jasmine is looking pretty sick. They agree she needs an IV bronchodilator and will pop down to review straight away.

You sit down to prescribe her treatment…

But what drug are you going to give?

You decide to give IV salbutamol as your first line agent

You recently read a large Cochrane review on second-line treatments for acute asthma. It was published last year and included 67 trials from 13 different Cochrane reviews dated up to the end of December 2019 (7). You don’t remember all the details but you do remember that NO single IV agent had been shown to reduce rates of escalation to PICU.

Jasmine is very tachycardic, but she’s also borderline hypotensive so on balance you decide this will be a better option than magnesium. The BTS guidelines suggest either salbutamol or magnesium can be used as first-line IV agent and you feel it’s the right choice in this particular scenario.  

You type up the script and ask Jasmine’s nurse to get it ready as quick as she can.

You decide to give IV magnesium as your first line agent.

You recently read a large Cochrane review on second-line treatments for acute asthma. It was published last year and included 67 trials from 13 different Cochrane reviews dated up to the end of December 2019. You don’t remember all the details but you do remember that NO single IV agent had been shown to reduce rates of escalation to PICU. Magnesium sulphate is your go-to IV drug for refractory wheezers, its recommended in the BTS guidelines and it hasn’t let you down so far.

You type up the script and ask Jasmine’s nurse to get it ready as quick as she can.

You decide to give aminophylline as your first line agent.

But your nurse in charge is reluctant. “We don’t typically use this first-line” he says…and it’s true, you don’t prescribe it often. You recently read a large Cochrane review on second-line treatments for acute asthma. It was published last year and included 67 trials from 13 different Cochrane reviews dated up to the end of December 2019. You don’t remember all the details but you do remember that NO single IV agent had been shown to reduce rates of escalation to PICU.

Your nurse in charge had read the same review and reminded you that it also found vomiting to be more common with aminophylline.

OK, we’ll go with magnesium then,” you say, it shouldn’t make too much of a difference –  she just needs something fast.

Finally, the infusion is up and running. You decide now is a good moment to grab a round of coffees for the team. But, to your horror, whilst standing in the queue, the crash buzzer goes off… you sprint back to the department wondering who on earth it can be for…

…and arrive to find Jasmine having CPR.

Jasmine turned pale after the infusion started, became more tachycardic, then hypotensive and then crashed.

The play specialist is crying as she thinks she overstimulated her with the bubbles. “It’s not that,” you reassure her, “I think we must have missed something here.”

But despite a sterling resuscitation and the team’s best efforts, Jasmine does not survive. Fortunately for you, this is not real life, it’s a PEM adventure and so we get to go back in time…..

And THIS time, you’re handed the gas before you write up the IV bronchodilator.

Oh rats,” you think. Tachycardia, hypotension, raised lactate. This must be sepsis. Hastily you prescribe 80mg/kg ceftriaxone and a 20ml/kg saline bolus.

But to your dismay this just puts Jasmine’s heart rate up even further.

At that moment your consultant arrives.

“Hmm… calcium’s a bit low,” they say.

Your mind is racing… why is the calcium low? Her lactate, her tachycardia, her poor response to bronchodilators and fluid is all starting to feel decidedly cardiac to you.

Jasmine starts to look drowsy and a worrying shade of pale. You order a portable CXR and your consultant suggests a dose of calcium gluconate – just in case. As all this is being organised, you recap the story so far.

“This is 23 month-old Jasmine. She presented with three days of coryzal illness followed by difficulty in breathing and wheeze. She’s had an oxygen requirement since she got here and was working hard with mild wheeze on auscultation. We gave salbutamol nebulisers plus ipratropium and a dose of steroids with little effect on her tachypnoea. She’s been here for about an hour and a half and has become more tachycardic, with a poor gas. We were about to give an IV bronchodilator,” you explain, “but with that gas I am really concerned we are missing something.”

Together you and your consultant re-examine Jasmine. She’s pale, peripherally mottled and tachycardic. Her BP is holding at 75 systolic. Her heart sounds are so fast you can’t tell if there’s a murmur or not. Her peripheral pulses are thready and those basal creps are now worse. Her liver is palpable 5cm below the costal margin

“Its got to be cardiac,” you conclude. “Shall we get her round to resus?”

Round in resus you pull up Jasmine’s x-ray. Her lungs look a little wet to you.

CXR of child with myocarditis

And it all starts to make sense. No wonder she didn’t get better with salbutamol – it never was bronchial asthma in the first place. It must have been cardiac wheeze secondary to rapid onset pulmonary oedema. “This must be a cardiomyopathy or myocarditis,” you say out loud. You know you know you need to support Jasmine’s sick myocardium with a vasoactive agent and fast.

But which one are you going to choose?

Adrenaline – a potent beta-agonist with alpha activity at higher doses; increases heart rate and contractility; good for low cardiac output states. “Yes, this would work here” your boss agrees..

Great choice. Time to move on.

Noradrenaline – a potent alpha-agonist with beta-agonist activity at higher doses; noradrenaline increases systemic vascular resistance by vasoconstriction and is good for distributive shock.

Hmmm…no, not norad” advises your consultant…

Try again

Milrinone – an inodilator that induces positive inotropy through phosphodiesterase inhibition, but simultaneously decreases systemic vascular resistance;  good for low cardiac output states. “This could work” your boss agrees, but they have never used it in ED before. Hmmmm…maybe not the best choice for now.

 Try again

Dopamine – a dopamine and adrenoreceptor agonist with dose dependent effects: inotropy at lower doses, vasoconstriction at higher doses; and additional effect to promote aldosterone secretion. At least you know how to give this peripherally, but you are not sure it’s the best option for Jasmine.

Try again

Dobutamine – an alpha and beta-agonist that produces increased myocardial contractility with little effect on heart rate and systemic vascular resistance; good for low cardiac output states. This could work, although you barely ever use it.

We can get some advice from our retrieval team” suggest your consultant “but I don’t think is the best choice for Jasmine”.

Try again

You call the local cardiac centre who agree, Jasmine should be treated as having cardiogenic shock and suggest that starting a peripheral or IO adrenaline infusion at 0.01mcg/kg/min is the safest first line option.

“What about milrinone?” you ask. They explain that they would prefer to wait until Jasmine’s BP is more stable as milrinone can vasodilate before it starts to work as an inotrope. It’s best given, they advise, once she’s safely arrived at their end and had an echo to confirm the diagnosis.

They would like you to intubate to reduce myocardial demand once the adrenaline infusion is up and request immediate transfer to their unit – no more fluid boluses. In fact, they suggest, have adrenaline boluses ready for intubation: draw up the arrest dose into a 10 ml syringe and dilute with saline so it can be given in 1ml aliquots at a tenth of the arrest dose to support the BP if needed.

If possible put in an arterial line, or at the very least cycle the BP every minute. Oh and of course, don’t forget an ECG.

Jasmine is successfully intubated for transfer using ketamine, rocuronium and fentanyl in a 1:1:1 ratio.

As you finally sit down to write some notes, the medical students from earlier approach.

“This has been fascinating,” they say. “We’d like to present this case at grand rounds. Myocarditis: the master of disguise. And we found this great paper…”

Freedman et al. Pediatric myocarditis: emergency department clinical findings and diagnostic evaluation. Pediatrics 120; 6:1278-85 December 2007 

Freedman and colleagues performed a retrospective review of paediatric patients who attended the Hospital for Sick Children in Toronto with myocarditis between May 2000 and May 2006. There were 16 cases of definite (biopsy-proven) myocarditis and 15 cases of probable myocarditis. And when looked at the demographics of the sample they found a few interesting things:

  • Age was not normally distributed, with peaks among children under three years and over 16 years of age
  • In their cohort:
    • 32% presented with predominantly respiratory symptoms
    • 29% had cardiac symptoms
    • 6% had gastrointestinal symptoms  
    • But this was significantly associated with age
  • Half of under 10’s had primarily respiratory symptoms
  • None of the under ten’s had cardiac symptoms or chest pain at presentation
  • The two children with gastroenteritis symptoms were also under ten.
  • Initial misdiagnosis with pneumonia or asthma happened in 57% of cases.
  • 25% of children were admitted with a different diagnosis to begin with.

This starts to make you feel a little better.

“But it’s not only symptoms that can be misleading,” the students continue. The paper looked at the relevance of investigations too:

  • Just over (55%) half of initial chest x-rays were abnormal.
  • Typical signs when present included cardiomegaly, pulmonary venous congestion and pleural effusion.
  • ECG was more sensitive with 93% abnormal at presentation

Signs included: ST or T wave abnormalities, axis deviation, ventricular hypertrophy, infarction pattern, decreased voltage, atrial enlargement and AV block.

  • Aside from troponin (which wasn’t assessed as it was measured at presentation in less than 30% patients), AST was the most useful biomarker for potential myocarditis and a value over 100 U/L was significantly associated with cardiac disease

Well, you think to yourself as Jasmine leaves the building with the retrieval team, sick but more stable, every day’s a school day. As you reflect on the biases influencing your decision making through Jasmine’s ED journey, you remind yourself to keep a more open mind in the future. And you save the date in your diary for the medical student’s grand round presentation.

Jasmine makes a complete recovery and one year later comes to visit you in PED. She and her Mum have been busy fundraising and she is here, full of 3 year old attitude, ready to donate the proceeds to your department.

But before we go, lets hop back in that PEM adventures time machine one more time and see what was the learning from Jasmine’s case.

Nebulised MgSO4

The MAGNETIC trial in 2013 was an RCT designed to compare standard acute asthma treatment with standard treatment plus nebulised magnesium sulphate (2).

Powell, C., Kolamunnage-Dona, R., Lowe, J., Boland, A., Petrou, S., Doull, I., Hood, K., Williamson, P. and MAGNETIC Study Group, 2013. Magnesium sulphate in acute severe asthma in children (MAGNETIC): a randomised, placebo-controlled trial. The Lancet Respiratory Medicine, 1(4), pp.301-308.

They randomised 500 children aged 2-16 years with acute severe asthma to receive either nebulised magnesium in addition to salbutamol or salbutamol plus placebo. They found no difference in the asthma severity score at 60 minutes post randomisation. However, they did note that magnesium made more difference to those with more severe symptoms at presentation and a short duration of wheeze.

Last year, a large multicentre Canadian study of over 800 2-17-year-olds with acute wheeze (3) showed absolutely no benefit of magnesium sulphate over placebo. They randomised children with persistent signs of moderate to severe wheeze after initial treatment with three albuterol and ipratropium nebulisers and steroids to receive either magnesium sulphate or placebo to be administered alongside three further albuterol nebulisers.  The primary outcome measure for this study was hospitalisation within 24 hours. They found no difference between groups in hospitalisation or change in asthma severity score at 4h post-treatment.

So, although the BTS guideline still does recommend this, in practice its not used widely in UK emergency departments and although it’s unlikely to do harm, it probably won’t make a huge difference to the patient in front of you.

Steroids for preschool wheeze

Two well-known studies on this topic are those by Foster in 2018 (4) and Panickar in 2009 (10) and for a great discussion on these have a read of this DFTB blog (11)

Panickar, J., Lakhanpaul, M., Lambert, P.C., Kenia, P., Stephenson, T., Smyth, A. and Grigg, J., 2009. Oral prednisolone for preschool children with acute virus-induced wheezing. New England Journal of Medicine360(4), pp.329-338.

In 2009, Panickar and colleagues performed a double blind RCT in children aged 10-60 months with acute virus induced wheezing across three UK centres (10). They randomised 700 children to receive a 5-day course of either prednisolone or placebo after initial albuterol treatment and measured the PRAM score at 4 hourly intervals from enrolment to hospital discharge.

Their primary outcome measure was duration of hospital stay and the trial found no significant difference between groups on this measure. There was also no difference in PRAM scores at any time interval or readmission within 1 month. And this held even when performing a subgroup analysis of children at higher risk of an atopic asthma phenotype. Of course, the caveat to this study, is the age range included in the trial. Infants in the ten months to 2 years age group show a degree of heterogeneity in disease phenotype; many will have a bronchiolitic illness rather than an inflammatory viral induced wheeze and respond differently to steroid medication (12).

Foster, S.J., Cooper, M.N., Oosterhof, S. and Borland, M.L., 2018. Oral prednisolone in preschool children with virus-associated wheeze: a prospective, randomised, double-blind, placebo-controlled trial. The Lancet Respiratory Medicine6(2), pp.97-106.

Foster and colleagues performed a similar trial in 2018 (4) randomising 600 children aged 24-72 months presenting with virus-associated wheezing, to receive prednisolone or placebo. They chose this age range specifically to avoid the confusion of including patients with bronchiolitis in the sample.

They also found that steroids made no difference to acute change in respiratory score or time to ED discharge. However, amongst children who were admitted to hospital, total length of stay in the steroid group was reduced. There was no difference in re-attendance or PICU admission but of note, children with the most severe symptoms or co-morbidities at presentation (for example, oxygen saturations <92% in air; a silent chest; shock or sepsis; previous PICU admission with wheeze; prematurity; other cardiac or respiratory disease) were excluded. So for this group, which would certainly include Jasmine, the question perhaps remains unanswered.

Wallace, A., Sinclair, O., Shepherd, M., Neutze, J., Trenholme, A., Tan, E., Brabyn, C., Bonisch, M., Grey, N., Johnson, D.W. and McNamara, D., 2021. Impact of oral corticosteroids on respiratory outcomes in acute preschool wheeze: a randomised clinical trial. Archives of Disease in Childhood106(4), pp.339-344.

A further trial, published last year by Wallace and colleagues (13), randomised 493 children aged 24-59 months to receive either prednisolone or placebo. They found no difference between groups in the primary outcome measure – change in baseline PRAM score at 24 hours and 7 days. However, they noticed with interest, that the median PRAM score at 24 hours was zero in both groups with only a small number of children remaining symptomatic at this time point.  This they argue, illustrates how viral-induced wheezing attacks may often be short-lived in nature and the most important benefits of steroids, if any, must occur within that initial 24-hour period.

Within the first 24 hours, they did find some benefit of prednisolone over placebo: those in the prednisolone group had significantly lower PRAM scores 4 hours after medication administration which translated into a reduced requirement for hospital admission, additional steroid or intravenous treatment. A particular strength of this study was the analysis of several subgroups for salbutamol responsiveness, positive Asthma Predictive Index and baseline severity. The subgroup analysis showed that the primary outcome measure (PRAM score at 24 hours and 7 days) was not modified by any of these factors, however, the analysis was not extended to the secondary outcomes (ie what happened within those first 24 hours).

This is a shame as it is increasingly well recognised that several different wheezing phenotypes exist and that these may determine response to standard asthma therapies. Ultimately, the answers we are looking for may come from studies such as the DOORWAY (Determinants Of Oral corticosteroid Responsiveness in Wheezing Asthmatic Youth) (14) project. This exciting study aims to identify genetic determinants of responsiveness to steroids so that one day clinical management can be better individualised.

Dexamethasone or prednisolone?

This is an interesting question that has been raised within the PEM community in recent years. Early studies show single dose dexamethasone is non inferior to a 3 day course of oral prednisolone for children attending ED with wheeze. It sorts out the respiratory symptoms, is overwhelmingly less likely to get vomited up and doesn’t need to be given by parents for two further days at home.

For example, the original trial by Cronin and colleagues showed no significant difference in day 4 respiratory score or unscheduled reattendance when they compared dex to pred for wheezing children aged 2-16 (5). This finding has been replicated in many subsequent trials as Wei and colleagues summarise in their recent systematic review (6).

Wei and colleagues looked at 7 trials comparing dexamethasone to prednisolone for the treatment of acute wheeze , specially aiming to compare relapse rates and adverse effects. Six out of the seven trials included children from age 2 to adult – avoiding the inclusion of those with potential bronchiolitis, but clearly including a mix of both atopic asthmatics and those with viral induced pre-school wheeze.  

Wei and colleagues found no significant difference between dexamethasone and prednisolone on relapse rate up to five days post treatment or 10-15 days of follow-up and this held whether children received one or two doses of dexamethasone. There was no difference in hospital readmission rates or adverse events between the two drugs, however the incidence of vomiting both in hospital and at home was significantly higher in the prednisolone group.

Sounds like a no-brainer then? Unfortunately, not quite. Conscious of the relatively small number of quality trials conducted on this topic, Wei and colleagues conducted a power calculation to determine the validity of their results. This showed the meta-analysis was underpowered to accurately answer the questions posed. Whilst their results are suggestive that dexamethasone is at least equivalent to prednisolone, they caution that further and larger studies on the topic are required before strong conclusions can be drawn.  In addition, further studies should try to differentiate dexamethasone response between pre-school wheezers and those with a more atopic phenotype as anecdotal evidence suggest there is likely to be a difference between these two groups.

Again, this is all going to come back to findings of projects such as DOORWAY which should one day help us to provide more nuanced care.

IV bronchodilators

Despite the fact that an acute exacerbation of wheeze or asthma represents the bread and butter of acute paediatrics, we have a yet to achieve consensus for the best way in which to treat it.  It is widely accepted that inhaled bronchodilators and steroids are the best first-line approach, but there are several options for second line IV treatment (IV beta-agonists, IV adrenaline, IV magnesium sulphate, IV methylxanthines and IV ketamine) and no evidence with which to separate them. A few years ago PERUKI conducted a survey to establish prescribing practices for second line asthma treatments amongst senior UK based ED clinicians (15) and this clearly illustrated wide variation in practice around the UK. Magnesium sulphate was the most frequently prescribed first IV infusion but this was by no means universal.

Last year a Cochrane review of systematic reviews on treatments for asthma (7) was conducted, the aim being to try and unravel the story here a little better. They included 13 Cochrane Systematic Reviews on various treatment options for acute asthma. Primary outcomes were length of stay, hospital admission, intensive care unit admission, and adverse effects. Four of the 13 reviews focussed on IV medication although none compared all three big players (beta agonists, magnesium sulphate and methylxanthines) head-to-head. No single agent was identified as being able to reduce risk of ITU admission. And no one single agent appeared markedly superior to the others for any of the primary outcome measures.

What we need, is a well-designed and adequately powered, large scale RCT to directly compare the three most commonly used IV bronchodilator treatments, including subgroup analyses in preschool and school‐aged children, and for varying degrees of asthma severity.


This case was a great illustration of the difficulties that can arise in the early identification of acquired cardiac pathology, particularly in younger children who do not tend to complain of cardiac symptoms and may present with a predominantly respiratory or non-specific picture. The key to diagnosis is recognising when there is a lack of expected response to treatment and picking up on the small signs that can give the game away. The astute amongst you may have noticed Jasmine’s unusually wide pulse pressure at presentation. Perhaps, if you had been the doctor examining, you’d have felt for the liver a little earlier on too?

From a PED management perspective the key to success is firstly in recognising the problem and getting early expert advice.

Myocarditis has been defined as an “inflammatory disease of the heart muscle” and has a variable clinical presentation, with several distinct disease phenotypes (16). As in Jasmine’s case, it is commonly viral in origin (think enterovirus/coxsackie/adenovirus and parvovirus). But there are some other important differentials to consider as well:

  • Familial Cardiomyopathy/metabolic
  • Cardiac Structural abnormality (ALCAPA/Coarctation)
  • Idiopathic dilated cardiomyopathy
  • Hypocalcaemia and Vitamin D deficiency (8)

Classic myocarditis may have a relatively insidious onset with worsening fatigue and exertional dyspnoea or in older teenagers may mimic an acute coronary syndrome. It is associated with echocardiographic findings of left ventricular dilatation (which may be indistinct from a dilated cardiomyopathy picture), reduced ejection fraction, segmental wall abnormalities +/- pericardial effusion (16).

Fulminant myocarditis is a distinct symptom complex, and when supportive care is administered in a timely fashion, typically enjoys a higher rate of complete recovery of function. It may present with a history of recent viral illness followed by sudden-onset heart failure usually within 2-4 weeks and usually has more severe ventricular dysfunction. In contrast to classic myocarditis, it has an echocardiographic phenotype of reduced left ventricular ejection, normal left ventricular cavity size, and increased septal thickening.

Fulminant myocarditis conversely is a distinct symptom complex. It typically follows a viral illness and presents with sudden onset heart failure as in our case above. Echocardiographic findings typically show reduced left ventricular ejection, normal left ventricular size and increased septal thickening. Heart size on chest x-ray may not be hugely increased (16). Provided appropriate supportive measures are initiated early, long-term prognosis is often better in this group (16).

Management – both in ED and PICU – is predominantly supportive.

Inotropes are the best way to support the child, like Jasmine, presenting in cardiogenic shock. And heart failure should be managed according to published guidelines once the child is stabilised (17). Adrenaline is recommended as a first line infusion where there is evidence of hypotension and poor end organ perfusion. Milrinone and/or dobutamine are of benefit once BP has stabilised (17). The child should be intubated and ventilated but make sure you’ve gone through your intubation checklist and be prepared for a bumpy ride as these patients are notoriously unstable and will arrest with even slight changes to their compensatory physiology.

Despite much debate and equivocal evidence of benefit (18), in PICU Jasmine received a dose of IVIG and over the course of 10 days was gradually weaned off milrinone.  She made an excellent recovery with a return to normal ventricular function 6 months later. Unfortunately, many children are not as lucky and will require ECMO – either as rescue therapy or as a bridge to transplant.

Jasmine was 23 months old, but for children under 10kg ECMO as a bridge is problematic, both ethically and clinically: there’s a small pool of eligible hearts and ECMO is a finite resource.  The answer may be a left ventricular assist device, where there have been growing reports of success, including amongst the very young (19) … but that’s for another PEM adventure.


  1. SIGN158 British guideline on the management of asthma: A national clinical guideline. First published 2003 Revised edition published July 2019
  2. Powell et al. Magnesium sulphate in acute severe asthma in children (MAGNETIC): a randomised controlled trial.  The Lancet Volume 1; 4: 301-308 June 2013
  3. Scuh at al. Effect of nebulized magnesium vs placebo added to albuterol on hospitalization among children with refractory acute asthma treated in the emergency department: a randomized controlled trial. JAMA. 2020;324(20):2038-2047.
  4. Foster et al.  Oral prednisolone in pre-school children with virus-associated pre-school wheeze: a prospective, double blind, randomised controlled trial. The Lancet. Volume 6, Issue 2. P97-106. February 2018.
  5. Cronin et al.  A randomized controlled trial of single dose oral dexamethasone versus multi-dose oral prednisolone for acute exacerbations of asthma in children who attend the emergency department.  Annals of Emergency Medicine: 67;5: 503-601 2016
  6. Wei at al. Oral Dexamethasone vs. Oral Prednisone for Children With Acute Asthma Exacerbations: A Systematic Review and Meta-Analysis. Frontiers in Pediatrics. 2019 Dec 13;7:503. doi: 10.3389/fped.2019.00503.
  7. Craig et al. Interventions for escalation of therapy for acute exacerbations of asthma in children: an overview of Cochrane Reviews. Cochrane Database Systematic Reviews. 2020 August 5;8:CD012977. doi: 10.1002/14651858.CD012977.pub2. PMID: 32767571.
  8. Maiya et al. Hypocalcaemia and vitamin D deficiency: an important, but preventable, cause of life-threatening infant heart failure. Heart 94.5 (2008): 581-584.
  9. Freedman et al. Pediatric myocarditis: emergency department clinical findings and diagnostic evaluation. PEDIATRICS 120; 6:1278-85 December 2007 
  10. Panickar et al. Oral prednisolone for preschool children with acute virus-induced wheezing. New England Journal of Medicine. 2009 Jan 22;360(4):329-38. doi: 10.1056/NEJMoa0804897. 
  11. Tessa Davis. Steroids for pre-school wheeze, Don’t Forget the Bubbles, 2018. Available at:
  12. Fernandes RM et al. Glucocorticoids for acute viral bronchiolitis in infants and young children. Cochrane Database of Systematic Reviews 2013, Issue 6. Art. No.: CD004878. DOI: 10.1002/14651858.CD004878.pub4).
  13. Wallace et al. Impact of oral corticosteroids on respiratory outcomes in acute preschool wheeze: a randomised clinical trial. Archives of Disease in Childhood2021;106:339-344.
  14. Tse SM et al. DOORWAY research group of the Pediatric Emergency Research in Canada (PERC) network. Genetic determinants of acute asthma therapy response in children with moderate-to-severe asthma exacerbations. Pediatric Pulmonology. 2019 Apr;54(4):378-385. doi: 10.1002/ppul.24247. Epub 2019 Jan 15.
  15. Morris et al. Which intravenous bronchodilators are being administered to children presenting with acute severe wheeze in the UK and Ireland? Thorax. 70(1):88-91. January 2015.
  16. Dasgupta et al. Myocarditis in the paediatric population: a review. Congenital Heart Disease. 2019;14:868–877.
  17. Kirk et al. The International Society for Heart and Lung Transplantation Guidelines for the management of pediatric heart failure: Executive summary. The Journal of Heart and Lung Transplantation, Vol 33, No 9, September 2014
  18. Robinson et al. Intravenous immunoglobulin for presumed viral myocarditis in children and adults. Cochrane Database Syst Rev. 2020 Aug 19;8:CD004370. doi: 10.1002/14651858.CD004370.pub4. PMID: 32835416.
  19. Ghelani et al. Demographics, trends and outcomes in pediatric acute myocarditis in the United States 2006 to 2011. Circulation: Cardiovascular Quality and Outcomes. 2012; 5:622-627.
Scurvy header image


Cite this article as:
Julia Hall and Abigail Lazenbury. Scurvy, Don't Forget the Bubbles, 2021. Available at:

A three-year-old boy with speech and language delay presents to the Emergency Department with a unilateral atraumatic limp. He is initially managed as per the ‘Limping Child Pathway’. At his follow up review, he is now non-ambulatory, resistant to examination and holds his legs in a flexed position.

He has an extensive array of normal investigations including basic blood tests, pelvis and bilateral leg x-rays and abdominal ultrasound. He subsequently has an MRI which shows florid symmetrical increased signalling in his long bones with a wide non-specific differential. He develops a small patch of petechiae on his ear.
Reviewing his history, it appears that his diet is extremely restrictive and made up of only lactose-free milk and cheesy biscuits.

Could this be scurvy?


Scurvy, or vitamin C deficiency, is a disease of malnutrition. It is one of the oldest nutritional deficiencies identified, and the source of one the world’s first randomized control trials. In 1753 James Lind published A Treatise of the Scurvy. Like a lot of research, this paper was widely ignored. It wasn’t until about 10 years later, when sailors got to try sauerkraut, wort, or syrup of oranges and lemons (all contain vitamin C) did the higher ups at the Admiralty begin to take notice.

Rime of the Ancient Mariner - all the sailors died of scurvy
Gustave Doré’s illustration from Coleridge’s Rime of the Ancient Mariner

Scurvy is rare in higher income countries and therefore often forgotten as a potential differential diagnosis.


Vitamin C, also known as ascorbic acid, is a water-soluble essential vitamin. It is found in citrus fruits, peppers, potatoes and broccoli. In babies, vitamin C is provided in the breast milk. Vitamin C has important roles in the body including wound healing, bone, cartilage and blood vessel maintenance and helps with the absorption of iron. It is also involved in fatty acid transport, neurotransmitter synthesis, prostaglandin metabolism and nitric oxide synthesis. 

Dietary doses of up to 100mg/day can be absorbed in the distal small intestine. It is renally excreted and therefore the kidneys are important in regulating vitamin C concentration in the blood. The World Health Organisation recommended daily allowance for infants and children is 25mg per day.

The clinical manifestations of scurvy result from disordered pathways that utilise vitamin C, such collagen and connective tissue synthesis. Symptoms can occur after just one to three months of inadequate vitamin C intake. 

Signs and symptoms 

Early manifestations of scurvy are often non-specific. Consider the infant with fatigue, anorexia, weight loss and low grade fever – these are all early signs of scurvy but scurvy was unlikely to have made it into your differentials list. Petechiae can also be present – you probably ran an FBC and CRP. But petechiae, follicular hyperkeratosis and perifollicular haemorrhage are all cutaneous manifestations of scurvy, while gingival signs include swelling, bleeding and loss of teeth.

Radiographic findings in scurvy
Case courtesy of Dr Matt Skalski, From the case rID: 19946

And consider the limping child. Arthralgia, limb and joint swellings, limp, inability to weight-bear are often the presenting features of children being brought to medical attention. Although rare, scurvy should be considered in the differential of the limping child once the more common causes have been ruled out.

Risk Factors 

In children of the developed world, risk factors for developing scurvy are severe dietary restriction of fruit and vegetables. These can be secondary to autism, developmental delay and psychiatric disorders, as well as the extremely fussy child.


Scurvy is a clinical diagnosis based on presentation of typical signs and symptoms alongside a dietary history of restrictive vitamin C intake for at least 1-3 months. Most laboratories cannot process ascorbic acid levels. If they can be measured then a level less than 11 umol/L would be considered deficient.

The diagnosis is, in the main, a clinical one. When a signs and symptoms respond to dietary changes or supplementation with Vitamin C then you know you are on the right track.

Classic bony signs on imaging include: periosteal oedema, sub-periosteal collections and sub-periosteal haematomas, lucent bands through long bone metaphyses, osteopenia and widening of the distal extremity of the femur. 


  • Vitamin C supplementation orally for children with 100-300mg for one month or until full recovery.
  • All children under five years of age are recommended to take a multivitamin (unless formula feeding as this is already fortified). 
  • Referral to a dietician for dietary education is imperative. 
  • Resolution of symptoms can start within 24 hours but may require a few weeks of treatment to fully resolve.

Two months later, the child was seen in paediatric outpatients running and jumping in the consulting room. They subsequently had an appointment with the dieticians who discussed dietary changes with the family and ensured that all calorie and nutrient requirements were being met. The child continued to have a restricted diet and will therefore need a multivitamin supplement long term. 

Scurvy is a preventable, easily treatable disease which due to its non-specific symptoms is often misdiagnosed or carries a delay in diagnosis, with patients presenting to healthcare professionals on multiple occasions. A good nutritional history is key to diagnosis. 

Selected references on scurvy

Agarwal A, Shaharyar A, Kumar A et al. Scurvy in pediatric age group- A disease often forgotten? Journal of clinical orthopaedics and trauma. 2015; 6(2): 101-7 https://doi:10.1016/j.jcot.2014.12.003

Alqanatish JT, Alqahtani F, Alsewairi WM, Al-Kenaizan S. Childhood Scurvy: an unusual case of refusal to walk in a child. Pediatric Rheumatology 2015; 13(1): 23 https://doi:10.1186/s12969-015-0020-1 

Chalouhi C, Nicolas N, Vegas N et al. Scurvy: A New Old Cause of Skeletal Pain in Young Children. Frontiers in Pediatrics. 2020; 8:8 doi:10.3389/fped.2020.00008 

De Ioris MA, Geremia C, Diamanti A et al. Risks of inadequate nutrition in disabled children: four cases of scurvy. Archives of Disease in Childhood. 2016; 101(9): 871  https://doi:10.1136/archdischild-2016-310911, https://doi:10.1136/archdischild-2016-310911

Kitcharoensakkul M, Schulz CG, Kassel R et al. Scurvy revealed by difficulty walking: three cases in young children. Journal of Clinical Rheumatology: practical report on rheumatic and musculoskeletal disease. 2014; 20(4): 224-228 https://doi: 10.1097/RHU.0000000000000101 

Noble JM, Mandel A, Patterson MC, Scurvy and rickets masked by chronic neurologic illness. Pediatrics. 2007; 119(3): e783-90 https://doi:10.1542/peds.2006-107

Pazirandeh S, Burns D. Overview of water-soluble vitamins. In: D, Seres, L, Kunins eds. UpToDate. 2020. Waltham, UpToDate [ Accessed 28th February 2021 ] Available from

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Weinstein M, Babyn P, Zlotkin S. An orange a day keeps the doctor away: scurvy in the year 2000. Pediatrics. 2001; 108 (3): E55. https://doi:10.1542/peds.108.3.e55

World Health Organization. Scurvy and its prevention and control in major emergencies [online]. World Health Organisation, 1999 [Viewed 28th February 2021]. Available from:

51st Bubblewrap header

The 51st Bubble Wrap

Cite this article as:
Currie, V. The 51st Bubble Wrap, Don't Forget the Bubbles, 2021. Available at:

With millions upon millions of journal articles being published every year it is impossible to keep up.  Every month we ask some of our friends from PERUKI (Paediatric Emergency Research in UK and Ireland) to point out something that has caught their eye.

Article 1: Anti-coagulation in CRRT

Chen Z, Wang H, Wu Z, Jin M, Chen Y, Li J, Wei Q, Tao S, Zeng Q. Continuous Renal-Replacement Therapy in Critically Ill Children: Practice Changes and Association With Outcome. Pediatr Crit Care Med. 2021 May 7. doi: 10.1097/PCC.0000000000002751. Epub ahead of print. PMID: 33965990.

What’s it about? 

This paper focuses on the paediatric patient outcomes for anticoagulant therapies used in continuous renal replacement therapy (CRRT) (heparin versus citrate).

The authors conducted a retrospective single centre audit over a 10-year period from 2010 to 2019 (289 patients included in the analysis) in Guangzhou, China. The median age of the patients was 4 years of age with a median fluid overload (FO) percentage at the initiation of the CRRT of 5.4%, and overall mortality of 46.3%.

Interestingly in 2015, the CRRT anticoagulant therapy practice was changed from heparin to citrate. There was no direct head-to-head comparison of the anticoagulants and in the paper 8 out of 10 patients received citrate anticoagulation. This paper assessed if the change in practice of anticoagulant had an impact on patient mortality.

The most common indications for CRRT in the paper were cytokine clearance 40%, acute kidney injury 23% and metabolic disease at 22%. In the paper, the heparin cohort had a higher mortality of 65% versus 47% in the citrate cohort. Interestingly if CRRT was initiated later (greater than 24 hours) then patients had a higher proportion of receiving vasoactive medication support, required longer mechanical ventilation days and had a greater fluid overload percentage.

Some limitations are that this is a single centre study, and the way in which they determined CRRT initiation time was time from admission to PICU to CRRT initiation time- which is not the usual way of evaluating early vs late CRRT.

Why does it matter? 

CRRT provides life-saving kidney support and assists with removal of electrolytes, fluid, and toxins from the body. Citrate anticoagulation in CRRT has offered patients an alternative to heparin. Heparin has the risk of heparin induced thrombocytopenia.

The emergence of citrate anticoagulant in CRRT over the last decade has offered promise for patients in this high-risk group and decreased mortality.

Clinically Relevant Bottom Line:

Paediatric patients presenting to hospital who require CRRT have a high risk of mortality. This paper concluded that a lower mortality with CRRT was associated with fluid overload % < 10%, CRRT initiation in less than 24 hours, and the use of citrate anticoagulant.

Reviewed by: Michele Cree

Article 2: It’s not always COVID

Snelson E, Roland D, Munro APS Throat and ear infections in children: URTI in the time of COVID-19Archives of Disease in Childhood – Education and Practice 2021;106:172-174.

What’s it about? 

This piece, prompted by restrictions presented by the COVID19 pandemic, discusses an alternative approach to the management of upper respiratory tract infections (URTI – tonsillitis and otitis media) in the UK.

The reduction in rheumatic fever incidence and vaccination against Haemophilus and Pneumococcus has resulted in a reduction in invasive URTI. The primary complications of URTIs are now mostly limited to peritonsilar abscess formation or mastoiditis. The incidence of both of these is not reduced significantly by antibiotic use (NNT >4000) and remain rare in children. The duration of tonsillitis symptoms following antibiotic treatment is only 18hours less, on average, and only if treatment is initiated before day 3 of symptom onset. In addition to this, antibiotics are demonstrated to cause many side effects including GI disturbance, allergy, and increased incidence of atopy and autoimmune conditions later in childhood.

The UK (NICE) guidance for otitis media was clarified in 2019. It now provides a graded approach of observation, delayed prescribing or same-day prescribing depending on the presence of systemic features, complications or in patients <2 years of age with bilateral AOM. Similarly, sore throat presentations are risk-stratified using FeverPAIN or CENTOR scoring – the former has not been validated in patients <3yrs and the latter was derived in an adult population.

Due to these guidelines frequently using the term ‘consider’ before suggested actions, the variation in clinical practice is not a surprise. This results in frustration for both clinicians in doubt and families expecting prescriptions..

Why does it matter? 

There is growing evidence that antibiotic use in URTI does not reduce symptom duration, and that the incidence of URTI associate complications is declining. This unfortunately has not detached clinicians’ hopes of reducing symptoms as a key factor in decision making.

COVID19 had a dramatic impact on clinical practice with the rise of virtual consultation and changes in health-seeking behaviour following government advice.

The Royal Children’s Hospital of Melbourne implemented a binary approach to reduce decision fatigue and improve antimicrobial guardianship. In this model, after the exclusion of sepsis and complications of URTI, AND if the patient is not classified as high risk (e.g. immunocompromised) then antibiotics are not immediately prescribed.

Clinically Relevant Bottom Line:

The proposed binary approach to decision making regarding antibiotic provision in URTI aims to reduce decision fatigue, unify the approach of clinicians, aid antimicrobial stewardship and efforts to inform health seeking behaviours.

For a round- up of the most up to date COVID literature in paediatrics why not visit

Reviewed by: Joshua Tulley

Article 3: A dipstick for diarrhoea?

Cotter JM, Thomas J, Birkholz M, et al. Clinical Impact of a Diagnostic Gastrointestinal Panel in Children. Pediatrics. 2021;147(5):e2020036954

What’s it all about?

This was a multicentre cross sectional-study of paediatric patients, in Colorado, who had stool testing from 2013 to 2017. The study looked at two time periods: 24 months before the introduction of rapid multiplex polymerase chain reaction gastrointestinal panel (GIP) and 24 months after the introduction of GIP. The GIP detects 22 enteric pathogens, including bacteria, viruses, and parasites with an aim to provide antibiotic susceptibilities. Stool cultures were additionally performed when the GIP was positive for Shigella or Salmonella.

The authors compared test use, pathogen detection and time to results. Among children who were hospitalized, they compared length of stay (LOS), ancillary testing including labs and imaging studies, time to treatment, and hospital charges.

After GIP was introduced, there was an increase in stool testing of 21%. There was a higher percentage of positive results (40% vs 11%). Among the 1,986 hospitalized children, only 3% received antimicrobials to treat bacteria/parasitic causes for diarrhoea. There was a significant decrease in time to result (4 vs 31 hours) and time to treatment (11 vs 35 hours). There was also a significant decrease in LOS by 2 days (3.1 vs 5.1 days). However, there was no statistical difference in LOS, ancillary testing, or charges in the overall population.

I would have liked to see whether there was a difference in rate of associated complications or adverse events in the pre and post GIP era among hospitalized children with community-acquired diarrhoea. This study was also conducted within a single healthcare system and in an ideal world should be investigated at other institutions.

Why does it matter?

Children get diarrhoea… a lot. Common culprits include viruses, bacteria, parasites and the occassional non-infectious aetiology. GIP allows for the testing of multiple organisms with faster turnaround of results, but it is also expensive.  We need to be judicious about which patients should undergo testing with GIP and determine whether results will impact clinical care.

The Bottom Line:

GIP may allow for faster turnaround of results, faster time to treatment, and decrease in LOS for a small subset of patients. Although the GIP yielded positive results in 4 out of 10 patients, most positive tests were due to viruses and 6 out of ten of GIP results were negative. Given that most cases of diarrhoea are self-limiting and can be managed with supportive care, the routine use of GIP does not seem cost-effective. Consider GIP (if available in your institution) if the pre-test probability for an actionable and treatable aetiology is high.

For more information on gastroenteritis why not visit Angharad Griffiths’ post at

Reviewed by: Dennis Ren

Article 4: Oxygen in African children with pneumonia

Maitland K, Kiguli S, Olupot-Olupot P et al. Randomized controlled trial of oxygen therapy and high-flow nasal therapy in African children with pneumonia. Intensive Care Medicine 2021;47(5):566-576

What’s it about?

This multicentre African study investigated which delivery method of oxygen support, children (age 28 days to 12 years) admitted with confirmed pneumonia (deemed severely hypoxic (Sp02 80-91%) or hypoxic (Sp02< 92%)) would need to decrease mortality. The trial was named COAST (The Children’s Oxygen Administration Strategies Trial). Those in the severely hypoxic arm (n=388) were randomised to high flow nasal therapy (HFNT) (n=194) or low flow oxygen (LFO) (n=194). Patients in the hypoxic arm (n=1454) were randomised to HFNT(n=363), LFO(n=364) or permissive hypoxia (n=727). HFNT was delivered by AIRVO2– initiated at room air and LFO was oxygen delivered by nasal cannula or standard masks. Ethical approval was sought.

Primary endpoints were mortality at 48 hours and up to day 28 post-randomisation. The entire trial was prematurely stopped due to a campaign in Uganda that deemed permissive hypoxia unethical.  Of the data collected, in the severely hypoxic group, 48 hours mortality was better using HFNT 9.3% vs 13.4% for LFO, demonstrating a 40% risk reduction in the HFNT arm.  For the hypoxic group, there was similar mortality at 48 hours across all arms (1.1% for HFNT, 2.5% for LFO and 1.4% for permissive hypoxia). Similar patterns were demonstrated at 28 days mortality. However, interpretation of the statistical significance of these results was severely limited by the inability to adequately power the study, due to early trial termination.

(For more information on High Flow see Padmanabhan Ramnarayan’s post on High Flow- When and How available at:  

(In addition to this great learning module on Pneumonia by Ellis Collins and Michelle Alisio:

Why does it matter?

In developing countries, the supply and demand of oxygen in hospitals can be financially and logistically challenging. Studies that explore the rationalisation of oxygen therapies that are clinically safe, as well as reduce cost burden are beneficial. This is also relevant, in recent times with the increased demand for oxygen therapy in the COVID-19 pandemic.

Although oxygen therapy is deemed a standard pneumonia treatment, there is evolving evidence of oxygen toxicity with over-use, thus needs more careful consideration.

The bottom line

The use of HFNT vs LFO vs permissive hypoxia in children admitted to hospital with pneumonia in low resource settings still remains unclear.  Although this study does not provide definitive data to inform treatment guidelines, it supports the need for future, adequately powered studies of a similar design to explore this further. Until then, clinicians should be guided by the World Health Organisation (WHO) ‘Hospital Care for Children’ guidance for best practice.

Reviewed by: Melanie Ranaweera

Article 5: Splenic injury? Off you go

Leah Plumblee et al, J Trauma Acute Care Surg.Isolated low-grade solid organ injuries in children following blunt abdominal trauma: Is it time to consider discharge from the emergency department?  2020;89: 887–893 DOI: 10.1097/TA.0000000000002899 PMID: 32769952

What’s it about?

In this study, the authors examine the rate of “major” intervention (surgery, angiographic embolization, or blood transfusion) received by patients with grade I-III solid organ injuries from blunt trauma. The authors performed a secondary analysis of data gathered from two previously conducted trials (PECARN Network). Their hypothesis was that patients with isolated grade I-III solid organ injuries would be unlikely to receive interventions, which would indicate that these patients could be managed by simple observation in the ED, followed by discharge instead of the traditional pathways of admission for overnight observation.

A total of 517 patients were assessed of whom 34 underwent a major intervention. None of the patients with isolated grade I-II solid organ injuries and only 2.6% of the isolated grade III injuries received a major intervention. Almost 1 in 10 had multiple low-grade injuries, and this did not increase the risk of intervention.

It should be noted however, that in the original studies, only 3% of these patients were discharged from the ED directly by the treating clinicians, suggesting that there was something pushing the original clinicians to admit most of these cases. The median length of stay was 2 days.

Additionally, it is important to highlight some patients were excluded from the original trial if they had a CT at their original institution before being transferred to a participating centre. This could be an important source of bias, if the original clinician was concerned enough to transfer a low-grade injury, then the likelihood of intervention is probably higher; but we do not know, as these patients were excluded from the original studies.

Why does it matter?

In contrast to adults, the majority of paediatric solid organ injuries are managed conservatively, particularly low-grade injuries from blunt trauma. The authors conclude that it is likely safe to discharge patients with grade I and II injuries without other significant injuries from the ED after a brief period of observation. While I agree it is unlikely that these patients would require what the authors define as “major” interventions. This definition is too narrow and there are a lot of important therapeutic interventions that are reasons to admit patients that have been excluded from the trial by this definition. Additionally, there were no attempts made to assess for other important factors addressed by admission such as follow up, MDT input and patient satisfaction. As a result, I find that I cannot agree with the sentiment expressed by the authors, while they have shown that this may be a safe option, they have provided insufficient evidence to demonstrate that it is an option that we should pursue. The author’s conclusions are unsupported by the evidence provided and represent too big of a leap. We have no idea what other services patients will miss from inpatient services.

Clinically Relevant Bottom Line:

Caution must be taken when discharging patients from the ED who have evidence of solid organ injury based on the conclusions of this study alone.

Reviewed by: Sean Croughan 

If we have missed out on something useful or you think other articles are absolutely worth sharing, please add them in the comments!

That’s it for this month. Many thanks to all of our reviewers who have taken the time to scour the literature so you don’t have to.

All articles reviewed and edited by Vicki Currie