PEM adventures chapter 4

Cite this article as:
Team PEM Adventures. PEM adventures chapter 4, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.33252
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.

Myocarditis

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.

References

  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:
    https://doi.org/10.31440/DFTB.14563
  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.

Croup

Cite this article as:
Laura Riddick. Croup, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.32637

It’s 0200 hours in the Emergency Department and you hear a seal …

As children have returned to school we have seen more croup through the ED so it’s time to refresh your memories!

What is it?

Viral laryngotracheobronchitis. It is essentially inflammation around the main large breathing structures and caused usually by parainfluenza 1 + 3. Other respiratory viruses including SARS-CoV-2 and RSV may also be involved. This inflammation causes a tell-tale cough and noisy breathing due to the obstruction to flow. There may be signs of increased work of breathing too such as sub-costal recession or a tracheal tug. They are generally quite well and are running around the waiting room!

Who gets it?

A lot of children – roughly 2-3% of all children per year! These kids are usually between six months and four years of age, and occurs at the beginning of autumn, though this spring we are seeing a lot of cases. Children with croup may present with a preceding coryza-like illness and a low-grade fever. This then develops into a barking “seal-like” cough and, for some reason, always seems worse at night. Boys are more commonly affected than girls, and some children seem to get it yearly.

How do we treat it?

This depends on your assessment of the child. Croup is a self-limiting viral illness and treatment tends to look to short term reduction in the inflammation to improve the work of breathing. Historically clinicians have used Westley scoring system to score croup and assess their severity before giving medication.

Westley Croup scxore
Westley Croup Score

In children who look unwell, it is important to not upset them by avoiding unnecessary interventions such as excessive handling or performing an ENT exam.

Steroids

If the child is able to take the medication, dexamethasone or prednisolone should be given to all cases of croup where any stridor or increased effort in breathing is present.

Dexamethasone appears to be more efficacious than prednisolone. It has an onset of action within 1 hour (30 minutes – 4 hours) and has a half-life of up to 36-72 hours (Schimmer 2005). There has been debate overdosing with doses of 0.15mg/kg, 0.3mg/kg and 0.6mg/kg of dexamethasone. Ultimately, 0.15mg/kg not inferior to 0.6mg/kg. At the time of writing both NICE and the BNFc recommend 0.15mg/kg as the initial dose of dexamethasone. If there are concerns about re-occurrence patients are occasionally sent home with an additional dose to be taken 12 hours later.

Prednisolone tends to be favoured in the primary care setting, at a dose of 1mg/kg with two additional daily doses. There appears to be no significant clinical difference between the two different steroids in terms of the need for additional treatment or length of stay. Dexamethasone was associated with a reduction in re-attendances, which may be due to the shorter half-life of Prednisolone (Gates 2018, Schimmer 2005)

Nebulised budesonide (2mg stat dose) is reserved for children who cannot take the dose. This may be because it was spat ou tor because they are working too hard to breathe. A Cochrane review in 2018 shows that budesonide is not superior to dexamethasone, with Westley Croup scores better in the dexamethasone group at 6 and 12 hours compared to budesonide. A combination of treatment does not appear to lead to additional benefit (Gates 2018)

Adrenaline/epinephrine

In severe cases, when the child has features of severe work of breathing, including significant recession, hypoxia or tiring, nebulised adrenaline has been used (0.4-0.5ml/kg, maximum 5ml of 1:1000). Adrenaline provides short term relief from respiratory distress and can be a bridge to getting steroids on board. The effects are short-acting and wear off after a couple of hours. It can be repeated every 30 minutes, although if you need repeat doses, anaesthetics and senior colleagues should be involved in this patients’ care.

How do we not treat it?

In the olden days parents tried treating croup at home with steam inhalation (not effective). In hospitals, humidified oxygen has also been tried though this has not been proven to be effective either (Moore 2007). Heliox (oxygen and helium combined) has also been looked at as it may improve airflow. The evidence is limited and safety and efficacy remain questionable (More, 2018). There is no evidence that salbutamol works in croup.

They sound better, what’s next?

If they are well and the stridor has resolved, patients can be discharged home with safety-netting advice. The effects of dexamethasone should last as croup itself is usually limited to 2-3 days of symptoms. Parents need to be aware that some symptoms of respiratory distress can return, usually the following night.

Patients may require a prolonged period of observation if:

  • stridor is still present at rest, or there is increased work of breathing
  • the child is very young (<3 months)
  • an adrenaline nebuliser had to be given
  • there is a past history of severe croup
  • there is a history of upper airway problems (i.e. laryngomalacia or subglottic stenosis)
  • concerns about the child returning (i.e. long-distance, social concerns)

When is it not croup?

  • Epiglottitis – a rare condition thanks to the HiB vaccine. A child would present with sudden onset, fever, drooling and looks unwell holding the head back and neck extended. This is a medical emergency and keeping the patient calm is paramount.
  • Tracheitis– thankfully also rare. It presents with the child acutely unwell after a prolonged course similar to Croup.
  • Anaphylaxis/allergy – this may be accompanied with angioedema, rash and wheeze, and requires swift treatment with IM adrenaline
  • Quinsy/retropharyngeal abscess
  • Foreign body – Usually the history would help suggest this, with a sudden onset history in a well-child.

COVID and croup

Most children admitted into hospital are now swabbed for COVID. This can provide a challenge – balancing upsetting the child (and making the upper airway obstruction worse) and performing an invasive swab. It is sensible not to swab the child whilst there is still concern about acute stridor and work of breathing..

There have been some case studies to suggest a small cohort of patients with croup who were SARS-CoV-2 positive are less responsive to the usual treatment (Venn 2020). These cases may need prolonged admission due to lack of response and the need for additional supportive therapy.

Selected references

  1. Al-Mutairi B, Kirk V. Bacterial tracheitis in children: Approach to diagnosis and treatment. Paediatr Child Health. 2004;9(1):25-30. doi:10.1093/pch/9.1.25
  2. Garbutt JM, Conlon B, Sterkel R, et al. The comparative effectiveness of prednisolone and dexamethasone for children with croup: a community-based randomized trial.  Clin Pediatr (Phila). 2013;52(11):1014–1021.
  3. Gates  A, Gates  M, Vandermeer  B, Johnson  C, Hartling  L, Johnson  DW, Klassen  TP. Glucocorticoids for croup in children. Cochrane Database of Systematic Reviews 2018, Issue 8. Art. No.: CD001955. DOI: 10.1002/14651858.CD001955.pub4. Accessed 28 April 2021
  4. Moore M, Little P. Humidified air inhalation for treating croup: a systematic review and meta-analysis.  Fam Pract. 2007;24(4):295–301
  5. Moraa I, Sturman N, McGuire TM, van Driel ML. Heliox for croup in children. Cochrane Database of Systematic Reviews 2018, Issue 10. Art. No.: CD006822. DOI: 10.1002/14651858.CD006822.pub5
  6. Schimmer B P, Parker K L. Adrenocorticotropic hormone: adrenocortical steroids and their synthetic analogs: inhibitors of the synthesis and actions of adrenocortical hormones. Goodman and Gilman’s the pharmacological basis of therapeutics, 9th edition. New York: McGraw‐Hill, 20051459–1485
  7. Smith DK, McDermott AJ, Sullivan JF. Croup: Diagnosis and Management. Am Fam Physician. 2018 May 1;97(9):575-580. PMID: 29763253.
  8. Sparrow A, Geelhoed G. Prednisolone versus dexamethasone in croup: a randomised equivalence trial. Arch Dis Child. 2006;91(7):580-583. doi:10.1136/adc.2005.089516
  9. Venn AMR, Schmidt JM, Mullan PC. A case series of pediatric croup with COVID-19 [published online ahead of print, 2020 Sep 15]. Am J Emerg Med. 2020;S0735-6757(20)30829-9. doi:10.1016/j.ajem.2020.09.034
  10. https://www.rch.org.au/clinicalguide/guideline_index/Croup_Laryngotracheobronchitis/
  11. https://cks.nice.org.uk/topics/croup/

Following bronchiolitis guidelines

Cite this article as:
Ben Lawton. Following bronchiolitis guidelines, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.32798

In 2016 our friends at PREDICT produced a robust, evidence-based guideline for the management of bronchiolitis. They assembled a diverse team of experts, decided on the key questions we ask ourselves when managing babies with bronchiolitis and then did a deep dive of the literature to provide answers to those questions. You can read the guideline here, or the DFTB summary here but the key messages will be familiar to regular readers of DFTB. The list of things that do not help babies under 12 months with bronchiolitis includes salbutamol, chest x-rays, antibiotics, nebulised adrenaline and steroids. In the real world, however, these ineffective treatments continue to be used – so what can we do about that? 

The authors of a new PREDICT study released in JAMA Pediatrics on 12 April 2021 sought to demonstrate whether a group of interventions they developed using theories of behaviour change would be effective in reducing the number of ineffective interventions given to bronchiolitic babies. 

Haskell L, Tavender EJ, Wilson CL, et al. Effectiveness of Targeted Interventions on Treatment of Infants With Bronchiolitis: A Randomized Clinical Trial. JAMA Pediatr. Published online April 12, 2021. doi:10.1001/jamapediatrics.2021.0295

Who did they study? 

This was an international multicentre cluster randomised controlled trial (RCT) involving 26 hospitals in Australia and New Zealand. It is described as a “cluster” RCT as randomisation was by hospital rather than by patient. The randomisation was a bit complicated. It was stratified to make sure secondary and tertiary hospitals from each country were represented in each group. Baseline data was collected from 8003 patient records from the three bronchiolitis seasons prior to the start of the intervention period. A further 3727 charts analysed from the season in which the intervention took place. The data from the three prior seasons were used to ensure baseline similarity between groups and to establish patterns of practice change that were already occurring. In short, this was a big study that ensured representation of both specialist children’s hospitals and mixed general hospitals. 

What did they do? 

Hospitals randomised to the intervention group received a package of interventions based on the Theoretical Domains Framework (TDF), developed following an earlier qualitative study that investigated why we do what we do when managing bronchiolitis infants. The TDF is one of the most commonly used frameworks in implementation science and is considered particularly good at identifying interventions to address barriers and facilitators that influence behaviour change. The package included:

  • Appointing clinical leads from medical and nursing streams in both emergency departments and inpatient paediatric units.
  • The study team meeting with those clinical leads to explore the local practice and any anticipated barriers to change.
  • A one day train-the trainer workshop to ensure clinical leads were comfortable using the educational materials provided to train local staff.
  • An education pack including a PowerPoint with scripted messages specifically designed to promote change, a clinician training video, evidence fact sheets, promotional materials and parent/caregiver information sheets.
  • Monthly audits of the first 20 bronchiolitis patients with the results shared and compared to the best performing hospital.

What about the control group?

Hospitals randomised to the control group were just left to their own devices for the year of the intervention period. They had access to the guidelines and were welcome to share that information as they would in any other circumstances. The intervention package was made available to control hospitals in the season following the study period. 

What did they show? 

The primary outcome was the proportion of infants who complied with all five of the Australasian Bronchiolitis Guideline recommendations known to have no benefit (chest x-ray, salbutamol, steroids, adrenaline, antibiotics). There was an 85.1% compliance rate in the intervention group compared to a 73% compliance rate in the control group. In other words, in hospitals that were part of the intervention group, an average of 85.1% of kids received care in line with the guidelines, compared to only 73% receiving guideline compliant care in control hospitals. This was a significant difference.

Secondary outcomes showed improvement was consistent in both the ED and inpatient phases of care. Unsurprisingly, there was no difference in hospital length of stay or admission rates to ICU. 

The DFTB verdict

On the surface this is a robust, well designed study showing that if we put some thought and some resources into supporting our colleagues in doing the right thing then babies with bronchiolitis will get better care in our hospitals. They won’t leave hospital any quicker and they won’t have a lesser chance of needing ICU but they will be exposed to fewer interventions that will not do them any good and may do them some harm. Dig a little deeper though and the big messages in this paper go way beyond the management of bronchiolitis. The implementation science based interventions used in this study can be adapted to anything, and though they have been shown to be effective in getting us to do the right thing here, we haven’t shown that their efficiency has been optimised yet. Great breakthroughs in novel medical science are exciting but there are huge improvements in care to be gained through getting the best care that we do know about to every patient every time. This paper should serve as fuel for the fires lighting implementation science’s journey from the shadows to the centre stage of improvement in clinical care. 

From the authors

The study’s senior author, Prof Stuart Dalziel gave DFTB the following take: 

“The key finding is that we can do better. By using targeted interventions, based on established behaviour change theories and developed from work looking at why clinicians manage patients with bronchiolitis the way they do, we can improve the management of patients with bronchiolitis such that it is more consistent with evidence based guidelines.

In the field of implementation science (IS) and knowledge translation (KT) a 14% improvement in care is a large change.

Changing clinician behaviour is complicated, this is especially so for de-implementation of medical interventions. Many factors influence clinician behaviour and it is thus perhaps naïve to think that a single intervention can cause a significant change to behaviour. For a number of decades the majority of clinical guidelines for bronchiolitis have emphasised that chest x-ray, antibiotics, epinephrine, corticosteroids and salbutamol are low-value care and not evidence based. Yet despite this consistent messaging from guidelines the use of these interventions has remained considerably higher than what it should be. While the interventions delivered in our study were not unique (site based clinical leads, stake holder meetings, train-the-trainer workshops, targeted clinical education, educational material, and audit and feedback) they were specifically developed, using an established framework for behavioural change, following a qualitative study that determined why clinicians managed bronchiolitis they way they do. This prior study, addressing the barriers and enablers to evidence based care, and the subsequent step wise approach to developing the targeted interventions that we used was critical in achieving the change in clinician behaviour observed in our randomised controlled trial”.

The study’s lead author, Libby Haskell, stated:

“Bronchiolitis is the most common reason for children less than one year of age to be admitted to hospital. We can improve the care of these infants, such that they are receiving less low-value care. In order to de-implement low-value care we need to first understand barriers and enablers of care, and then develop targeted interventions, built on robust behavioural change models, to address these. This approach can be used to improve care for other high volume conditions where we see considerable clinical variation in care and with clearly established clinical guidelines on appropriate management.”

Let us know what you think in the comments below 

High flow therapy – when and how?

Cite this article as:
Padmanabhan Ramnarayan. High flow therapy – when and how?, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.31730

Isn’t nasal high flow just a fancy name for plain old high flow oxygen? Or is it CPAP-lite? For a therapy that has become so popular in less than a decade, amazingly, there is more opinion sloshing around than proper scientific evidence…

OK, back up, what is Nasal High Flow therapy?

Nasal high flow therapy (NHF), aka high flow nasal cannula therapy (HFNC), is a non-invasive mode of respiratory support, involving the delivery of heated (to 37° C) and humidified (to nearly 100% relative humidity) gas (oxygen and/or medical air) through nasal cannulae at high gas flow rates. What is a “high” gas flow rate is still not uniformly defined (some studies say >2 L/min and others >4 L/min). In physiological terms, to provide the true benefits of “high flow”, the gas flow rate should exceed the patient’s maximal peak inspiratory flow rate (roughly 8-10 x normal minute ventilation).

Makes sense, but what is a child’s peak inspiratory flow rate?

Short answer – it changes according to the age and the extent of respiratory distress. For example, a 4 kg baby breathing at 40 breaths/min and inhaling a tidal volume of 5 ml/kg (=20 ml) would have a minute ventilation of 0.8 L/min and a peak inspiratory flow (PIF) rate of nearly 3 L/min. However, the same infant would have a much higher PIF in respiratory distress. Matching the maximal PIF rate by aiming for roughly 8-10 x normal minute ventilation (in this case, 8-10 x 0.8 L/min = 7-8 L/min) is the key principle of NHF therapy. NB: Magically, the 8 L/min flow rate in this baby is also 2 L/kg/min (more on that later!)

Got it. But when should I start NHF in the ED?

Case 1. A previously healthy 4-month old infant is seen in the emergency department with a two-day history of coryza and poor feeding. On examination, he has mild/moderate subcostal recession and a respiratory rate of 60 bpm. His oxygen saturation in room air is 89%. Would you start nasal high flow?

This baby most likely has mild viral bronchiolitis and the main question is whether to start standard oxygen therapy (SOT) via nasal cannulae or NHF. The most useful clinical outcomes we are interested in are transfer to paediatric intensive care (PICU) and the need for endotracheal intubation.

What does the evidence say?

A recent systematic review (Lin J et al. Arch Dis Child 2019) is an obvious starting point. For the outcome of transfer to PICU, only two RCTs were included (Franklin et al. NEJM, 2018; Kepreotes et al. Lancet 2017). The overall risk ratio was 1.30 (95% CI 0.98, 1.72) indicating no significant difference between NHF and SOT, although there was a tendency to favour SOT.

Similarly, only two RCTs were included for the outcome of intubation (Franklin et al. NEJM, 2018; Yang et al. Chinese Pediatric Emergency Medicine, 2017). The overall risk ratio was 1.98 (95% CI 0.60, 6.56), again with no significant difference between NHF and SOT. So, not much joy from the systematic review…

Considering that Franklin et al dominated the systematic review in terms of sample size, it is useful to look at this RCT in a bit more detail, from a PICO point of view as well as the flow of patients through the RCT.

Population: Infants <12 months of age with bronchiolitis and needing supplemental oxygen

Intervention: NHF at 2 L/kg/min

Control: Standard oxygen therapy

Outcome: Escalation of care due to treatment failure (composite outcome)

A few reflections on the outcomes of infants in this RCT: although nearly double the number of infants randomised to SOT “failed treatment” compared to NHF, it is notable that over 75% of infants randomised to SOT did not “fail”; the majority of those who did “fail” SOT were rescued by NHF; and since NHF “failure” automatically led to PICU transfer, in effect, more infants were transferred to PICU in the NHF group than in the SOT group (12% vs 9%). Essentially, this RCT could be considered a trial of ‘immediate’ NHF versus ‘rescue’ NHF, as covered by us here previously.

Bottom line: There is no advantage to starting NHF as first-line therapy in an infant with mild bronchiolitis. A more clinically and cost-effective strategy would be to use NHF as ‘rescue’ therapy when standard oxygen therapy has failed.

Case 2. An ex-prem born at 24 weeks gestation, now 4 months old, is seen in the emergency department with a 24-hour history of coryza and cough. On examination, he has moderate/severe subcostal recession and a respiratory rate of 80 bpm. His oxygen saturation in room air is 85%. Would you start nasal high flow?

This baby is much sicker, with significant past medical history, and most likely has moderate/severe bronchiolitis. Would NHF be more useful as first-line therapy in this infant, where previously nasal CPAP would have been an option – can NHF be used as ‘CPAP-lite’? A really useful clinical outcome to focus on is endotracheal intubation.

What does the evidence say?

Lin et al summarise the evidence in their recent systematic review. For the outcome of intubation, 4 RCTs were included, but the total number of patients included were low (n=264). Intubation rates were identical in the NHF and CPAP groups (5.3%), with a risk ratio of 0.96 (95% CI 0.35, 2.61). So, there is not much evidence to support the use of NHF compared to CPAP, although quite notably, the rate of adverse events was lower in the NHF group (8% vs 21%).

Bottom line: There is no clinical advantage to starting NHF as first-line therapy in an infant with moderate to severe bronchiolitis to avoid intubation. However, its adverse event profile and tolerability by infants might make NHF more appealing as first-line therapy.

When should I start NHF in the HDU?

Case 3: A 5-year old boy with cerebral palsy and epilepsy is admitted to the paediatric HDU bed with fever, cough and respiratory distress. On examination, he has moderate subcostal and intercostal recession and a respiratory rate of 45 bpm. His oxygen saturation in room air is 88%. Would you start nasal high flow?

In this older child with a complex past medical history, is starting NHF, compared to either standard oxygen or CPAP, beneficial in terms of avoiding the need for endotracheal intubation?

What does the evidence say?

A recent systematic review (Luo J et al. Journal of Pediatrics, 2019) is an obvious starting point. In the comparison of NHF versus SOT, 5 RCTs were included, although 2 were focussed on bronchiolitis (previously covered – Franklin et al and Kepreotes et al). The other 3 RCTs were small (Chisti et al. Lancet, 2015; Ergul et al. Eur J Pediatrics, 2018; Sittikharnka et al. Indian J Crit Care Med 2018) with just 300 patients in total. The overall risk ratio for intubation from these 3 studies alone (calculated specifically for this post) was 0.72 (95% CI 0.38, 1.36). Similarly, in the comparison of NHF versus CPAP, 4 RCTs were included but 2 were in bronchiolitic infants (covered earlier). The other two RCTs (Ramnarayan et al. Crit Care 2018; Chisti et al. Lancet 2015) included just 187 children. The overall risk ratio for intubation based on these two RCTs (calculated for this post) was 2.14 (95% CI 0.93, 4.92) indicating a tendency for a higher intubation rate with NHF in older children.

Bottom line: In an older child, intubation was not less frequent when NHF was used compared to SOT as first line therapy. There was a tendency for NHF to be associated with a higher intubation rate compared to CPAP.

Great – what is the best way to provide NHF?

Starting gas flow rate

Milesi et al showed in physiological studies in infants aged <6 months with bronchiolitis that the work of breathing is reduced considerably when the gas flow rate is set at nearly 2 L/kg/min. In their cohort of 21 infants (mean weight 4.3 kg), the measured work of breathing was lowest at a flow rate of 7 L/min (compared to 1, 4 and 6 L/min). Similarly, in children up to the age of 3 years with pneumonia, work of breathing was reduced by nearly 20% at a flow rate of 1.5 L/kg/min compared to 0.5 L/kg/min (Weiler et al. Journal of Pediatrics 2017). Usual adult flow rates range from 50-60 L/min.

In summary, the optimal gas flow rate does not increase in a linear fashion with increasing age/weight, instead it goes from nearly 2 L/kg/min in infancy to nearly 1 L/kg/min in young adults.

RCTs of different starting flow rates

There have been two RCTs comparing NHF flow rates in bronchiolitis (Yurtseven A et al. Ped Pulm 2019; Milesi et al. Intens Care Med 2018). In the former, 1 L/kg/min (n=88) was compared to 2 L/kg/min (n=80) in infants <24 months with clinical severe bronchiolitis presenting to the emergency department. The primary outcome was ‘treatment failure’ within 24 hours. There was no significant difference in treatment failure between the two flow rates (1 L/kg/min: 11.4%; 2 L/kg/min: 10%). The second RCT compared 2 L/kg/min (n=142) with 3 L/kg/min (n=144) in infants aged <6 months with moderate/severe bronchiolitis. The primary outcome was treatment failure within 48 hours. There was no significant difference in treatment failure between the two groups (2 L/kg/min: 38.7%; 3 L/kg/min: 38.9%).

A useful chart with suggested starting flow rates based on weight is used in the ongoing FIRST ABC clinical trial of NHF versus CPAP.

Nasal cannula size

There are different nasal cannula sizes available based on the manufacturer. The general rule of thumb is that the cannula prongs should be no more than 50% of the diameter of the nostril to avoid inadvertent occlusion of the nasal passages. It is also advisable to start the gas flow rate at a low rate and then increase gradually over 10-15 min to avoid patient discomfort. Pacifiers may be useful in babies to prevent mouth opening.

Weaning NHF

There are no RCTs comparing weaning strategies for NHF. Clinical practice is also highly variable – in a global survey of practice in over 1000 PICU professionals by Kawaguchi et al, 68% weaned the FiO2 first to a threshold value (e.g. 0.40) and then weaned the flow rate gradually, 11% weaned the FiO2 first to a threshold value (e.g. 0.40) and then stopped NHF, and 4% weaned the flow rate alone without weaning the FiO2. The FIRST ABC RCT algorithm for the weaning of NHF provides a weight-based approach to a one-step weaning process and suggested clinical thresholds for weaning and stopping NHF.

The take homes

  • Nasal high flow is a form of non-invasive respiratory support that sits somewhere between standard oxygen therapy and nasal CPAP.
  • In infants with mild bronchiolitis, there is no clinical (or cost) benefit in starting NHF as first-line treatment – rather, NHF is best used as a ‘rescue’ therapy after standard oxygen.
  • In infants with moderate/severe bronchiolitis, NHF may be a useful first-line therapy owing to its ease of use and since it is better tolerated by infants, however there is no clinical benefit compared to nasal CPAP.
  • In older children with respiratory failure, there is little RCT evidence to guide practice – however, there is no clear benefit of starting NHF over and above standard oxygen. NHF may be associated with a higher intubation rate compared to CPAP in older children.
  • There is no RCT evidence to support either 1, 2 or 3 L/kg/min NHF flow rates in infants with bronchiolitis; however, physiological evidence suggests that nearly 2 L/kg/min is associated with reduction in work of breathing. Suitable flow rates in older children approximate 1.5 L/kg/min and in young adults, 1 L/kg/min.
  • There is no RCT evidence to support one way of weaning over another – the most common practice seems to be to reduce FiO2 to below 0.40, followed by a reduction in the NHF flow rate.
  • Ongoing RCTs such as the FIRST ABC trial will help address the question whether NHF is non-inferior to CPAP in critically ill children.

Nebulised magnesium sulphate for asthma?

Cite this article as:
Abdul Safras. Nebulised magnesium sulphate for asthma?, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.31503

Acute asthma is a common presentation to the Paediatric Emergency Department. Treatment is adjusted depending on the child’s clinical acuity, but commonly includes inhaled salbutamol (a beta-2 agonist), oral corticosteroids, and – in more severe cases – inhaled ipratropium (an anticholinergic). However, some patients with moderate to severe asthma do not respond to this treatment.

 Magnesium sulphate is commonly used intravenously as an escalation of care, with evidence supporting reduced hospital admission in children. The 2019 NICE-accredited BTS / SIGN guideline on the management of asthma suggests magnesium sulphate can be nebulised with salbutamol and ipratropium in children with a short duration or acute severe asthma with oxygen saturations below 92%. But how effective is nebulised magnesium sulphate?

Schuh S, Sweeney J, Rumantir M, et 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 Clinical Trial. JAMA. 2020;324(20):2038–2047. doi:10.1001/jama.2020.19839

Clinical question

What is the effectiveness of nebulized magnesium added to inhaled short-acting beta-agonists in children and adolescents with acute asthma in the emergency department who remain in moderate or severe respiratory distress after evidence-based standardized initial therapy?

Design and setting

A randomized double-blind parallel-group clinical trial conducted over 8 years from September 2011 to November 2019, in 7 tertiary-care paediatric emergency departments in Canada. Randomization allocations were concealed to maintain blinding.

PICO image

Population

Children 2 to 17 years of age were eligible if they had a diagnosis of asthma made by a physician, had a previous episode of acute wheeze, and had persistent moderate to severe asthma after completing 1 hour of initial treatment. This treatment included systemic steroids, three doses of inhaled ipratropium bromide and three doses of inhaled salbutamol.

Intervention

Three consecutive nebulisers, consisting of 5 mg of salbutamol (known as albuterol in Canada) and 600 mg (1.2 mL) of magnesium sulphate.

Control

Three consecutive nebulisers containing 5mg of salbutamol, but instead of magnesium sulphate, the nebulisers contained 1.2 mL of 5.5% saline placebo.

The magnesium and placebo solutions were identical in volume, colour, taste, and smell, both in the steady state and during nebulization. Study participants, research nurses, ED staff, and the study analyst were blinded to the treatment assignment.

Outcome

The primary outcome was whether the treating physician decided to hospitalise children in the study due to persistent respiratory distress or the need for supplemental oxygen within 24 hours of randomisation.

The secondary outcomes included adverse effects, changes in PRAM score, respiratory rate, oxygen saturations or blood pressure, hospitalisation or revisits within 72 hours or administration of IV magnesium after the experimental therapy.

Exclusions

Several exclusion criteria were applied. Children requiring immediate airway management; children who received IV magnesium prior to enrolment; children with comorbidities such as chronic lung disease, cardiovascular, kidney, neurologic, or other systemic disease; and children with a known hypersensitivity to magnesium. Families without adequate command of the English or French language, without telephone or e-mail contact information, and those previously enrolled were also excluded.

What is the PRAM score?

PRAM (Paediatric Respiratory Assessment Measure) is a 12-point clinical scoring system that captures a patient’s asthma severity using a combination of scalene muscle contraction, suprasternal retractions, wheezing, air entry and oxygen saturation. PRAM was originally developed for patients aged 3 – 6 years and subsequently validated in children aged 1 to 17 years old.

Asthma scores are commonly used in the USA and Canada, however, are much less frequently used in the UK, Ireland, Australia and NZ. A recent PERUKI survey found that none of 59 hospitals routinely collected enough information to be able to calculate a PRAM score for asthma patients.

That being said, a PRAM score of 4-7 is considered “moderate” asthma, while 8 or more suggests “severe” illness.

Analysis

Of a total of 5846 screened patients, 4332 met various exclusion criteria (the most common was the 2740 patients who had a PRAM score of 4 or less after initial therapy), 273 declined participation, and another 423 did not participate, mostly due to absence of a primary caretaker.

818 children were randomised and the results of 816 children were analysed (two children were excluded, one from each group, because they were lost to follow or not eligible).

What did they find?

The primary outcome was hospital admission within 24 hours. 178 of the 409 children in the magnesium sulphate group (43.5%) were hospitalised, compared to 194 of the 407 children in the placebo group (47.7%). The difference between groups was 4.2%, however, the 95% confidence intervals range from -11% to 2.8%, suggesting that there may be no significant difference.

The were no differences in any secondary outcomes between the two groups: no difference in change in PRAM score from baseline at 240 minutes (4 hours); no difference in hospitalisations; no difference in revisits within 72 hours; and no difference in administration of IV magnesium after the experimental therapy.

There were relatively more adverse events in the magnesium group than the placebo group, but more serious adverse events in the placebo group. All observed serious adverse events consisted of admissions to PICU and none were attributed to the experimental therapy.

There was no difference in outcome between “intention to treat” analysis (all patients enrolled in the study) and “per protocol” analysis (those who completed all three assigned treatments), and no difference demonstrated for those with more severe asthma.

Clinical bottom line

Children with acute asthma who received nebulised magnesium with salbutamol did not have a significantly lower hospitalisation rate than those given salbutamol alone. This study suggests that patients who present with moderate to severe asthma will not benefit from nebulized magnesium sulphate added to salbutamol.

Will it change my practice? – Simon Craig

This is a well-conducted study from the Pediatric Emergency Research Canada (PERC) network and highlights how challenging it is to conduct high-quality research. The authors made an incredible effort to recruit over 800 patients from 7 hospitals over an 8-year period.

Although magnesium alone has some bronchodilator properties (when compared to placebo), it doesn’t look like it’s worth adding to inhaled salbutamol for children who are still unwell after initial asthma therapy.

This study also makes me wonder how good IV magnesium really is… It will be very interesting to see the various paediatric emergency research networks try to tackle large multicentre trials to answer some of the big “IV therapy for asthma” questions. Australian, UK and Irish guidelines don’t recommend inhaled magnesium, and I doubt they will change as a result of this study.

ng key info for the paper

References

Chalut, D.S., Ducharme, F.M., & Davis, G.M. (2000). The preschool respiratory assessment measure (PRAM): A responsive index of acute asthma severity. Journal of Pediatrics, 137(6), 762-768.

Ducharme FM, Chalut D, Plotnick L, Savdie C, Kudirka D, Zhang X, Meng L, McGillivray D. The Pediatric Respiratory Assessment Measure: a valid clinical score for assessing acute asthma severity from toddlers to teenagers. J Pediatr. 2008 Apr;152(4):476-80, 480.e1. doi: 10.1016/j.jpeds.2007.08.034. Epub 2007 Oct 31. PMID: 18346499.

Cheuk DK, Chau TC, Lee SL. Ameta-analysis on intravenous magnesium sulphate for treating acute asthma. Arch Dis Child. 2005;90(1):74-77. doi:10. 1136/adc.2004.050005

Liu X, Yu T, Rower JE, Campbell SC, Sherwin CM, Johnson MD. Optimizing the use of intravenous magnesium sulfate for acute asthma treatment in children. Pediatr Pulmonol. 2016;51(12):1414-1421. doi:10.1002/ppul.23482

https://www.chusj.org/CORPO/files/32/32ba0b8c-4894-4d8e-87ca-a46e4c0924a5.pdf

https://www.asthmahandbook.org.au/acute-asthma/clinical/add-on-treatment

It’s Only Wheeze – Treatment Is Simple, Isn’t It?: Meredith Borland at DFTB19

Cite this article as:
Team DFTB. It’s Only Wheeze – Treatment Is Simple, Isn’t It?: Meredith Borland at DFTB19, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.20828

Meredith Borland is a paediatric emergency physician and the Director of Emergency Medicine at Perth Children’s Hospital in Perth, Western Australia. She was a founding member of the PREDICT Executive and is the current chair of PREDICT.

Last year at DFTB18, Meredith continued an ongoing discussion about the use of steroids in wheeze. This year, she took us on a journey through an emergency department visit for a number of children who may or may not receive various interventions. This was a fun, interactive and thought-provoking talk that highlighted some common differences in practice.

#doodlemed on this talk by @char_durand below

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.

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.

Bronchiolitis: Ed Oakley at DFTB19

Cite this article as:
Team DFTB. Bronchiolitis: Ed Oakley at DFTB19, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.22370

When a medical student starts their paediatric ED rotation they need to know three key illnesses and that will cover the majority of patients that they see. To round out the ABC trifecta of asthma and crapping (acute gastroenteritis) we have bronchiolitis. At #DFTB19 Ed Oakley from PREDICT gave us the latest.

 

 

 

DoodleMedicine sketch by @char_durand-done live from Australia via the DFTB19 streaming video link!

 

 

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. 

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.

iTunes Button
 

 

Common Rashes Module

Cite this article as:
Aoife Fox. Common Rashes Module, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.27731
TopicCommon rashes
AuthorAoife Fox
DurationUp to 2 hours
Equipment requiredNone
  • Basics (10 mins)
  • Main session: (2 x 15 minute) case discussions covering the key points and evidence
  • Advanced session: (2 x 20 minutes) case discussions covering grey areas, diagnostic dilemmas; advanced management and escalation
  • Game
    Quiz (10 mins)
  • Infographic sharing (5 mins): 5 take home learning points

We also recommend printing/sharing a copy of your local guideline.

Definitions/rash description:

  • Macule: a flat area of colour change <1 cm in size (e.g., viral exanthem [such as measles and rubella], morbilliform drug eruption).
  • Patch: a large macule >1 cm in size (e.g., viral exanthem [such as measles and rubella], morbilliform drug eruption).
  • Papule: a raised area <1 cm in size (e.g., wart).
  • Nodule: a larger papule, >1 cm in size (e.g. nodular prurigo). 
  • Plaque: a flat-topped raised area (a cross between a nodule and a patch; e.g., psoriasis).
  • Vesicle: a small fluid-filled lesion (blister) <0.5 cm in size (e.g. varicella, eczema herpeticum).
  • Bulla: a larger vesicle >0.5 cm (e.g. bullous impetigo).
  • Pustule: a pus-filled lesion (e.g. folliculitis).
  • Wheal: a transient raised papule or plaque caused by dermal oedema (e.g. urticaria)
  • Scale: flakes of stratum corneum (e.g. eczema, psoriasis).
  • Crust: dried serum, blood, or purulent exudate on the skin surface (e.g. impetigo).
  • Erosion: loss of epidermis, heals without scarring (e.g. Stevens-Johnson syndrome, toxic epidermal necrolysis).
  • Ulcer: loss of epidermis and dermis, heals with scarring (e.g. venous ulcer, pyoderma gangrenosum).
  • Excoriation: loss of epidermis following trauma such as scratching (e.g. pruritus).
  • Fissure: a split in the skin (e.g. angular cheilitis, palmoplantar keratoderma).
  • Lichenification: thickening of the skin with accentuation of skin markings (e.g. chronic eczema, lichen simplex chronicus).
  • Purpura: an area of colour change (red or purple) due to bleeding into the skin; does not blanch on pressure (e.g. vasculitis, disseminated intravascular coagulation).
  • Petechia: a pin-point purpuric lesion (e.g.,vasculitis, disseminated intravascular coagulation).
  • Ecchymosis: a larger area of purpura (e.g. vasculitis, disseminated intravascular coagulation).
Some important points to note in history:
  • Where did the rash start?
  • Sequence of the rash?
  • Type of rash?
  • Time of onset and duration?
  • Involvement of palms and soles?
  • Involvement of mucous membranes?
  • Involvement of conjunctiva?
  • Desquamating?
  • Systemic involvement?
  • Associated symptoms – fever/cough/conjunctivitis/runny nose/sore throat/strawberry tongue/itchiness/pain/weakness/headache/lymphadenopathy/swollen extremities/nausea/vomiting/diarrhoea? 
  • Exposures – immunizations/pets/foreign travel/bites (insects/ticks)/recent injury to skin/sexual history/sick contacts?

Common childhood rashes

The terminology for all but fifth disease is not used anymore, however, should anyone be curious here they are:

Also known as..What causes it?When?What rash?Where is the rash?FeverAssociated findings
First diseaseMeaslesParamyxovirusWinter – spring Erythematous, confluent, maculopapularBegins at the hairline spreads inferiorlyHigh feverKoplik spots, cough, coryza and conjunctivitis, Forchheimer spots
Second diseaseScarlet feverStreptococcus pyogenesAutumn – spring Generalised erythema with a sandpaper textureBegins on the face and upper part of trunk and spreads inferiorlyHigh feverPastia lines, Forchheimer spots, strawberry tongue, exudative pharyngitis, abdominal pain, rheumatic fever, circumoral pallor
Third diseaseRubellaRubivirusLate winter – spring Rose-pink, maculopapularSpreads inferiorlySlightly high feverLymphadenopathy, arthralgias, Forchheimer spots
Fourth diseaseThe existence of “fourth disease” is controversial. It was described as a generalised maculopapular rash and desquamation. This exanthema may be staphylococcal scalded skin syndrome
Fifth diseaseSlapped cheekParvovirus B19Winter and spring“Slapped cheek” appearance, lacy reticular rashErythematous cheeks, reticular extremities Slightly high feverRash, waxes and wanes over weeks, arthritis, aplastic crisis
Sixth diseaseRoseola Human herpesvirus 6 and 7SpringRose-pink, maculopapularNeck and trunk High feverLymphadenopathy, febrile seizures, Nagayama spots
Others of note..ChickenpoxHerpes zoster virusLater winter and early springVesicles on erythematous base, crustsBegins on face and trunk and spreads centripetallyHigh feverPruritus
Hand-foot-and-mouthCoxsackie A virusLate summer or early winterElliptical vesicles on an erythematous base, oral vesicle, erosionsMouth, hands and feetHigh feverVesicles on the hands, feet and in the mouth

Forchheimer spots: rose coloured spots on the soft palate that may coalesce into a red blush and extend over the fauces

Koplik spots: clustered white lesions on the buccal mucosa. They are pathognomonic for measles.

Pastia lines: where pink or red lines formed of confluent petechiae are found in the skin creases.

Nagayama spots: erythematous papules on the mucosa of the soft palate and the base of the uvula. You may see these present on the fourth day in two thirds of patients with roseola.

(based on case from RCEM Learning RCEM Learning – Common Childhood Exanthems)

Mark is a 3-year-old boy brought to the ED by his mother with a rash, temperatures and decreased oral intake. His older brother has a similar rash and illness and mum reports that there was an outbreak of chickenpox in the older brother’s school. 

On exam you note a quiet child with a diffuse vesicular rash. On palpation he has generalised lymphadenopathy.

What are the differentials of chicken pox in this case?

What is the incubation period of chicken pox? How long will Mark be infective?

What investigations are necessary?

How would you manage this illness? What treatment would you give?

What patients would you give anti-VZV immunoglobulin to?

Mark’s mum tell you that she has a 2-week old baby at home – what will you do?

What complications of chickenpox can occur?

Mum tells you that the children’s childminder is pregnant what advice do you give?

Discussion point – Do you use NSAIDs?

(Diffuse) disseminated gonococcaemia

(Local) hand, foot and mouth (coxsackievirus)

(Local) herpes zoster

Staphylococcal bacteraemia

DFTB – Exclusion period for infections

The incubation period for chicken pox is usually 10-21 days. The infectivity period starts when symptoms first appear and lasts until all the lesions have crusted over. This is usually around 5-6 days after the onset of the illness, with most crusts disappearing by 20 days.

Chicken pox is a very common illness and the vast majority of cases can be managed symptomatically at home. Prolonged fever >4 days should prompt the suspicion of complications of varicella such as secondary bacterial sepsis. Under these circumstances, patients should be examined carefully with appropriate blood test work up and a chest x-ray, depending on their clinical presentation.

Oral acyclovir has been shown to reduce the effects of chicken pox, for example the number of lesions and duration of fever, if used within 24 hours of the onset of rash in immunocompetent children. Oral acyclovir has not been shown to reduce the incidence of varicella zoster virus pneumonia or other complications when compared to placebo. Cochrane results do not support the widespread use of acyclovir in immunocompetent children.

Pediatric EM Morsels – Chicken Pox

It is used for high risk patients including, immunocompromised children, newborns with maternal Varicella that develops 5 days before to 2 days after delivery, premature babies and hospitalized infants.

Paediatrics Open – Management of varicella in neonates and infants

Asymptomatic newborn in contact with VZV from any infected subject

The mother is proved seropositive:
Very low risk of disease in the baby.
No treatment should be provided.

Observance of the baby at home and encourage parents to come back if any clinical sign or symptom appears in the 2 weeks after contact.

The mother is proved seronegative or refuses testing:
Treat the baby with acyclovir PO 80 mg/kg/day divided into four doses to start 7 days after infective contact and administer during 7 days.

Careful surveillance of the baby during the risk period. Indication and duration of hospitalisation (with airborne and contact precautions) should be discussed in each case depending on child clinical status, parental compliance and social setting. If any doubt, hospitalisation with optimal medical surveillance are warranted during the risk period.

Pneumonia

Bacteraemia

Encephalitis

Bacterial superinfection of skin

Problems may arise where there is a failure to recognise the complications of secondary streptococcal or staphylococcal infections or to appropriately manage high-risk groups. A prolonged fever for more than 4 days in a child with chicken pox, for example, should prompt the suspicion of secondary bacterial complications.

A range of complications including pneumonia, bacteraemia and encephalitis are increasingly being recognised. Neurological complications may occur without a preceding rash.

The incidence of congenital varicella syndrome is low if maternal infection occurs before 20 weeks of gestation. Congenital varicella syndrome is associated with shortened limbs, skin scarring, cataracts and growth retardation.

RCOG – Chickenpox in Pregnancy

The childminder should contact her own GP. She should avoid contact with children until establishing her risk of contracting VZV. 

DFTB – Varicella and NSAIDs

There is a long history of anecdotal evidence associating invasive group A Strep (GAS) complications, or severe skin and soft tissue infections (SSTIs) with exposure to NSAIDs. 

There are currently 5 papers, ranging from 1997 to 2008 which try to answer this question. Almost all the studies used a case-control method to try and answer this question. Where they took a group of children who had varicella and the outcome of interest (invasive GAS infection, severe SSTI), and compared them to a group of children who had varicella and did not get these outcomes, seeing which groups were more likely to have had ibuprofen.

The studies are pretty heterogeneous, so unsurprisingly the results varied. These studies all found an association, but they generally all suffer from the same big problem, which is confounding by indication. It might not be that ibuprofen causes complications, but rather bad varicella needs ibuprofen, and is also more likely to get complications anyway. As the famous saying goes, “Correlation does not equal causation”. The absolute risk increase of GAS complications or SSTIs is 0.00016% in the worst case scenario. 

NICE advises against giving ibuprofen due to the uncertainty but you must risk assess the clinical scenario yourself. 

(Based on a case from the American Academy of dermatology – American Academy of Dermatology – Viral exanthems)

Caleb is a 9-year-old boy who presents for evaluation of fever and rash. His mother noted a fever of 40 °C two days ago. He appeared well and was eating and playing normally, so his mother was not alarmed. After the fever resolved, Caleb developed red rash that progressed rapidly over the past 24 hours.

What is the most likely diagnosis?

What are the differentials?

What is the cause of roseola?

Who gets it?

How is it spread?

What are the signs and symptoms of roseola?

How is it diagnosed?

What is the treatment?

What are the complications from roseola?

Roseola

Measles

Rubella

Erythema infectiosum (fifth disease)

It is caused most commonly by human herpesvirus 6 (HHV-6) and less commonly by human herpesvirus 7 (HHV-7).

Children aged 6 months – 4 years are most typically affected. Most children (86%) will have had roseola by the age of 1 year. It is rarely seen in adults and infection is thought to confer lifelong immunity.

It is spread person-to-person via the saliva of asymptomatic family members. The incubation period is 9-10 days.

It results in an acute febrile illness lasting between 3 and 7 days, which is then followed by the characteristic rash of roseola in around 20% of infected children. 

The prodrome to the rash is a high fever (39-40 °C), palpebral oedema, cervical lymphadenopathy and mild upper respiratory symptoms. The child appears well. As the fever subsites the exanthem appear. This consists of a pink macules and papules surrounded by white halos. It begins on the trunk and spreads to the neck and proximal extremities. Nagayama spots may occur on the soft palate and uvula. The rash is non-itchy, painless and does not blister.

Diagnosis is usually based solely on the characteristic history and physical exam. 

Roseola is usually benign and self-limiting. Rest, maintaining fluid intake and paracetamol for fever is all that is usually required. Treatment may be necessary for atypical cases with complications and immunosuppressed patients. 

Complications are rare in most children.  The most common complication is febrile convulsion that occurs in 5-15% of children.

Acute encephalitis, hepatitis, myocarditis, haemophagocytic syndrome and infectious mononucleosis-like illness occur very rarely. 

Reactivation of HHV-6 with drug exposure can lead to drug-induced hypersensitivity syndrome, which results in fever, rash, pneumonia, hepatitis, bone marrow suppression and encephalitis. 

Simple Febrile Convulsions generally occur in children aged from 6 months to 5 years. They are common affecting 1 in every 20 children. The most common causes are viral URTIs, ear infections, bacterial tonsillitis and UTIs. 

They are generalised seizures, which last less than 15 minutes and occur only once during 24 hours. 

The recurrence risk depends on child’s age at presentation: 1 year old: 50% recurrence;

2 year old: 30% recurrence

Where there are no neurodevelopmental problems and no family history of epilepsy, the subsequent risk of epilepsy is 1% (equivalent to the population risk).

A 5-year-old girl, Emma, attends the ED with after being unwell for the last 3 days. It initially started out with fever, headache and a sore throat. She then developed a rash 24 hours ago. Her parents report that the rash started on her abdomen and spread to the neck and arms and legs and it feels rough to touch. 

On exam she has a sandpaper type rash on her trunk and limbs which is more pronounced in flexures. 

What is the most likely diagnosis?

What other symptoms might Emma have?

What is it caused by?

What are the differential diagnoses?

How is the diagnosis confirmed? What investigations will you do?

What is the treatment? Why do you treat?

Discussion point – Evidence for antibiotic therapy 

What are the possible complications? How can you categorise them?

What advice do you give to Emma’s parents in order to prevent transmission of Scarlet fever?

Is there anything else you need to do?

Scarlet fever 

The symptoms of Scarlet fever start with fever (over 38.3°C), sore throat and general fatigue/headache/nausea. 12-48 hours later a rash appears on the abdomen and spreads to neck and extremities. 

Characteristic features of the rash are a rough texture (like sandpaper) and worse in the skin folds e.g. groin, axilla, neck folds (Pastia’s lines). 

Other symptoms include white coating on tongue which then peels and leaves a ‘strawberry tongue’; flushed red face with perioral pallor and cervical lymphadenopathy. Most symptoms resolve within a week. After the symptoms have resolved it is common to get peeling on the fingers and toes. 

In Emma’s case the other symptoms that you would look for are – cervical lymphadenopathy, white tongue or strawberry tongue and a flushed face with peri-oral pallor. 

Scarlet fever is caused by the bacterium Streptococcus pyogenes (also known as group A streptococcus, or GAS). It can be found on the skin or in the throat, where it is usually unproblematic in asymptomatic carriers – 20% of children are colonized. 

However, certain virulent forms of S. pyogenes carry genes that code for streptococcal superantigens, including pyrogenic exotoxins, which can cause non-invasive infections such as scarlet fever. The typical rash is caused by the exotoxin.

They include measles, glandular fever, slapped cheek infections, other viral pathogens, Kawasaki disease, staphylococcal toxic shock syndrome, and allergic reactions.

The diagnosis is clinical. A throat swab is not routinely recommended, although during specific outbreaks Public Health England might advise this.

Streptococcal antibody tests are used to confirm previous group A streptococcal infection. They may be of value in patients with suspected acute renal failure, acute glomerulonephritis or rheumatic fever.  

Antistreptolysin O (ASO) test is the most commonly available streptococcal antibody test. ASO titres peaks 2-4 weeks after an acute infection and returns to normal over the next 6-12 months. Streptolysin O is produced by almost all strains of S. pyogenes (group A streptococci) and many group C and group G beta-haemolytic streptococci. 

Anti-deoxyribonuclease B (anti-DNase B (ADB)) titres rise after both pharyngeal and skin infections. DNase B is produced by group A streptococci and is therefore more specific than the ASO antibody test.

General guidance for patients may include advice on rest, drinking plenty of fluids, good hygiene measures to minimise the risk of cross-infection, and the use of paracetamol to reduce discomfort and high temperature.

Overall, the evidence base for the management of scarlet fever is limited, and there is a need for more evidence of the benefits and harms of antibiotics.

Public Health England, NICE and the Department of Health in Western Australia recommend treating people with scarlet fever with antibiotics regardless of severity of illness to speed recovery, to reduce the length of time the infection is contagious, and to reduce the risk of complications.

Recommended antibiotic therapy is Penicillin V QDS x 10/7 or azithromycin OD x 5/7 if penicillin allergic. 

Complications of Scarlet Fever are much the same as complications of strep tonsillitis. They are divided into suppurative, and nonsuppurative.

Suppurative complications occur due to the infection spreading and include otitis media; mastoiditis; sinusitis; peritonsillar abscess; meningitis; endocarditis; retropharyngeal abscess; and invasive group A strep (IGAS).

Non-suppurative complications occur later and occur mainly in untreated patients. They are rheumatic fever and post-strep glomerulonephritis.

IGAS is not common in children, but those at increased risk are children with co-morbidities, immunocompromised children, and those with co-existing chickenpox.

(DFTB – Exclusion period for infections)

Children should be excluded from school until they have had 24 hours of antibiotics.

Check if you need to contact the public health authorities – scarlet fever is a notifiable disease in many jurisdictions e.g. England, Wales, Northern Ireland and Western Australia. 

(Based on Life in the Fast Lane case – LITFL – Kawasaki Disease)

Alex, a 4 year-old boy has been brought to the emergency department by his worried parents. He has had fevers for the past 6 days. They are concerned because he is not getting better despite repeated visits to a number of doctors. Each time they were told he had a viral illness.

On examination you note the presence of bilateral conjunctivitis, and erythematous rash on his torso and limbs, a 4 cm tender left-sided cervical lymph node and a diffusely red pharynx.

What is the most likely diagnosis?

How is the diagnosis made?

Who gets this condition?

What are the important differential diagnosis?

What investigations should be performed?

What complications may occur?

What specific treatment is required?

Discussion point – Incomplete Kawasaki Disease: Another child, Sarah, attends the ED with 6 days of fever. On exam you find a strawberry tongue and cervical lymphadenopathy >1.5cm. No other signs of Kawasaki disease are present. What might you consider?

Discussion point – Is there a roll for steroids in Kawasaki disease?

Kawasaki disease, also known as Mucocutaneous Lymph Node Syndrome, this vasculitic disorder was first described by Dr. Tomisaku Kawaski in 1967. It is of uncertain etiology, but may be a post-infectious condition.

The diagnosis is made on the basis of the following clinical criteria (A + B):

A.Fever ≥5 days
B.At least 4 of the 5 following physical examination findings:
1.Bilateral, nonexudative bulbar conjunctival injectionbilateral scleral injection with peri-limbic sparing
2.Oropharyngeal mucous membrane changespharyngeal erythema, red/cracked lips, and a strawberry tongue
3.Cervical lymphadenopathywith at least one node >1.5 cm in diameter
4.Peripheral extremity changesacute phase: diffuse erythema and swelling of the hands and feetconvalescent phase: periungual desquamation (weeks 2 to 3)The diffuse palmar erythema seen in KD is in contrast to the discrete macular lesions of various viral illnesses (e.g., measles) that can sometimes be seen on the palms and soles.
5.A polymorphous generalized rashNon-vesicular and non-bullousThere is no specific rash that is pathognomonic for KD

The manifestations may appear sequentially rather than concurrently. Atypical cases may not meet all the criteria but may still have the same risks of cardiac complications. These 

‘incomplete’ cases occur more often in infants less than 6 months-old — further investigations (see Q5) should be performed if fever of 5 days and 2 or 3 of the other criteria are present.

Kawasaki disease may occur in any child of any age, and even adults in some cases. However, it is more common in:

  • children aged < 5 years
  • child of Asian descent
  • males (RR 1.5)

Diagnosis may be difficult as Kawasaki disease may mimic a number of other conditions:

  • Viral exanthemas including measles
  • Streptococcal disease (e.g. scarlet fever, toxic shock syndrome)
  • Staphylococcal disease (e.g. scalded skin syndrome, toxic shock syndrome)
  • Bilateral cervical lymphadenitis
  • Leptospirosis and rickettsial diseases
  • Stevens-Johnson syndrome and Toxic Epidermal Necrolysis
  • Drug reactions including mercury hypersensitivity reaction
  • Juvenile Chronic Arthritis

Echocardiography —
this is the most important investigation to assess for cardiac complications.
If no abnormalities on presentation the study should be repeated in 4-6 weeks.

Laboratory tests
Rule out other causes:
— ASOT, AntiDNAse B, throat swabs, blood cultures
Non-specific findings seen in Kawasaki disease include:
— FBC: normochromic anaemia and leucocytosis; thrombocytosis (in the 2nd week)
— LFT changes and hypoalbuminemia
— increased CRP and ESR
— Sterile pyuria of ≥10 WBCs per high-power field

Cardiac complications:

  • Carditis during the febrile phase
    — myocarditis with ST-T changes (25%), pericardial effusions (20-40%), valvular dysfunction (1-2%) and cardiac failure (~5%)
  • Coronary vessel abnormalities (occur in 20% of cases if untreated and <5% if treated; peaks at 2-4 weeks)
    — aneurysm formation may lead to fatalities from thrombosis, rupture or ischemia-related dysrhythmia (usually within 6 weeks of onset, but may occur many years later.

Kawasaki disease is a vasculitis that can potentially affect almost any organ, it is commonly associated with:

  • arthritis
  • keratitis and uveitis
  • diarrhoea, vomiting and gallbladder disease
  • coryza and cough

IV immunoglobulin and aspirin

IV immunoglobulin

  • 2g/kg IV over 10 hours
  • ideally start within 10 days of the onset of the illness
  • a second dose may be given if fevers persist

Aspirin

  • 3-5 mg/kg PO daily for 6-8 weeks
    (when laboratory parameters have fully normalised)
  • some advise higher doses of aspirin until the patient is afebrile or 48-72 hours, but others argue this offers no benefit in addition to treatment with IV immunoglobulin.

Despite these therapies 2-4% of cases still go on to develop coronary artery abnormalities. Corticosteroids may be considered in refractory cases, although there is little evidence supporting their use.

Another child, Sarah, attends the ED with 6 days of fever. On exam you find a strawberry tongue and cervical lymphadenopathy >1.5cm. No other signs of Kawasaki disease are present. What might you consider?

Incomplete Kawasaki disease

DFTB – Kawasaki Disease

Very easily missed
Makes up 15-20% of all cases
Patients with incomplete KD, particularly those <6 months of age and older children, may experience significant delays in diagnosis and these children are at high risk of developing coronary artery abnormalities.

Consider KD if:

  • Infants <6 months old with prolonged fever and irritability
  • Infants with prolonged fever and unexplained aseptic meningitis
  • Infants or children with prolonged fever and unexplained or culture-negative shock
  • Infants or children with prolonged fever and cervical lymphadenitis unresponsive to antibiotic therapy
  • Infants or children with prolonged fever and retropharyngeal oroparapharyngeal phlegmon unresponsive to antibiotic therapy

Fever and pyuria in an infant or young child may be diagnosed as a urinary tract infection, with subsequent development of rash, red eyes, and red lips attributed to an antibiotic reaction. Irritability and a culture-negative pleocytosis of the cerebrospinal fluid in an infant with prolonged fever suggestive of aseptic meningitis (or if antibiotics have been given, partially treated meningitis) may cause a diagnosis of KD to be overlooked. Cervical lymphadenitis as the primary clinical manifestation can be misdiagnosed as having bacterial adenitis. Gastrointestinal symptoms are considered for surgical causes, other physical findings of KD can be overlooked.

Toxin-mediated illnesses, such as group A streptococcus infections (e.g. toxic shock syndrome and scarlet fever) can also present with fever, rash, mucous membrane involvement and abnormal extremity findings. Desquamation in Kawasaki disease tends to affect the hands and feet as it does in scarlet fever and toxic shock syndrome; however, in Kawasaki disease, it usually begins in the periungual region. In scarlet fever, the desquamation tends to be diffuse and flaking, whereas in Kawasaki disease it tends to be sheet-like.

BMJ – Kawasaki disease

Children with measles and Kawasaki disease tend to be very irritable and inconsolable. It can be difficult securing the diagnosis of Kawasaki disease as the clinical features may appear sequentially rather than at the same time. In Kawasaki disease there may be presence of erythema and induration at the BCG immunisation site as there is cross reactivity between the heat-shock protein and the T-cells of patients with Kawasaki disease. 

The temperature in measles may exceed 40°C but tends to fall after day 5 of the illness. Koplik spots are not seen in Kawasaki disease and the morbilliform rash of measles begins from the ears and hairline and starts to fade by day 4; after day 7 brownish staining may be seen due to capillary haemorrhage. Desquamation in severely affected cases of measles can occur but is not seen in the hands and feet. In measles, clinical improvement typically begins within 2 days of appearance of the rash.

This table can help distinguish between differentials:

(Cochrane – Using steroids to treat Kawasaki disease)

A Cochrane review published January 2017 concluded “steroids appear to reduce the risk of heart problems after Kawasaki disease without causing any important side effects. They also reduce the length of symptoms (fever and rash), length of hospital stay, and blood markers associated with being unwell. Certain groups, including those based in Asia, those with higher risk scores, and those receiving longer steroid treatment, may have greater benefit from steroid use, especially with decreasing rates of heart problems, but more tests are needed to answer these questions”.

What disease is associated with dermatitis herpetiformis?

A: Herpes

B: Coeliac disease

C: Atopic dermatitis

D: Melanoma

The correct answer is B.

In coeliac disease, there are IgA antibodies against gluten that cross-react with reticulin fibres that anchor the basement membrane to the dermis. Thus, IgA is deposited at the tips of dermal papillae, presenting as grouped pruritic vesicles, papules or bullae. Usually found on elbows.

What is the most common causative agent of erythema multiforme?

A: Penicillin and sulphonamides

B: Systemic lupus erythematosus

C: HSV infection

D: Malignancy

The correct answer is C.

HSV is the most common etiologic agent of EM, which presents as a targetoid rash and bullae. All the other options are also associated with the disorder, but less commonly.

What disorder is characterised by an initial ‘herald patch’ which is then followed by scaly erythematous plaques usually in a ‘Christmas tree’ distribution?

A:    Pityriasis rosea

B:    Herpes

C:    Varicella zoster virus

D:   Erysipelas

The correct answer is A.

Pityriasis rosea classically presents with a salmon coloured solitary patch ‘herald patch’ which enlarges over a few days followed by generalised bilateral and symmetric macules with collarette scale. Pruritus is sometimes present. It itself resolves within 6 – 8 weeks.

What is the infective agent implicated in acne? 

A: Staphylococcus aureus

B: Streptococcus pyogenes

C: Staphylococcus epidermidis

D: Propionibacterium acnes

The correct answer is D.

Propionibacterium acnes infection produces lipases resulting in inflammation and breakdown of sebum, leading to pustule formation.

Which of the following statements about the treatment of measles is correct?

A: No specific antiviral therapy is recommend for immunocompetent patients 

B: Prevention of spread of measles depends on prompt immunization of people at risk of exposure or people already exposed who cannot provide documentation of measles immunity

C: Recommend supportive care with antipyretics, fluids and rest

D: All of the above

The correct answer is D.



Please download our Facilitator and Learner guides

Asthma Module

Cite this article as:
Miriam Saey Al-Rifai. Asthma Module, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.27232
TopicAsthma
AuthorMiriam Saey Al-Rifai
DurationUp to 2 hours
Equipment requiredNone
  • Basics (10 mins)
  • Main session: (2 x 15 minute) case discussions covering the key points and evidence
  • Advanced session: (2 x 20 minutes) case discussions covering grey areas, diagnostic dilemmas; advanced management and escalation
  • Sim scenario (30-60 mins)
  • Quiz (10 mins)
  • Infographic sharing (5 mins): 5 take home learning points

We also recommend printing/sharing a copy of your local guideline.

Joseph, a 10 year old boy comes into the ED. He is a known asthmatic on treatment. He appears breathless with an audible wheeze. He is able to talk in complete sentences. He has a RR of 25, sats of 94%, pulse of 100 and his PEF is 60% of normal.

What is the severity score of this child’s asthma presentation?

What investigations and treatment options should you consider?

How do you decide when it is safe to discharge home?

The boy is 3 years old with the same presentation – his mum asks you if her son has asthma. What is your response?

When seeing a child with an acute asthma attack, the initial assessment is key to establishing the severity of the attack as this influences ongoing management. 

The following clinical signs should be recorded:

Pulse rate – Increasing tachycardia generally denotes worsening asthma; severe airway obstruction can result in pulsus paradoxus and a fall in heart rate in life-threatening asthma is a preterminal event.

Respiratory rate and degree of breathlessness –  Ie too breathless to complete sentences in one breath or to feed.

Use of accessory muscles of respiration – subcostal, intercostal recessions, tracheal tug. You can also assess by palpation of neck muscles. Also consider including a prolonged expiratory phase.

Amount of wheezing – which might become biphasic or less apparent with increasing  airways obstruction. Silent chest is an indicator of life threatening asthma. It is important to auscultate and document any improvement with treatment.

Degree of agitation and conscious level – always give calm reassurance.

Observations

  • Include general observations.

CXR

  • NOT routinely advised. A chest X-ray should be performed if there are persisting unilateral signs suggesting pneumothorax, inhaled foreign body, lobar collapse or consolidation and/or life-threatening asthma not responding to treatment.

Blood Gas

  • Only indicated if not responding to treatment or needing further escalation of care

Oxygen 

  • If any life threatening features or sats <94%. Aim for sats 94-98%

Inhaled β2 agonist 

  • Salbutamol up to 10 puffs via spacer (1 puff = 5 breaths) assess after 15 mins and repeat if necessary. If sats <94% use,or patient refusal/poor inhaler technique use salbutamol nebulisers (2.5 – 5mg).
  • Continuous nebulisation may be better, as intermittent may result in rebound bronchoconstriction. 

Ipratropium Bromide 

  • If symptoms are refractory to initial β2 agonist treatment, add ipratropium bromide (250 micrograms/dose mixed with the nebulised β2 agonist solution) every 20-30 mins for the first two hours in severe asthma attacks. This should then be tapered to 4-6hrly before being discontinued. However, there are no clinical trials supporting ipratropium use beyond the first hour or first 3 doses in children (EMCases).
  • In a systematic review and meta-analysis comparing the use of beta-agonists plus anticholinergics with beta-agonists alone, combination therapy was associated with significantly lower hospitalisation rates and improvements in asthma scores and pulmonary function test results (EMCases).

Oral steroids 

  • Give oral steroids in the management of acute asthma attacks. Dexamethasone is starting to be used more, as a once only dose, but there is no evidence for benefit over Prednisolone, so not recommended yet. 

Nebulised Magnesium 

  • Nebulised magnesium sulphate is not recommended for children with mild to moderate asthma attacks. The RCT entitled MAGNETIC trial in 2013 of about 500 children showed that MgSO4 nebulisers added to the salbutamol and ipratropium bromide nebuliser in the first hour, for kids with acute severe asthma, significantly improved asthma severity scores without any increase in adverse events.

Antibiotics 

  • Insufficient evidence to refute or recommend.

Burst therapy – improves forced expiratory volume with an earlier peak response, and prevents deterioration between doses. Salbutamol 100 mcgs x 10 puffs via inhaler & spacer every 20 mins for 1 hour. Add ipratropium bromide 20 mcgs (x 4 puffs < 5 years, x 8 puffs > 5 years) together with salbutamol as above for severe cases.

BTS/SIGN – Children can be discharged home once requiring no more than 3-4 hourly inhalers (based on a randomised controlled study in 1999), PEF >75% and sats >94% . 

Safe follow up

  • Reducing regime of salbutamol inhaler therapy with a clear plan as to when to come back to hospital (ie. requiring >10 puffs in 4 hours)
  • Ensure good inhaler technique/correct fitting spacer mask. Advise to use the B-agonist BEFORE the inhaled steroid and to wash the mouth out after the steroid inhaler to prevent thrush.
  • If the parent/carer of the child smokes, advise them to stop.
  • Address potentially preventable contributors to the exacerbation, such as exposure to trigger factors
  • Ensure the patient is discharged home with 3-5 days oral steroids. Some trusts are now given single dose Dexamethasone, although prednisolone is still in the national guideline (https://www.stemlynsblog.org/dexamethasone-asthma-children/). 
  • Primary care follow-up in 24-48hrs
  • If second attack in 12 months refer to a secondary care asthma clinic.

Wheeze is a common presentation in the ED and its diagnoses and management differs depending on the age of the child and the detail in the history (Snelson et al, 2019). 

An age based approach to wheeze in children

Bronchiolitis

  • Slow onset of symptoms. 3-4 day period of worsening cough, poor feeding, wheeze and respiratory distress due to inflammation of the airways.

Viral Wheeze

  • Rapid onset of wheeze and respiratory distress over hours due to bronchospasm.

Asthma

  • Described above. 

The age based approach to wheeze can be explained by the changes in a child’s immune system:

  • At birth and in the first few months, immunity is largely provided by maternal antibodies. These antibodies offer protection from most simple viral infections. Acute atopic IgE mediated reactions are very rare. If infections do occur it is likely to be serious bacterial infections. In addition the baby’s own immune system is not yet fully turned on and the response to infection is therefore muted, making the recognition of sepsis difficult in this age group.
  • Preschool age children no longer rely on maternal antibodies. However, their own immune system is still not fully developed. They compensate for this by having heightened and indiscriminate responses to infections. They produce lots of white blood cells, but do not yet have circulating antibodies. You are more likely to see associated problems of viral infections in this age group like transient synovitis. Atopy is becoming more common now. Sepsis is also difficult to recognize in this age group due to the extreme reaction to often uncomplicated viral infections. These children present with viral wheeze. It is worth knowing that there are wheezy presentations in this age group that can look a lot like viral wheeze.  These include bronchomalacia, acute allergy, and cardiac failure due to e.g. acute myocarditis.
  • Older children have a more mature immune system and response to infection is like that of an adult. As the response to infection is less vigorous and indiscriminate than the pre-schoolers, some specific infections like Varicella can cause severe reactions in these children. These children are more likely to have asthma. True asthma is rarely seen under the age of 5 as it requires a fully matured immune system to develop.

Management

  • By looking at the history we can direct our inhaled beta agonist treatment to one that matches a story consistent with bronchospasm. This would include children with likely viral wheeze and asthma.  
  • The best evidence for the use of oral steroids for viral wheeze between the ages of 1 and 5 would suggest that the following group are most likely to have a small benefit (https://gppaedstips.blogspot.com/search/label/Asthma):
  • Children with a diagnosis of asthma
  • Children who have required substantial amounts of inhaled beta-agonist prior to presentation
  • Children whose severity and lack of response to treatment with beta-agonists requires admission to hospital
  • Joseph has presented with features of a moderate asthma attack
  • This can be managed with beta 2 agonist therapy and oral steroids
  • Once Joseph does not need beta 2 agonist bronchodilation for more than 4hrs and obs remain stable he can be safely discharged home with safe follow up.
  • The 3 year old presenting with the same symptoms of sudden onset wheeze and breathlessness, likely has a diagnosis of viral wheeze. They would benefit from beta 2 agonist bronchodilation. They are too young to be diagnosed with asthma, but risk factors for developing asthma could be explored in the history.

Leila, a 13 year old female, known asthmatic on treatment, presented to ED breathless and finding it hard to speak in full sentences. Her oxygen saturations are 92%, HR 130 and RR 35

What is the severity score of this child’s asthma presentation?

What investigations and treatment options should you consider?

When do you need to re-assess response to treatment to decide on discharge vs escalation?

  • In this instance, Leila falls into the acute severe asthma presentation. 
  • As her sats <94% oxygen needs to be given via a facemask. 
  • Beta 2 agonist bronchodilator via a nebuliser (preferably oxygen driven) to be given due to sats <94% and she falls into the severe category. 
  • Oral steroids must be given. This can be given as IV Dexamethasone if too unwell/vomiting.
  • Re-assess response to treatment after 15 minutes. 
  • If no improvement after 15 minutes give a further two beta 2 agonist nebulisers and add Ipratropium Bromide nebuliser. 
  • A consideration of nebulised Mg can be given in acute severe asthma.
  • Plan for admission, escalate and refer to paediatrics for consideration of second line treatment.

Do you know how to use a spacer?

Leila has not improved despite the treatment given in ED as outlined in case 2. Her sats are now 89%, she appears cyanosed and has a poor respiratory effort. On auscultation her chest is quiet. What are the next steps that need to be taken?

How would you rate the severity score of this presentation?

What investigations or treatment needs to be considered?

Which IV medications if any should be used? 

Which important differentials need to be considered?

What escalation plans need to be put in place?

Children with continuing severe asthma despite optimal first-line treatments, frequent nebulised β2 agonists and ipratropium bromide plus oral steroids, and those with life-threatening features, need urgent review by a specialist with a view to management in an appropriate high-dependency area or transfer to a paediatric intensive care unit to receive second-line intravenous therapies. It is important to do a blood gas prior to starting bronchodilators to measure the pCO2 and also to monitor side effects of salbutamol (decreasing potassium and lactic acidosis).

PERUKI (Paediatric Emergency Research in the UK and Ireland network) is a research collaborative of paediatric-specific and mixed adult and paediatric emergency departments (EDs). In 2015 PERUKI carried out a study looking at the variation in practise of the use of IV bronchodilators as a second line treatment in the management of acute asthma in children. There was a large discrepancy between what clinicians felt was the appropriate management and what they actually administered. A survey of 183 clinicians in 30 EDs revealed that when escalating to intravenous bronchodilators, 99 (54%) preferred salbutamol first line, 52 (28%) magnesium sulfate (MgSO4) and 27 (15%) aminophylline. 87 (48%) administered intravenous bronchodilators sequentially and 30 (16%) concurrently, with others basing approach on case severity. 146 (80%) continued inhaled therapy after commencing intravenous bronchodilators. 

Of 170 who used intravenous salbutamol, 146 (86%) gave rapid boluses, 21 (12%) a longer loading dose and 164 (97%) an ongoing infusion, each with a range of doses and durations. Of 173 who used intravenous MgSO4, all used a bolus only. What this demonstrates is the considerable variability in practise and opinion. 

So what is the evidence? (Cochrane review)

IV salbutamol 

  • There have not been enough trials to form a robust evaluation of its benefits.

IV MgSO4 

  • Appears to be safe and beneficial in severe asthma

IV aminophylline 

  • Improves lung function within 6hrs. However, there is no apparent reduction in symptoms, number of nebulised treatments or length of hospital stay. We do not know the impact on oxygenation, PICU admissions or need for NIV. 

IV ketamine 

  • There has only been 1 study conducted, which reveals no known benefit in non intubated children. 

In one RCT comparing IV aminophylline, salbutamol and magnesium in 100 children, a bolus of magnesium sulphate was shown to reduce clinical symptoms faster than the other treatments. There were no significant side effects documented in the magnesium sulphate group. A systematic review of four paediatric trials comparing IV salbutamol with IV aminophylline demonstrated equivalence.

In children who respond poorly to first-line treatments, consider the addition of intravenous magnesium sulphate as first-line intravenous treatment (40 mg/kg/day).

Consider early addition of a single bolus dose of intravenous salbutamol (15 micrograms/kg over 10 minutes) in a severe asthma attack where the child has not responded to initial inhaled therapy. It is not clear whether IV bolus vs infusion is more beneficial. Prior to IV salbutamol administration insure blood potassium is checked and on cardiac monitor. If using an IV infusion monitor lactate to check for toxicity. 

Consider aminophylline for children with severe or life-threatening asthma unresponsive to maximal doses of bronchodilators and steroids. Some of the side effects include abdominal pain, anxiety, headache, nausea, palpitations and seizures. Toxicity can occur with aminophylline. This presents as vomiting (which may be severe and intractable), agitation, restlessness, dilated pupils, sinus tachycardia, and hyperglycaemia. More serious effects are haematemesis, convulsions, and supraventricular and ventricular arrhythmias. Severe hypokalaemia may develop rapidly especially in combination with salbutamol.

Ensuring you have appropriately assessed and optimised their condition

Reassess the patient?

  • Consider revisiting history, respiratory examination and consider adjuncts to assessment such as a capillary or venous blood gas.

Have you exhausted medical management?

  • ? adrenaline ? ketamine ?heliox 

What could be missing? 

  • Consider your confidence of whether you have the right diagnosis or if there is a need to assess for a secondary pathology such as pneumonia, foreign body, anatomic airway anomalies, airway compression by masses/lymph nodes, cardiac disease? Some can be excluded with a good history. Do you need to further investigate with bloods, CXR? Do you need to append your management and provide antibiotic coverage? Do you need to assess for a complication from treatment e.g. pneumothorax.

Escalation options

  • Have you sought a senior review/notified the admitting paediatrician?
  • Do you need an ICU consult, NETS consult or retrieval to a tertiary centre?
  • How long are you comfortable to wait to see if there is a response to IV bronchodilation?

Non invasive ventilation 

  • Is there any evidence in acute asthma attack?
  • What settings/mode would you use?

Does this child need to be intubated?

  • How would you determine this?
  • Who should be involved in the conversation? Who should perform the intubation?
  • What sedation would you use?
  • What equipment would you use?
  • What settings would you use?

Alternative treatment options

Adrenaline

Give for severe or life threatening asthma – if the diagnosis is in doubt. 

Asthma and atopy often co-exist – and in these patients death from anaphylaxis is more likely. So if a patient fails to respond to initial therapy, the diagnosis of anaphylaxis needs to be considered. In addition nebulised Adrenaline causes bronchodilation.  

Heliox 

May improve respiratory score, but it probably won’t reduce the risk of admission. Nor should you use it in routine asthma to stave off intubation (PEMBlog). Can be considered in the ICU setting with maximum oxygen therapy has failed. 

Ketamine

Limited number of trials with mixed outcomes on the benefits of Ketamine. However, it is safe at dissociative dosages, and is a reasonable option when all others measures have failed.

NIV

A few case reports and observational studies of the use of BiPAP in pediatric asthma show some promise. The one RCT of only 20 patients does show a benefit in clinical asthma scores, respiratory rate, and supplemental oxygen need. There is no evidence that it prevents the need for intubation (Basnet S et al, 2012).

Critical care input is the next step for children with severe asthma not responding to treatment or with any life threatening features. There are a number of ongoing trials on the use of ketamine, sevofluorane and NIV, but the evidence is currently lacking so they’re not recommended by BTS/SIGN.

A 15 year old male has been brought into resus with features of life threatening asthma. Pre hospital the paramedics gave continuous salbutamol nebulisers, 500mcg Ipratropium nebulisers and 0.5mg IM Adrenaline. The attending medical team in resus administered 2g IV Mg over 20 mins and a bolus of 250mcg IV Salbutamol. The patient then became unresponsive with no respiratory effort.

What are the next steps that need to be taken?

What is the ‘deadly triad’ in asthma?

What are the key ALS modifications in asthma arrest?

In the pre-hospital setting, paramedics usually give IM Adrenaline to cover for the possibility of a diagnosis of anaphylaxis. 

In this case the patient has arrested. As soon as this has been identified, CPR needs to be initiated as per the ALS guidelines.

The cause of cardiac arrest in asthma is a result of the ‘deadly triad’:

Important modifications and considerations in managing cardio respiratory arrest in asthma (RCEMLearning – https://www.rcemlearning.co.uk/foamed/arrest-asthma/):

  1. Intubate Early

Due to the need for high inflation pressures, an endotracheal tube (ETT) is needed. In addition this protects the airway from the increased risk of regurgitation and aspiration.

  1. Ventilate with caution

The European Resuscitation Council recommends 8-10 breaths per minute with the lowest tidal volume required to see the rise and fall of the chest, to avoid dynamic hyperinflation. Tachypnoea must be avoided as this reducses expiratory time, thus increasing the residual volume in the alveoli. This auto PEEP increases intrathoracic pressure which reduces venous return, impeding CPR. 

  1. Manual chest deflation

If the patient has a hyperinflated chest/poor excursions of the chest wall, disconnect the ETT and apply manual pressure to the patient’s chest to expel the trapped air. 

  1. Consider tension pneumothorax

If ETT disconnection does not improve ventilation, consider performing a bilateral thoracostomy.

  1. Rehydrate

Dehydration and reduced intravascular volume compromises effective CPR. It also causes mucus to be thicker which can plug small airways. So ensure you give IV fluids. 

  1. GIVE ADRENALINE! – Utilise its bronchodilator effect. 

In an acute asthma exacerbation in children, monitoring the oxygen sats is important because:

A: Hypoxaemia is an early sign of clinical deterioration 

B: Sats <95% may suggest the need for prolonged bronchodilator therapy

C: Hypoxaemia occurs in the presence of life threatening asthma. Children may have normal sats for some time before critical desaturation occurs.

D: Sats >96% supports the decision to safely discharge home

The correct answer is C.

In an acute asthma attack hypoxic vasoconstriction occurs. This is coupled with decreased blood flow to the under ventilated lung (matching pulmonary perfusion with alveolar ventilation). 

In the hospital setting SaO2<91% may be a helpful predictor of prolonged frequent bronchodilator therapy more than 4 hours and SaO2 of <89% is associated with a need for bronchodilator therapy over 12 hours.

Hypoxaemia and hypocarbia only occur in the presence of life threatening asthma. Children may have normal sats for some time before critical desaturation occurs. Whilst low oxygen saturations mean that a patient is unwell it should be clinically obvious at this point.  Low oxygen saturations may also represent a degree of mucus plugging that may be helped with repositioning.

Hyperoxia can lead to absorption atelectasis as well as intra-pulmonary shunting with subsequent reduction in cardiac output. In addition concerns have been raised that oxygen administration may lead to potential delay in recognising clinical deterioration.

What is an appropriate length of time to stretch children in the ED prior to discharge?

A: After two sets of 3-4hrly inhaler/nebulisers

B: After they reach the first 3-4 hrs post last inhaler/nebuliser

C: After two sets of 3hrly

D: After 1 hour, if obs are completely normal and has had a consultant review

The correct answer is B.

BUT this is based on a randomised control trial in 1999. The most recent study in 2018 suggests that there is no benefit to 4hours vs 3hrs, and in fact 3 hrs post inhalation resulted in a reduction in length of stay. A recent retrospective analysis study in Australia looked at discharging children after 1 hour. They suggested that children that were clinically ‘well’ at 1 hour were likely to go home and if they were showing any moderate symptoms at one hour would likely need to be admitted. There is no strong evidence or recent studies, which is why there is such variation in practice. 

Under what circumstances would you choose to administer a beta agonist via nebuliser as opposed to a pMDI with a spacer?

A: When the child has become more tachycardic with worsening salbutamol induced tremor

B: In severe or life threatening asthma or when under the age of 1yrs old/learning difficulties

C: If the pMDI is ineffective

D: Some departments prefer nebulisers as it is cheaper than inhaled preparations

The correct answer is B.

Cochrane review 2013 – “Metered-dose inhalers with a spacer can perform at least as well as nebulisation in delivering beta-agonists in children with acute asthma”

Salbutamol has systemic side effects – tremor and increased pulse rate were more common when using nebulisers. SIGN/BTS guidelines state to give nebulisers in severe or life threatening asthma. Nebulisers are also preferential in very young children, or those with learning difficulties, as coordinating breathing with an inhaler can be difficult. Cost savings can be made with inhaled preparations. 

When is intubation indicated in paediatric asthma presentations?

A: When the HR > 160 OR the RR > 60

B: When you have given all first line and second line treatment and trialled NIPPV and the patient has still not improved. 

C: The child looks exhausted with worsening hypercapnia and changes in mental status. 

D: When the child has a history of fast deterioration and need for intubation

The correct answer is C.

Up to 26% of children intubated due to asthma suffer complications including pneumothorax, impaired venous return, and cardiovascular collapse because of increased intrathoracic pressure. Mechanical ventilation during an asthma exacerbation is associated with an increased risk of death and should therefore be a last resort. The decision to intubate should be based on clinical judgement as opposed to any one observation or blood result. Some variables to consider for intubation are worsening hypercapnia, patient exhaustion and changes in mental status (EMCases).

You have a 4 yr old, with two days of wheeze, coryzal symptoms and one day of increased work of breathing symptoms. You suspect that this may be viral induced wheeze. How do you manage this child?

A: Burst therapy with salbutamol. 

B: 6-10 puffs of salbutamol and reassess. If severe symptoms give oral steroids. 

C: Humidified air nebuliser and antipyretics for fever. 

D: 6-10 puffs of salbutamol and Ipratropium bromide nebuliser. If severe symptoms give oral steroids.

The correct answer is B.

At what age would it be appropriate to consider a trial of ventolin for potential viral induced wheeze? 

  • (Note – This is a good opportunity to survey your team and colleagues to see what the practice is at your local department). 
  • Regarding this grey area question, in Australian practice, some clinicians will trial salbutamol for potential viral induced wheeze if the child is 12 months or older. Other doctors may wish to trial if the child is slightly younger (e.g. from 10 months) if they have a strong family history of asthma and atopy or if they have had previous ventolin use reported by their family with good effect. The younger the child is, the less likely that the story and case is to fit viral induced wheeze.

If you are not sure if the child is presenting with asthma or viral induced wheeze, but they are displaying severe symptoms – it is advisable to give steroids. But be cautious in giving too many courses of steroids if presenting frequently to the ED.

M Balfour-Lynn (1996) Why do viruses make infants wheeze?, Archives of Disease in Childhood  74: 251-259

MO Stormon, CM Mellis, PP Van Asperen, HA Kilham (2002) Outcome evaluation of early discharge of asthmatic children from hospital: A randomized control trial, Journal of quality in clinical practise, Vol 19, issue 3, 149-154

Huay-ying Lo, Amanda Messer, Jennifer Loveless, Esther Sampayo, Robert H. Moore, Elizabeth A. Camp, Charles G. Macias and Ricardo Quinonez (2018) Discharging Asthma Patients on 3-Hour β-Agonist Treatments: A Quality Improvement Project, Hospital Pediatrics, 8 (12) 733-739

Basnet S, Mander G, Andoh J, Klaska H, Verhulst S, Koirala J (2012) Safety, efficacy, and tolerability of early initiation of noninvasive positive pressure ventilation in pediatric patients admitted with status asthmaticus: a pilot study. Pediatr Crit Care Med 13(4):393-8.

Snelson, E (2019) A simple model for understanding the causes of paediatric wheeze, Paediatrics and Child Health, Volume 29, Issue 8, Pages 365-368

DFTB – Managing acute asthma, Simon Craig (2017)

DFTB – Asthma for ambos (2016)

DFTB – Are nebulisers or spacers better for managing acute asthma (2013)

DFTB – The curious incident of the wheeze in the night

PEMBLOG – Heliox in the emergency department (2017)

EMCases – Management of acute paediatric exacerbations (2016)

BTS/SIGN British guideline on the management of asthma in children (2019)

PaediatricFOAM – ventilation strategies for the critically ill asthmatic (2019)

RCEMLearning – Arrest in asthma

gppaedstips.blogspot.com – The NYCE guideline for viral induced wheeze – Let’s clear a few things up (2019)



Please download our Facilitator and Learner guides

Bronchiolitis Module

Cite this article as:
Tessa Davis. Bronchiolitis Module, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.27061
TopicBronchiolitis
AuthorTessa Davis
DurationUp to 2 hours
Equipment requiredNone
  • Basics (10 mins)
  • Main session: (2 x 15 minute) case discussions covering the key points and evidence
  • Advanced session: (2 x 20 minutes) case discussions covering grey areas, diagnostic dilemmas; advanced management and escalation
  • Sim scenario (30-60 mins)
  • Quiz (10 mins)
  • Infographic sharing (5 mins): 5 take home learning points

We also recommend printing/sharing a copy of your local guideline.

A 7 month old infant presents on Day 4 of the illness. He has mild to moderate work of breathing. Sats 95% in air. He is taking around half his normal feeds.

What investigations and treatment options should you consider?

Why doesn’t salbutamol work in this age group?

How do you know when to admit?

See the PREDICT systematic review of all treatments

  • Salbutamol – there is no benefit in using salbutamol in infants with bronchiolitis (and some evidence of adverse effects)
  • Nebulised adrenaline – no clinically useful benefit (there is evidence for temporary effect but not for improvement in outcome)
  • Nebulised hypertonic saline – there is weak evidence of a reduction in length of stay of 0.45 days. However when two studies were removed, both of which used a different discharge criteria than most hospitals, there was no benefit. This is not recommended routinely, although the authors suggest that it should be used only as part of an RCT
  • Glucocorticoids – no benefit
  • Antibiotics – not recommended (The risk of a secondary bacterial infection is very low, and there is potential harm from giving antibiotics)
  • Oxygen – no evidence of benefit in infants with no hypoxia, and low level evidence that maintaining the sats over 91% with oxygen actually prolongs the length of stay. There are no reports of long-term adverse neurodevelopmental outcomes in infants with bronchiolitis, however there is also no data on the safety of targeting sats <92%. Commence oxygen therapy to maintain sats over 91%.
  • Sats monitoring – there is moderate evidence suggesting that continuous sats monitoring increases the length of stay in stable infants
  • High flow – there is low to very-low level evidence of benefit with high flow
  • Chest physiotherapy – not recommended
  • Saline drops – routine saline drops are not recommended but a trial with feeds may help
  • Feeds – both NG and IV are acceptable routes for hydration

See Beta receptor mythbusting (from https://gppaedstips.blogspot.com/)

A 6 month old infant presents on Day 3 of the illness. She has moderate to severe work of breathing. Sats are 91% in air. She is struggling to feed at home.

What management options would you consider?

See the PARIS Paper

This is the biggest and most robust trial yet done to assess the value of high-flow in bronchiolitis. The primary outcome shows that there is a role for high-flow in the non-ICU management of this disease. Importantly PARIS has shown in a large cohort of children that high-flow, when used within the parameters of the trial protocol, does not lead to an increase in adverse events which in-turn suggests the increased patient:nurse ratios for kids on high-flow that are often mandated by hospital policies may not be necessary (depending on the severity of disease of course). Some caution must be used around the potential for erroneous use of the high-flow circuits themselves and the interpretation of early warning scores in the context of high-flow use.

PARIS was supported with significant nursing education resources potentially reducing errors to a level that were below what could be expected with the standard resourcing of mixed EDs and other environments where high-flow use in children may be infrequent. As with many grey areas in medicine protocols as to how we use high-flow vary by institution with little more than opinion to guide them.

Though neither the intention nor the conclusion of this paper in showing the progress of such a large number of children on high-flow, this trial also provides a basis for more robust decision making around how we use high-flow itself.

NICE feeding guidance

  • Give fluids by nasogastric or orogastric tube in children with bronchiolitis if they cannot take enough fluid by mouth.
  • Give intravenous isotonic fluids (see the NICE guideline on intravenous fluids therapy in children) to children who: do not tolerate nasogastric or orogastric fluids; or have impending respiratory failure.

Do you know how to set up high flow? (8 minutes)

How to set up Airvo 2 (Optiflow)  (3.5mins)

How to use Airvo 2 (6 mins)

You have a 12 month old, with two days of coryza and one day of increased work of breathing symptoms.

How do you manage them?

How do you figure out whether they have bronchiolitis or VIW?

Practically speaking, we know that bronchiolitis and viral induced wheeze have two quite different management pathways, but it is not as if a child moves from being 12 months old to 13 months old and therefore cannot have bronchiolitis (or vice versa for viral induced wheeze). These conditions as previously mentioned, exist on a spectrum. 

  • What has been the onset of symptoms? Progressive over days is most consistent with bronchiolitis. Onset of wheeze and respiratory distress over hours is most consistent with bronchospasm (viral induced wheeze).
  • What has been the pattern of their work of breathing? 
  • How significant is the work of breathing? 
  • What are the auscultation findings – is there presence of focal findings? Wheeze? Crackles? 
  • Is this affecting the child functionally with feeding or sleeping difficulties?
  • If auscultation is suggestive of possible viral induced wheeze or at least, a component of wheeze that may be responsive to bronchodilators (If wheeze is present and no crackles or focal findings) and presuming the child has more than just mild work of breathing -then we suggest this may be a possible candidate for viral induced wheeze.  
  • (Note – This is a good opportunity to survey your team and colleagues to see what the practice is at your local department). 
  • Regarding this grey area question, in Australian practice, some clinicians will trial salbutamol for potential viral induced wheeze if the child is 12 months or older. Other doctors may wish to trial if the child is slightly younger (e.g. from 10 months) if they have a strong family history of asthma and atopy or if they have had previous ventolin use reported by their family with good effect. The younger the child is, the less likely that the story and case is to fit viral induced wheeze.

It would be prudent to give 6 puffs (or do you use another number?) and reassess following to see if there is any improvement or change.

You’ve started high flow 2L/kg for a four month old with bronchiolitis, moderate work of breathing and saturations of 88% and titrated FiO2 up to 30% to maintain saturations. However they are still intermittently desaturating so you titrate them up to 40% FiO2.

They have ongoing work of breathing with a respiratory rate of 60-70.

What are your next steps?

Consider revisiting history, respiratory examination and consider adjuncts to assessment such as a capillary or venous blood gas.

  • For example, Do they have an NG tube on free drainage, are they nil by mouth and on IV fluid support at ⅔ maintenance
  • Are their family actually compliant with this or have also been feeding them via a bottle? 
  • Are they working harder to breathe because they are getting “hangry” and might actually tolerate a continuous NG or comfort feed?
  • Consider whether the HFNP has led to no change, improvement and then deterioration or simple worsening of symptoms due to patient distress.
  •  If no improvement was observed on commencement – it may be worth de-escalating them – ie. lower flow rates or low flow nasal prongs

Consider your confidence of whether you have the right diagnosis or if there is need to assess for a secondary pathology such as pneumonia, foreign body, cardiac contribution? Do you need to further investigate with bloods, CXR? Do you need to append your management and provide antibiotic coverage? Do you need to assess for a complication from treatment e.g. pneumothorax.

  • Have you sought a senior review/notified the admitting paediatrician?
  • Do you need an ICU consult, NETS consult or retrieval to a tertiary centre?
  • How long are you comfortable to wait to see if there is a response to high flow?
  • What settings would you start on?
  • Where could you move up to (in terms of peep, FiO2)
  • How soon would you reassess – what are you looking for?

  • How would you determine this?
  • Who should be involved in the conversation? Who should perform the intubation?
  • What sedation would you use?
  • What equipment would you use?
  • What settings would you use?

In bronchiolitis, children do not respond to salbutamol because:

A: They don’t have beta receptors until they are older.

B: The beta receptors are immature and do not begin functioning correctly until the child is older.

C: The large amount of secretions interfere with it and prevent it binding to the receptors

D: There is no bronchospasm for the salbutamol to act on.

The correct answer is D.

All humans have beta receptors. Foetuses develop them from around 15 weeks gestation and are therefore born with them. Developing beta receptors after 1 year of age is a common paediatric myth! In fact, in bronchiolitis, there is no bronchospasm in the same way as there is in viral induced wheeze. Bronchiolitis is a illness developing gradually over 4 days and then slowly improving. Patients have increased mucous rather than bronchospasm, which does not respond to a bronchodilator.

A 3 month old baby presents to ED with coryza, cough, and poor feeding. Breastfeeding is going ok, but the baby is feeding for shorter periods, more frequently than usual. She is having wet nappies as normal. Saturations are 93% on room air, RR is 62, and there is moderate subcostal recession with some nasal flaring. Which of the following is an indication to admit this baby to hospital?

A: The reduced breastfeeding

B: The oxygen sats

C: The work of breathing

D: The age of the baby

The correct answer is C.

The criteria for admission usually are:

  • feeding less than half of usual, or less wet nappies
  • saturations less than 92% on air
  • increased WOB
  • apnoeic episodes

Risk factors such as:

  • Ex-prem
  • Age less than 12 weeks or less than 37 weeks CGA
  • history of lung disease or congenital heart disease or neurological problems
  • smoke exposure

In clinical practice, you would use your judgement to assess if hospitalisation was necessary. Social concerns should always be considered.

In this case, the baby is maintaining good urine output and the feeds, although shorter, are more frequent. The age alone is not an indication for admission. Obviously, an O2 requirement would be an indication for admission but most units would consider sats of 92% or less as reduced. There is significantly increased work of breathing with recession and nasal flaring, however, so this would be the main indication for admission.

You have a 10 month old baby with bronchiolitis who is to be commenced on high flow. Which of the following is false?

A: Nasal prongs size should be estimated based on the width of the patient’s nostrils.

B: Patients can be NG fed immediately once on high flow. 

C: High flow improves the functional residual capacity.

D: The humidified oxygen help clearing mucous secretions.

The correct answer is B.

Patients on high flow will likely need an NG inserted due to abdominal distention, but should usually not be fed for the first couple of hours on high flow. The aim of high flow is to provide humidified, high flow to improve clearance of secretions and to increase the functional residual capacity. Together this should reduce the work of breathing.



Please download our Facilitator and Learner guides

Managing cough: Adam Jaffe at DFTB19

Cite this article as:
Team DFTB. Managing cough: Adam Jaffe at DFTB19, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.22157

Adam is a respiratory physician at Sydney Children’s Hospital. He spoke about all things wheezy in Melbourne for DFTB18.  In this talk from our London conference, he deals with that bane of parents’ lives – the coughing child.

 

 

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.

iTunes Button
 

Selected references:

Chang AB. Cough, cough receptors, and asthma in children. Pediatric pulmonology. 1999 Jul;28(1):59-70.