Emergency ambulance transport in those with Autistic Spectrum Condition

Cite this article as:
Vicki Marchant. Emergency ambulance transport in those with Autistic Spectrum Condition, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.33246

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

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

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

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

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

From a Different Perspective…..

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

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

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

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

The Autistic Spectrum

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

Autistic Symptoms and Coping Mechanisms

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

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

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

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

Tips to Remember

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

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

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

PEM adventures chapter 4

Cite this article as:
Team PEM Adventures. PEM adventures chapter 4, Don't Forget the Bubbles, 2021. Available at:
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.
Scurvy header image

Scurvy

Cite this article as:
Julia Hall and Abigail Lazenbury. Scurvy, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.33473

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

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

Could this be scurvy?

Definition

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

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

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

Pathophysiology

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

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

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

Signs and symptoms 

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

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

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

Risk Factors 

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

Diagnosis

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

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

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

Management

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

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

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

Selected references on scurvy

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

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

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

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

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

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

Pazirandeh S, Burns D. Overview of water-soluble vitamins. In: D, Seres, L, Kunins eds. UpToDate. 2020. Waltham, UpToDate [ Accessed 28th February 2021 ] Available from https://www.uptodate.com/contents/overview-of-water-solube-vitamins

Ratanachy EK, Sukswai P, Jeerathanyasakun Y, Wngtapradit L. Scurvy in pediatric patients: a review of 28 cases. Journal of the Medical Association of Thailand. 2003; 86(3): S734-S740

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

World Health Organization. Scurvy and its prevention and control in major emergencies [online]. World Health Organisation, 1999 [Viewed 28th February 2021]. Available from: https://apps.who.int/iris/bitstream/handle/10665/66962/WHO_NHD_99.11.pdf?ua=1

Peripheral IV cannulation

miniMAGICal thinking

Cite this article as:
Amanda Ullman, Tricia Kleidon and Elizabeth Andresen. miniMAGICal thinking, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.33480

18-month-old Byron presents to ED with septic arthritis. You know you need to take cultures, so you think you might pop a peripheral intravenous cannula in his antecubital while you’re there – he’ll need intravenous (IV) antibiotics for sure, maybe some fluids. He’s toddler-level chubby, and not exactly compliant.

Time for a deep breath.

Inserting peripheral intravenous catheters (PIVCs) is a core skill in paediatric acute care. We often make a quick decision to insert a PIVC in order to ensure accurate diagnosis and commence important treatments. We often worry about our capacity to insert the PIVC, especially in children like Byron. The vessels can be hard to visualise and palpate, and putting a young child going through a painful procedure can be stressful for all concerned.

But quick decisions have consequences

We know that PIVCs can result in harm. Multiple insertion attempts, extravasations, and infections are all a risk. They often stop working prior to the completion of treatment. PIVCs last only 48 hours, on average, in children and young people. When they fail, we not only pause treatment, but we frequently have to start the process all over again. According to children (and their families) cannulation is the most stressful part of their healthcare experience.

Think carefully about the IV, before it is inserted.

We have an array of IV devices and a variety of places to insert them. In 2020, the Michigan Appropriateness Guide for Intravenous Catheters (miniMAGIC) was published. Its aim was to improve the safe selection of IVs in children across a range of indications. You can read them (open access) here; or download the app for Google or Apple.

In Queensland (Australia) we have developed our first practice targets to improve IV selection, insertion, and securement based on miniMAGIC, and thus reduce IV associated harm. We are currently rolling them out at Queensland Children’s Hospital (Australia). These are:

Paediatric IVC and miniMAGIC

Improving device selection

Peripheral devices (like PIVC or midline catheters) should only be used for peripherally compatible therapies, outside of an emergency or crisis

To ensure safe administration of ‘at risk’ infusates, we consider:

  • Is this PIVC working? Check for good flow prior to administration
  • Is this PIVC optimally placed? Ideally, it should be away from a joint?
  • Are we giving this medication slowly and with enough dilution? Check the Paediatric Injectable Guidelines (PIG)
  • Is this PIVC site visible? It shouldn’t be coverfed up with crepe bandages

We are proactive in our device planning:  

  • If the child needs >2 days of IV therapy, make sure the PIVC is optimally positioned (e.g., in forearm)
  • If the child needs >5 days of IV therapy, consider a midline catheter

STOP and THINK, Make a plan! If this PIVC stops working, do we need to replace it immediately or are there other options? If this child is going to theatre, can we have the device ‘upgraded’?

Peripherally Inserted Central Catheters (PICCs) should not be inserted for antibiotic administration without discussion with the Infectious Diseases team. We use the minimal lumens necessary for treatment (NO just in case PICC/additional lumens).

Improving device insertion

Inserted them away from joints, where possible, looking for visible AND palpable vessels in the forearm. If there is nothing obvious it is time to turn to the trusty ultrasound machine if you have the skills. Even when we place topical anaesthetics, we pop some on the mid-forearm rather than antecubital fossa.

When faced with a child without palpable or visible vessels, don’t have multiple IV insertion attempts. Instead, refer early to an experienced clinician (+/- USG).

Improving device securement

keep the cannula visible, clean and secure
  • Keep it visible: Do not use crepe bandages; use tubular bandages.
  • Keep it clean: Use sterile products
  • Keep it secure: Use two points of securement

Take a look at Henry’s Twelve tips to placing a well secured PIVC.

For Byron, this means we consider the planned duration of intravenous antibiotics, assess his vessels, and our skills. If practical, Byron would have a PIVC inserted in the forearm (most likely via USG) where we can simultaneously take blood cultures. We would also consider an upgrade to midline or PICC, once the cultures and sensitivities are known, providing a better understanding of the actual duration of therapy and targeted antibiotic therapy.

We are evaluating the project, to see its impact on PIVC related morbidity. Based on the impact of MAGIC on adults, this is likely to be considerable (read here).

Another way to make sticking children with sharp needles less painful for everyone.

Want some top tips on paediatric cannulation? Watch our paediatric cannulation video on the DFTB YouTube channel here.

Neonate resus update 2021

2021 Resuscitation Council UK Guidance: What’s new in neonates?

Cite this article as:
Anandi Singh, Jilly Boden and Vicki Currie. 2021 Resuscitation Council UK Guidance: What’s new in neonates?, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.33461

We’ve looked at the changes in the paediatric resuscitation guidelines, here we take a closer look at neonatal guidelines.

Supporting transition at birth

There are no major changes for the newborns (just yet), but there is clarification on certain practices since the last 2015 update.

The umbilical cord: Leave it hanging?

We should delay clamping the cord for sixty seconds after the first cry. Researchers are looking at the benefit of beginning resuscitation whilst the cord still remains intact. Immediate cord clamping (ICC) has been shown to significantly reduce ventricular pre-load while simultaneously adding to left ventricular afterload.

If delayed cord clamping (DCC) is not possible, ‘milking of the cord’ can result in some transient benefits. There may be less need for inotropic support and fewer transfusions but no overall reduction in morbidity or mortality in the premature. There is insufficient data to suggest any benefit in babies 34 weeks to term. Milking of the cord is not recommended below 28 weeks as one large study was terminated early after babies were found to have higher risk of intraventricular haemorrhage.

Inflation and ventilation breaths: Increased pressure

When delivering inflation breaths, the resuscitation guidelines recommend slightly increased pressures than before

<32 weeks gestation, 25cm H2O for peak inspiratory pressure
>32 weeks, we should be using 30cm H2O initially slowly titrating up to achieve good chest wall movement.

Set the PEEP at at 5cm H2O for all babies that need assisted ventilation.

Laryngeal Mask Airways

LMAs are better than (in systematic review of 7 studies, N=794) bag-mask ventilation. Using them reduces the need for intubation and the duration of ventilation, though the evidence was low/moderate quality. The updated guidelines suggest more proactive use of an LMA in babies >34weeks and >2kgs.

Oxygen: Start low

  • For babies >32/40, the guidelines remains unchanged, start in air, monitor SpO2 and increase as needed. It can take several minutes to reach normal saturation levels.
  • For babies born between 28-32 weeks gestation, a small amount of supplemental oxygen (21-30% FiO2) may help with the effort of breathing and reduce mask ventilation time.
  • Start babies born before 28 weeks gestation on 30% FiO2.
  • Turn the FiO2 immediately up to 100% if you have to start chest compressions.

Thick Meconium: Don’t rush to suction

In the past, if a ‘non-vigorous’ baby (i.e. hasn’t cried yet), was delivered through thick meconium, you were supposed to visualise the cords with a laryngoscope and suction before providing inflation breaths. There wasn’t great evidence for this and the thought was that it simply delayed ventilation in an otherwise apnoeic baby.

What about adrenaline dosing?

There are still a few studies looking at the dosing of adrenaline in neonates but now the recommended dose is 20 micrograms/kg (0.2 mL/kg of 1:10,000 adrenaline (1000 micrograms in 10 mL)).  This should be repeated every 3-5 minutes as needed.

Focus on temperature: Aim for 36.5-37.5°C

The admission temperature of all (non-asphyxiated) babies across all settings and gestational ages, is a strong predictive factor for morbidity and mortality.

  • Use heated and humidified gases from the outset if you can, for babies born <32 weeks. A meta-analysis of 2 RCTs (N=476) suggested that this reduced the rate of hypothermia on admission by 36%.
  • Skin-to-skin care may be enough to keep >32 week babies warm, though a study focusing on 28-32+6 gestation babes suggested that this may be sub-optimal compared to conventional means of warming (a mix of radiant heaters, plastic bags, heated mattresses etc).

For each 1 degree Celsius decrease in admission temperature below the recommended range, an increase in the baseline mortality by 28% has been reported.

Emergency access: You know the drill

Umbilical catheterisation remains the prime means of vascular access.   If this is not an option, then use intraosseous access to give emergency drugs and volume.  Simulation studies suggest that the IO route may be quicker, though not without risk. Adverse events such as osteomyelitis, compartment syndrome and fractures have occurred.

Neonatal resuscitation updates

Stopping resuscitation should be considered by the team if there is no response after 20 minutes and reversible (e.g. tension pneumothorax, hypovolaemia, equipment failure) have been discounted.

Selected references

Resuscitation Council UK Guidelines 2021 https://www.resus.org.uk/library/2021-resuscitation-guidelines

Madar J et al European Resuscitation Council Guidelines 2021: Newborn resuscitation and support of transition of infants at birth (2021). https://doi.org/10.1016/j.resuscitation.2021.02.014

ERC Guidelines 2021: https://cprguidelines.eu/

Wyckoff MH, ET AL. Neonatal Life Support Collaborators. Neonatal Life Support 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Resuscitation. 2020 Nov;156:A156-A187.  https://doi.org/10.1016/j.resuscitation.2020.09.015 Epub 2020 Oct 21. PMID: 3309891

Paediatric resus update 2021

2021 Resuscitation Council UK Guidance: What’s new in paediatrics?

Cite this article as:
Anandi Singh, Jilly Boden and Vicki Currie. 2021 Resuscitation Council UK Guidance: What’s new in paediatrics?, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.33450

You are working in Paeds ED. The alert phone rings for a 2-year-old boy coming in a cardiac arrest. You hear some colleagues talking about Plasmalyte, capnography, and reduced respiration rates. Don’t panic! You had heard somebody mention that there were new resuscitation guidelines out though you’ve not read them yet. How much could have really changed?

Let’s take a step back. Where do these resus guidelines come from?

The Resuscitation Council UK recently issued their 2021 guidelines. They are tailored to UK clinical practice and derived from the European Resuscitation Council (ERC) 2021 Guidelines. The International Liaison Committee on Resuscitation (ILCOR) is responsible for the International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations (CoSTR). This consensus document is then used by international member organisations to develop guidelines. They are updated roughly every five years. CoSTR 2020 formed the ERC 2021 guidance.

The guideline development process utilised systematic reviews, scoping reviews, evidence updates and engagement from worldwide stakeholders (including members of the public and cardiac arrest survivors).

The 2021 Resuscitation Council UK Guidance covers both adult and paediatric basic and advanced life support. We have reviewed the corpus of generic guidance, some key additions and the main changes to both paediatric and neonatal life support algorithms.

The new guidelines do not specifically include the management of arrest secondary to COVID-19. You can be find them at https://www.resus.org.uk/covid-19-resources.

Epidemiology of Paediatric Cardiac Arrest

Epidemiology of paediatric cardiac arrest

Changes in paediatric resuscitation

Paediatric Basic Life Support

There are a few minor changes in 2021 to the paediatric BLS guidelines. They all apply to children up to 18 years of age (except for newborns).

Initial Assessment

Assess for signs of life simultaneously with the delivery of rescue breaths. If there are no signs of life, start chest compressions immediately after initial rescue breaths (you do not need to pause here).

Deliver five rescue breaths followed by ventilation breaths with compressions at a ratio of 15:2.

Emphasis on achieving high quality CPR

We should use mobile phones on loudspeaker for dispatcher guidance on how to deliver CPR or to summon emergency medical services (EMS) without leaving the victim.

Whilst the majority of paediatric cardiac arrests are respiratory in nature, effective chest compressions still play their part. Do these on a firm surface( so not a bed) and to a depth of at least one third the anterior-posterior diameter of the chest (or by 4cm in an infant and 5cm in a child). The rate remains at a rate of 100-120/min. The chest needs to fully recoil after each compression and around 80% of the CPR cycle should be composed of compressions.

Airway

The Resus Council recommend cuffed endotracheal tubes in children, if intubation is needed, and uncuffed tubes in neonates (Ed. note-we’ll look at this another day). Monitor this cuff pressures and try to keep it below 20mmHg.

Breathing

Target oxygen saturations (SpO2) of 94-98% with as little supplemental oxygen as possible. Avoid giving pre-emptive oxygen therapy without signs of hypoxemia or shock and try to avoid readings of up to 100% – unless in situations such as carbon monoxide poisoning. Hyperoxia appears to be almost as harmful as hypoxia.

High-flow nasal cannula oxygen (HFNC) or continuous positive airway pressure (CPAP)/non-invasive ventilation (NIV) support should be considered in children that have adeqaute respiratory drive but are not responding to low-flow oxygen. Bag-mask ventilation (BMV) is recommended in children with inadequate respiratory drive. If oxygenation/ventilation doesn’t improve, or ventilation may be ongoing, it is time for more advanced airway techniques – supraglottic airway devices (SGA) or endotracheal intubation.

Changes to paediatric resuscitation guidelines

Monitor capnography

End-Tidal CO2 monitoring is the gold standard, whether using an SGA or bag-valve-mask ventilation. Waveform capnography can reliably confirm tracheal tube placement when has a perfusing rhythm, as long as they are over two kilos in weight. There is a reasonable correlation between ETCO2 and PaCO2 but the guidelines do not go so far as suggesting a threshold ETCO2 or PaCO2 for stopping the resuscitation attempt.

What can the ETCO2 waveform tell us in resuscitation?

Use of end-tidal in paediatric resus

Circulation

No single finding can reliably identify the severity of circulatory failure. We still need to reassess frequently and after every intervention. This can be done by monitoring mean arterial blood pressure, trends in lactate, urine output and, if competent, ultrasound findings.

Vascular Access

Peripheral intravenous (IV) lines are the first choice for vascular access but it’s just two attempts and you are out. Then it is time to move on.

Intraosseous (IO) access is the primary rescue alternative. Remember it can be painful so give proper intraosseous analgesia before giving the first fluid bolus in every (awake) child.

A balanced approach to fluids

In children with shock, use a 10 mL/kg fluid bolus repeated up to 40-60 mls/kg.

How much should we give? There is an emphasis on smaller volumes with careful reassessment after each bolus to enable early identification of signs and symptoms of fluid overload. These include hepatomegaly, bilateral basal lung crackles, and jugular venous distention. Current evidence shows that a restrictive approach to fluid therapy is at least as effective as larger volumes.

In children with shock secondary to haemorrhage, we need to keep crystalloid boluses to a minimum (max 20mls/kg). Early use of blood products is the way to go in children who present with severe trauma.

Having decided to give fluid, what should we give? Balanced isotonic crystalloids (e.g. Plasmalyte) are the first choice with 0.9% sodium chloride being an acceptable alternative. Saline can induce hyperchloremic acidosis and may be associated with a worse outcome. The evidence for Hartmanns/Ringer’s lactate is still limited and shows ‘no more than a trend’ (?) towards a better outcome – so this is still left a bit unclear… Don’t use dextrose-based solutions for volume replacement – these will be redistributed rapidly away from the intravascular space and will cause hyponatremia and hyperglycaemia which may worsen neurological outcome.

Consider using permissive hypotension (mean arterial blood pressure (MAP) at 5th percentile for age) in traumatic injury. Be mindful that It is contraindicated in children with traumatic brain injury. You need to maintain a reasonable cerebral perfusion pressure. The Resus Council UK guidelines recommend giving tranexamic acid (TXA) to all children requiring transfusion after severe trauma and/or significant haemorrhage, as long as it is within three hours of injury

Vasoactive drugs need to be started early In children with persistent decompensated circulatory failure. Noradrenaline or adrenaline are recommended as first-line agents. Vasoactive drug choice may be directed by individual patient circumstances once more detailed information about the pathophysiology is available..

Dopamine is no longer recommended but can be used if adrenaline and noradrenaline are not available.

Cardiac Arrest in Special Circumstances

Specific approach to CPR needed during specific conditions such as cardiac surgery, neurosurgery, trauma, drowning, sepsis, and pulmonary hypertension. However, there are no major changes to any of these guidelines.

When managing traumatic cardiac arrest we need to fix the reversible causes.

Traumatic cardiac arrest guidelines

We need to start simultaneous chest compressions whilst treating these causes. This trumps adrenaline use. Though exceedingly rare we should think about thoracotomy in paediatric TCA patients with penetrating trauma with or without signs of life on ED arrival.

Extracorporeal Life Support (ECLS)

Extracorporeal cardiopulmonary resuscitation (E-CPR) is the implementation of veno-arterial extracorporeal membrane oxygenation (VA-ECMO) in a patient with refractory cardiac arrest. E-CPR should only be considered if it is readily available and there is a (presumed) reversible cause.

For specific subgroups of children with decompensated cardiorespiratory failure (e.g. severe refractory septic shock or cardiomyopathy or myocarditis and refractory low cardiac output), the pre-arrest use of ECLS can be lifesaving and provide end-organ support, preventing cardiac arrest.

Post-cardiac arrest care

Avoid hypoxia, hypotension and fever in children and infants who have a return of spontaneous circulation (ROSC) following cardiac arrest. Targeted temperature management of children post-ROSC should comprise active treatment with either normothermia or mild hypothermia and continuous invasive temperature monitoring.

Changes in adult resuscitation guidance

Are you curious about the big people?

For the adults, there are no major changes in ADULT BLS/ ALS 2021 guidelines. The guide states that a child is any person up to 18 years – in terms of when we switch from paediatric to adult algorithm. If the child looks like a child, we use the paediatric algorithm. If it turns out that your patient looks more youthful than they actually are then little harm will ensue. They also recommend a stepwise approach to airway management. The expert consensus is that: providers with a high first-pass success rate should perform tracheal intubation.

The use of adrenaline is controversial. We don’t have great evidence for either the dosing or the timing of doses. A large trial in the UK (PARAMEDIC 3, expected Autumn 2021) will look in more detail at the timing of adrenaline and the potential benefits of an IO first approach.

There is a greater emphasis on POCUS and ECMO. This reflects the increasing evidence as a rescue therapy in certain adult patients in cardiac arrest. There is an increasing role of point-of-care ultrasound (POCUS) in peri-arrest care for diagnosis, but it requires a skilled operator, and the need to minimise interruptions during chest compression.

As with the paediatric population: there is a greater recognition that patients with both in- and out-of-hospital cardiac arrest have premonitory signs, and that many of these arrests may be preventable.

What else is in the guidance?

Health inequality (HI) and it’s impact on cardiac arrest outcome

There is vast inequality in the incidence of cardiac arrest, use of bystander CPR and the distribution of public access defibrillators. Deprived areas, and areas with a greater proportion of residents from minority ethnic backgrounds, have a higher incidence of cardiac arrest, lower incidence of bystander CPR and lower access to public access defibrillators. This needs further discussion and research. Teaching CPR to children in all schools would be a way of improving some of these inequalities.

Improving education and systems can save (more) lives

50% of out-of-hospital cardiac arrests (OHCAs) are witnessed. Bystanders perform CPR in 70% of these. Public education is crucial in saving lives. In 2018, 59% of members of the public in the UK reported having received training in CPR and 19% in how to use an automated external defibrillator (AED).

In 2019, over 291,000 people in the UK were trained in CPR as part of World Restart a Heart Day. Teaching the essential core skills in resuscitation will improve patient survival.

How to get better at paediatric resus

Technology-enhanced education, as well as simulation, can be used to improve teaching and engage learners. Social media and smartphone apps can be used to engage the community. A new section has been added to the guidance named ’Systems Saving Lives’ with the intended audience being governments, managers in health and education systems, health care professionals, teachers, students and members of the public. By emphasising the importance of the connections along the Chain of Survival, we can improve the performance of resuscitation systems.

4 Key areas that have been highlighted are:

What's new in paediatric resus guidelines

Ethics

Another key area in the new guidelines is around integrating decisions about CPR in advanced treatment plans (e.g. Recommended Summary Plan for Emergency Care and Treatment (ReSPECT) process). The guideline highlights the need for communication strategies and interventions to support discussions with patients and their family around resuscitation.

What might we see in the next revision…

  • Could IO become the first choice route of adrenaline?
  • Will we still be using adrenaline in all arrest situations?
  • Will (ab)normal saline be removed entirely?
  • Will we have more concrete evidence on using Hartmann’s/ Ringer’s Lactate in resuscitation fluids?
  • Will we have more information on the barriers and motivators to bystander CPR and AED use in respect of ethnic, socio-economic, cultural and educational background?

Selected references for the updated Resuscitation Council UK guidelines

Resuscitation Council UK Guidelines 2021 https://www.resus.org.uk/library/2021-resuscitation-guidelines

Madar Jet al European Resuscitation Council Guidelines 2021: Newborn resuscitation and support of transition of infants at birth (2021). https://doi.org/10.1016/j.resuscitation.2021.02.014 ERC Guidelines 2021: https://cprguidelines.eu/

Wyckoff MH, ET AL. Neonatal Life Support Collaborators. Neonatal Life Support 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Resuscitation. 2020 Nov;156:A156-A187.  https://doi.org/10.1016/j.resuscitation.2020.09.015 Epub 2020 Oct 21. PMID: 3309891

Much ado about Meckel’s

Cite this article as:
Peter Tormey. Much ado about Meckel’s, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.33008

Robert is a 14-year-old boy who re-presents to ED with a history of rectal bleeding. He has had four or five episodes of passing bright, red blood PR over the last three days, having been a previously well child. He has also had four or five episodes of non-bilious vomiting.

Mum has noticed that he has now become pale and lethargic.

On his first presentation to ED, two days prior, the working diagnosis was bacterial gastroenteritis. His haemoglobin at that time was 99g/L. It has fallen to 45g/L on this presentation.

On examination, he is very pale, his heart rate is 120, and his blood pressure 95/65.

What are your differentials at this point?

Infectious

  • Bacterial: Campylobacter, Salmonella, Shigella, E. coli, Yersinia, C. difficile
  • Viral: rotavirus, COVID-19

Inflammatory

  • Inflammatory bowel disease

Vascular

Bowel obstruction

  • Intussuception
  • Malignancy

Others

  • Meckel’s diverticulum
  • Anal fissure
  • Haemorrhoids
  • Trauma/NAI

What investigations would you perform?

  • Bloods: FBC, U+E, LFTs, CRP, ESR, VBG, blood culture, coagulation screen
  • Stool culture, stool for C.difficile
  • Covid swab
  • Abdominal ultrasound
  • CT abdomen/pelvis
  • Colonoscopy
  • Meckel’s scan

What is Meckel’s Diverticulum?

You may remember “The Rule of Two’s” from medical school.

MD is a congenital abnormality of the small intestine that is present in 2% of the population. 2% of these people will become symptomatic. It is 2 inches long and 2 feet from the ileocoecal valve. There can be 2 types of ectopic tissue: gastric or pancreatic. There is a 2:1 male preponderance.1,2,3

MD comprises the three layers of the intestinal wall and is, therefore, a true diverticulum.3 It results from the incomplete obliteration of the omphalomesenteric duct. The omphalomesenteric duct connects the yolk sac to the intestinal tract during early foetal life and is usually obliterated by the seventh week of gestation. Failure to regress can result in a spectrum of abnormalities, including: MD, patent vitelline duct, fibrous band, sinus tract, umbilical polyp and umbilical cyst.3

Comparison between vitelline fistula and meckel's

What happens to the symptomatic 2%?

The presentation of MD is highly variable. It is best to consider the different presentations based on the underlying anatomical or pathological processes the diverticulum can undergo.

1. It gets in the way

The abnormal anatomy in MD can lead to intestinal obstruction. In children, this usually presents as intussusception or volvulus.3

The diverticulum acts as the lead point in intussusception. These patients present with abdominal pain. The symptoms can be non-specific, particularly in pre-verbal children. They are “off form”, or parents complain about poor feeding, constipation, abdominal distension. As you can see from Robert’s case, intussusception can also lead to massive GI haemorrhage.

Volvulus of the intestine may occur around the fibrous cord that connects the Meckel’s to the umbilicus.4

2. The ectopic gastric tissue can cause an ulcer

The ectopic gastric mucosa in the diverticulum can secrete acid which results in ulceration of the small bowel. This usually presents as painless bleeding, which can be massive in nature.3 It may also present due to anaemia from chronic bleeding. The bleeding is usually dark red or maroon in colour.3 Robert’s Technitium-99m scan (or Meckel’s scan) was positive, suggesting the presence of gastric mucosa, so he may have intussusception plus ulceration, both leading to his massive GI haemorrhage.

3. It gets angry

As the Meckel’s is a blind ending diverticulum, it can undergo a process of inflammation, similar to appendicitis. Obstruction at the base of the diverticulum leads to bacterial overgrowth and inflammation. This can present with fever, vomiting and abdominal pain, which is often indistinguishable from acute appendicitis. The MD may also perforate, leading to diffuse peritonitis and  a very unwell patient.

As these symptoms are all non-specific, it is important to think of MD as a diagnosis in children presenting with any of the symptoms above.

How is it diagnosed?

MD requires a high index of clinical suspicion to aid diagnosis. Most imaging modalities are non-specific but can still be helpful. X-ray or ultrasound may show a small bowel obstruction and intussusception.5 Finding a normal appendix on ultrasound, may lead to careful consideration of MD as an alternate cause.

A Meckel’s scan may be performed. This is a nuclear medicine scan using Technitium-99m, which accumulates in the ectopic gastric mucosa (see Image 2).5 The test is reliant on the presence of gastric mucosa, which is only present in 4.6-71% of symptomatic MD.5 Premedication with H2 antagonists may increase the accuracy of the scan.5

Radionuclide Meckel scan
Case courtesy of Radswiki, Radiopaedia.org. From the case rID: 11598

MD is often only confirmed on exploratory laparoscopy or laparotomy.

How is it treated?

Definitive treatment is surgical resection of the diverticulum, either laparoscopically or by laparotomy. Simple diverticulectomy and closure of the ileum is acceptable except in cases of GI bleeding where the ulcer may extend to the adjacent ileum, in which case segmental resection with re-anastomosis of the small bowel should be carried out.4

Robert’s haemoglobin is 45. He requires multiple transfusions with packed red cells, FFP and fibrinogen. He is stabilized and transferred to PICU.

He has an emergency OGD and colonoscopy. They do not reveal the source of bleeding. His abdominal ultrasound shows a small bowel intussusception, suspicious for Meckel’s diverticulum (MD). He has a Meckel’s scan which confirms MD. He undergoes surgical resection of the diverticulum and recovers well.

Who was Meckel?

Johann Friedrich Meckel (the younger) was a German anatomist whose principle interest was the study of congenital malformation and the developmental aspects of the lungs and bloods vessels.6

Interestingly, MD was first described by Wilhelm Fabricius Hildanus, a German Surgeon, in 1598.7 It wasn’t named, however, until Meckel reported his research on the diverticulum’s anatomy and embryology in 1809.

He is also responsible for the medical eponyms Meckel cartilage and Meckel syndrome.

He is called Johann Friedrich Meckel The Younger because his grandfather was called by the same name and was also an anatomist, as were his father, younger brother and son.

You can find out more about him and the Meckel anatomist dynast on LITFL.

References for Much Ado about Meckel’s

1. Meckel’s Diverticulum [Internet]. [cited 2021 Apr 1]. Available from: https://pedemmorsels.com/meckels-diverticulum/

2. Rule of 2s in Meckel diverticulum | Radiology Reference Article | Radiopaedia.org [Internet]. [cited 2021 Apr 1]. Available from: https://radiopaedia.org/articles/rule-of-2s-in-meckel-diverticulum-1

3. Keese D, Rolle U, Gfroerer S, Fiegel H. Symptomatic Meckel’s Diverticulum in Pediatric Patients—Case Reports and Systematic Review of the Literature. Front Pediatr [Internet]. 2019 Jun 26 [cited 2021 Apr 12];7(JUN):267. Available from: https://www.frontiersin.org/article/10.3389/fped.2019.00267/full

4. Ivatury RR. Meckel’s diverticulum and the eponymous legend. Vol. 87, Journal of Trauma and Acute Care Surgery. Lippincott Williams and Wilkins; 2019. p. 451–5.

5. Hansen C-C, Søreide K. Systematic review of epidemiology, presentation, and management of Meckel’s diverticulum in the 21st century. Medicine (Baltimore) [Internet]. 2018 Aug 1 [cited 2021 Apr 12];97(35):e12154. Available from: https://journals.lww.com/00005792-201808310-00091

6. Johann Friedrich Meckel The Younger • LITFL • Medical Eponym Library [Internet]. [cited 2021 Apr 12]. Available from: https://litfl.com/johann-friedrich-meckel-the-younger/

Defining Learning Disability

Cite this article as:
Liz Herrieven. Defining Learning Disability, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.33287

In all areas of paediatric practice (and beyond), we come into contact with children with a learning disability, learning difficulties or autism. Terminology is important, not only for making sure we understand a child’s diagnosis properly, but also for providing the best possible care. Getting it right can also help gain the trust of parents and carers who will often know far more about appropriate language use than we clinicians. This guide aims to describe the key points to remember – some of them easier to grasp than others.

Learning Disability

Let’s start with learning disability or LD. 2.5% of the children in the UK have a learning disability, yet it’s one of the most commonly confused terms. Probably the most pragmatic and descriptive definition is that used by Mencap, a UK charity supporting people with LD: “A learning disability is a reduced intellectual ability and difficulty with everyday activities – for example household tasks, socialising or managing money – which affects someone for their whole life.” The World Health Organisation keeps it short, although open to discussion and interpretation. For them it’s “a state of arrested or incomplete development of mind.”

Having a learning disability means an individual will not only find learning difficult but also face challenges with retaining, processing, reasoning and deducing information. Some people will find different areas of learning more challenging than others. Children with Down syndrome have a relative strength in visual learning and find learning or remembering auditory information more difficult. Building on strengths can help to balance out some of the more challenging areas. Some people with LD may be able to communicate very well, even if they struggle to understand all of what is communicated to them but many will have an associated speech and language problem.

The term intellectual disability, or ID, is used rather than LD, to signify that the condition affects intellect and is lifelong. This fact is important – the individual will need support, depending on their level of disability, for the whole of their life. There are many causes of LD, all involve the developing brain – genetic or chromosomal conditions, intrauterine infections, perinatal hypoxic brain injury to name but a few. After the brain has developed, such an insult is described as an acquired brain injury.

The level of disability may be mild, moderate or severe, depending on IQ, although this is rarely formally calculated and actually doesn’t really add much. Support and care should be tailored to an individual’s needs rather than their IQ.

The term PMLD is used to describe individuals with Profound and Multiple Learning Disability. These patients may have fairly complex comorbidities alongside severe learning disabilities. They can affect not only their ability to learn and process information, but also their ability to communicate and to be independent.

Learning Difficulty

A learning difficulty is very different to a learning disability, and is far more common. Things like ADHD, dyspraxia or dyslexia are all examples of a learning difficulty. They all make learning more difficult, but don’t affect overall intellect or IQ.

Autism

Autism, or an autistic spectrum condition (ASC), is not itself a learning disability, although about one-third of people with ASC will also have LD. The National Autistic Society (UK) describes autism as “a lifelong developmental disability which affects how people communicate and interact with the world”. There are lots of different elements, each of which may be present to a greater or lesser extent within one individual, so each autistic person is different from the next. The autistic spectrum is not a linear thing, with someone being more or less autistic. “High functioning” or “low functioning” are not particularly appropriate terms either. It’s more helpful to think about how someone’s autistic features affect them. The most common features include social communication difficulties, sensory processing disorder and restrictive or repetitive movements.

Social communication difficulties include challenges in interpreting body language or facial expression, and reading hidden meaning into words or phrases, particularly when metaphors are used. Sensory processing difficulties involve the body misinterpreting sensations. A light touch may be perceived as very painful whilst a deeper touch may be more comforting. Bright lights or certain noises could be very distressing. Restrictive or repetitive movements are often comforting, or theymay distract from upsetting or uncomfortable situations.

ASC was more commonly known as ASD, or autistic spectrum disorder. The move to calling it a condition, instead, is an attempt to remove unnecessary negativity. ASC encompasses many other conditions such as that previously known as Asperger syndrome. This name is no longer preferred – Hans Asperger has a troubling history. It was used to describe people with normal or even high intelligence, coupled with autistic features. Other conditions included under the ASC umbrella include PDD (pervasive developmental disorder) and PDA (pathological demand avoidance).

Person First vs Identity First Language

We use person-first language for many conditions. Someone with asthma is not defined by their asthma but has a whole identity of their own, so they are described as someone with asthma. Someone with Down syndrome may share certain physical features with someone else with Down syndrome, but they have their own identity and character which is very different from that of others with Down syndrome, so they are described as a person with Down syndrome, not a Down’s person or, even worse, a Downs.

Child with learning disability

Many autistic people feel that their autistic features form part of their identity – that they would be a very different person if they did not have autism, so they describe themselves as autistic, rather than a person with autism. You can read more about person first vs identity first language here.

And if you can’t remember what to say when?

Ask! It’s always better to ask someone how they would prefer to be described than to guess. All people. whether they have LD, a learning difficulty or ASC are individuals and will have their own preferences, likes and dislikes. Getting the language right can be a great start, but being honest and open when you’re not sure is a very close second.

Supraglottic airway devices

Cite this article as:
Jessica Rogers. Supraglottic airway devices, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.32780

Endotracheal intubation (ETI) in children is thankfully rare and our first pass success rate could definitely do with some improvement.

It is difficult to compare the efficacy of various advanced airway techniques in children. There are ethical implications, of course, but also marked differences in ages and in the potential aetiology of the arrest. There is often time to talk with the intensive care team and make a plan based on the best airway for that given situation. Similarly, the operating theatre, home of many an airway trial, is a very different environment. We’ll look at advanced airways in cases of cardiac/respiratory arrest. Be mindful there will always be a difference in timing and skill set between out-of-hospital cardiac arrest (OHCA) to in-hospital cardiac arrest (IHCA).

There are few actual studies comparing the advanced airway treatments used during cardiac arrest management in children. There are even fewer studies surrounding the use of supraglottic airways (SGAs) in children. Most of these are observational studies.

ILCOR currently recommends endotracheal intubation (ETI) as the ideal way to manage an airway during resuscitation. They also state that supraglottic airways are an acceptable alternative to the standard bag-valve-mask ventilation (BVM). There are very few clinical trials in children on which these recommendations are based (and certainly none of rigorous design in the last 20 years). Due to this lack of evidence, they commissioned a study as part of the Paediatric Life Support Task Force.

Lavonas EJ, Ohshimo S, Nation K, Van de Voorde P, Nuthall G, Maconochie I, Torabi N, Morrison LJ, DeCaen A, Atkins D, Bingham R. Advanced airway interventions for paediatric cardiac arrest: a systematic review and meta-analysis. Resuscitation. 2019 May 1;138:114-28.


Lavonas et al. (2018) carried out a systematic review and meta-analysis on the use of advanced airway interventions (ETI vs SGA), compared to BVM alone, for resuscitation of children in cardiac arrest. Only 14 studies were identified. 12 of these were suitable for inclusion in the meta-analysis. They were mostly focused on OHCA. There was a high risk of bias and so the overall quality of evidence was in the low to very low range. The key outcome measure was survival to hospital discharge with a good neurological outcome. The analysis suggested that both ETI and SGA were not superior to BVM.

So now, let’s cover some of the literature on the use of supraglottic airway devices. These are mostly based on studies in adults.

The ideal ventilatory device

  • …is easy to set up and insert by anyone so it doesn’t matter what the make-up of the team is
  • …is quick to set up and quick to insert. This reduces the time taken away from other important tasks and allowing that all-important ‘bandwidth’
  • …allows for minimal risk of aspiration
  • …provides a tight seal to allow for high airway pressures if needed
  • …is sturdy enough that the patient cannot bite through it and cut off their own oxygen supply
  • …provides an option to decompress the stomach via the same device
  • …has minimal risk of accidental misplacement or loss of airway once inserted

If this sounds too good to be true, it is. No one device combines all of these essential features. This leaves us deciding which is most suited to the patient in front of us.

sizing chart for supraglottic airway devices
Rather than tape the i-gel to the cheek it is often easier to use traditional tube ties to secure the airway

It is very difficult to compare SGAs with endotracheal tubes (ETT). An ETT is a ‘definitive airway’ that provides protection against aspiration. This does not mean that SGAs are a ‘lesser’ option. An SGA is still an ‘advanced airway’ and more effective than using a bag-valve-mask technique. It is important to remember that advanced airways have their pros and cons. Whilst they may improve a patients’ likelihood of survival with good neurological recovery, there can be associated complications.

Table showing advantages and challenges of bag-valve mask compared to supraglottic airway devices

The science behind supraglottic airways

So what does the science say? There are few trials in children but there have been several seminal papers released on advanced airway techniques in adults. Whilst not directly related to children, they do raise some interesting points of comparison between devices.

Benger JR, Kirby K, Black S, Brett SJ, Clout M, Lazaroo MJ, Nolan JP, Reeves BC, Robinson M, Scott LJ, Smartt H. Effect of a strategy of a supraglottic airway device vs tracheal intubation during out-of-hospital cardiac arrest on functional outcome: the AIRWAYS-2 randomized clinical trial. Jama. 2018 Aug 28;320(8):779-91.

This multicentre, cluster randomised trial, was conducted by paramedics across four ambulance services in England. It compared supraglottic devices to tracheal intubation in adult patients with OHCA looking at their effect on functional neurological outcome. This study only included patients over the age of 18. They found no statistically significant difference in 30-day outcome (the primary outcome measure) or in survival status, rate of regurgitation, aspiration or ROSC (secondary outcomes). There was a statistically significant difference when it came to initial ventilation success. Supraglottic airways required less attempts, but their use also lead to an increased likelihood of the loss of an established airway

So what does this mean? The main concern that gets bandied around when discussing SGAs is the higher risk of aspiration. If there was no difference in risk, would that change your mind?

Jabre P, Penaloza A, Pinero D, Duchateau FX, Borron SW, Javaudin F, Richard O, De Longueville D, Bouilleau G, Devaud ML, Heidet M. Effect of bag-mask ventilation vs endotracheal intubation during cardiopulmonary resuscitation on neurological outcome after out-of-hospital cardiorespiratory arrest: a randomized clinical trial. Jama. 2018 Feb 27;319(8):779-87.

This was a multicentre, randomised clinical trial in France and Belgium looking at OHCA over a 2-year period. Again this study enrolled adults over 18 years old. They looked at the non-inferiority of BVM vs ETI with regard to survival with favourable neurological outcome at 28 days. Responding teams consisted of an ambulance driver, a nurse and an emergency physician. The rate of ROSC was significantly greater in the ETI group but there was no difference in survival to discharge. Overall, the study results were inconclusive either way.

If survival to discharge is unaffected, should we all be spending time training and maintaining competency or should endotracheal intubation be kept only for those who practice it regularly in their day job?

Wang HE, Schmicker RH, Daya MR, Stephens SW, Idris AH, Carlson JN, Colella MR, Herren H, Hansen M, Richmond NJ, Puyana JC. Effect of a strategy of initial laryngeal tube insertion vs endotracheal intubation on 72-hour survival in adults with out-of-hospital cardiac arrest: a randomized clinical trial. Jama. 2018 Aug 28;320(8):769-78.


This cluster-randomised, multiple crossover design was carried out by paramedics/EMS across 27 agencies. It looked at adult patients receiving either laryngeal tube or endotracheal intubation and survival at 72 hours. Again, they only included adults over 18 with non-traumatic cardiac arrest. They found a ‘modest but significant’ improved survival rate in the LMA group and this correlated with a higher rate of ROSC. Unfortunately, this trial included a lot of potential bias and the study design may not be robust enough to back up the level of difference.

Could the survival rate be explained by first-pass success and less time spent ‘off the chest’ during initial resuscitation? No study is perfect. Always critically appraise for yourself and check if study results are applicable to your local population and own practice before changing anything.

More questions than answers

After reading the science (and please do go take a deeper dive into those papers and appraise them for yourselves), let’s tackle some common queries.

SGAs are so easy you can just whack it in and done!

No. Getting the SGA in is only the first step. Even then, you need to be sure you have picked the appropriate size and assessed for leaks. SGAs are much more likely to become dislodged and lead to an unexpected loss of airway. Generally, we are not as meticulous about securing them as we should be. Ideally, use a tube tie to secure it in place and monitor the position (in relation to the teeth). Some SGAs have a black line on the shaft that should line up with the incisors (beware this may only be present in the larger sizes). Just like ETTs, they require you to check for adequate ventilation via auscultation, ETCO2 and listening for an obvious leak.


It’s okay if there is a leak at the start as the gel will mould as it heats up

No. There is no evidence to suggest the shape of i-gels (this is usually the model clinicians are referring to in this instance) will mould to the inside of the larynx. Researchers have tried heating up the material and there is no statistical change in the leak. If you do have a significant leak, consider re-positioning, swapping out for a different size or using a different model. You may find a small leak that disappears over time. Over time, the airway jiggles around and sits better.


You should always decompress the stomach when you put in an LMA

Possibly. This is not routinely found in guidelines as it is seen as more of a fine-tuning procedure. It can take time and resources away from other critical tasks (such as chest compressions, IV access, optimal ventilation) but if you have the resources to do so, without affecting the basics of good resuscitation care, then it is a good option if ventilation is not as optimal as it could be. This is particularly important in children. We know that they are at higher risk of diaphragmatic splinting from overzealous ventilation so the early insertion of a nasogastric tube can really improve things.

Laryngoscopy should be used before every SGA insertion

Possibly. Some places have started to mandate laryngoscopy because they have missed obstruction by a foreign body, or to allow better suctioning and improve the passage for insertion. There is an argument that the SGA may sit better if inserted with the aid of a laryngoscope as, in a number of cases, it hasn’t been inserted deeply enough. Laryngoscopy is a complex skill, that takes regular practice and comes with its own challenges (damage to mouth/teeth, additional time taken, higher skill set needed).

Once inserted, SGAs can be used alongside continuous chest compressions

Possibly. This really needs to be considered on a case-by-case basis. SGAs are an advanced airway and can be used with continuous chest compressions to increase cerebral perfusion pressures. It is up to the individual clinician to monitor and decide if the ventilatory support they are giving is adequate during active compressions. In cases where the arrest is secondary to hypoxia (as in many paediatric arrests) it may be easier, and more useful, to continue with a 30:2 or 15:2 ratio to ensure good tidal volumes are reaching the lung. Some studies have shown little difference comparing the 30:2 approach to continuous ventilation.

Troubleshooting

This is the same in both SGAs and ETTs.

  • Patient issues – vomit, secretions, bronchospasm, position, change in intrathoracic / intrabdominal pressures, and in SGAs there is a risk the epiglottis has moved and is covering the opening of the device
  • Device issues – position, size, biting/kinking of an ETT
  • Equipment issues – ventilator settings, connections, oxygen supply

Remember, if you are really struggling, take a second to consider if you might be in a “can’t intubate, can’t ventilate” type of situation. Check out this article, which takes a closer look at this rare scenario.

The bottom line is, we just do not know what is best in our paediatric population. Due to lack of scientific evidence, we often have to rely more on operator skill, available equipment and previous experience.

Selected resources on supraglottic airways

Check out the ‘Roadside to Resus: Supraglottic airways’ podcast from The Resus Room

PHEMcast also have podcasts on ‘The LMA’ and ‘The collapsed infant’

Nasal injuries

Cite this article as:
Ragavan Navaratnam. Nasal injuries, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.33108

13-year-old Freya (she/her) has been tackled in rugby and fell onto her nose. It bled initially and her mother has brought her as it is really swollen and looks wonky. “Is it broken, doctor?”

Nasal injuries in children are frequently encountered in paediatric emergency departments. One third of all nasal fractures occur in children, accounting for 60% of all facial fractures seen in the emergency department. The nose is the second most commonly injured site on a child and is more commonly seen in males. The most common locations of injury to the nose are: the nasal tip, the dorsum, and nasal root region with only 32% of injuries involving the nasal skeleton.

Nasal fractures are more common after three years of age, and unlikely below the first year of life, as the nasal bones are hardly ossified. But the bones aren’t the only thing you need to look out for; nasal obstruction and septal haematomas are important to identify and treat urgently.

History

Nasal trauma in children commonly arises following: falls, contact sports and automobile crashes, typically involving bicyclists or pedestrians. Non accidental injury also must be considered as a potential mechanism.

Important aspects of history should include:

  • mechanism
  • if there was any deformity immediately
  • new-onset nasal obstruction.
  • bleeding
  • anosmia

It is also important to note any previous nasal injury or pre-existing deformity.

Examination

Children with facial trauma are usually apprehensive, so any examination may be limited due lack of cooperation.  Pain relief and play therapy will go a long way. Bleeding and swelling often accompany injuries and can limit a thorough examination. Applying local pressure may be necessary prior to starting a formal examination.

Inspection

The examination should start with inspection of the nose and the surrounding facial structures.  It is important to note:

  • Periorbital bruising in the absence of other orbital findings is suggestive of a nasal fracture.
  • External nasal deformity, epistaxis, oedema, and bruising is highly suggestive of a septal injury. Any deformity more be masked by swelling.
  • A flattened, broad nose with an increase of the inner canthal distance and associated with vertical orbital displacement is suggestive of a naso-orbito-ethmoid fracture. The normal mean inner canthal distance is 16 mm at birth and increases to 25 to 27 mm in the mature female and male face, respectively, although there is ethnic variation.

The intranasal cavity should be assessed with a nasal speculum to exclude a septal injury. A septal haematoma can arise without the presence of any external signs. The septum should be examined for the presence of fractures, displacement, lacerations, discoloration, and abnormal swelling. Don’t forget that the nasal septum may be acutely or chronically deviated so you may need to ask about this in the history. Sometimes looking at an old photo helps.

The key findings suggestive of septal hematoma include:

  • An asymmetrical septum with a blue/red discolouration
  • Swelling of the nasal mucosa that obstructs the nasal passage
  • The size of the mass does not change with the application of topical vasoconstricting agents.

Most times a septal haematoma looks like a blueberry up the nostril.

Palpation

After inspection, the nasal bones should be palpated for tenderness, deformity, mobility and  crepitus, although realistically poking a bruised nose may be too painful to tolerate. It is important to note:

  • Tenderness over the frontal sinus may indicate frontal sinus fractures.
  • Tenderness to palpation of the tip of the nose may be suggestive of a septal hematoma
  • Tenderness and instability on palpation of the anterior nasal spine from beneath the upper lip may indicate a significant septal injury.
  • Malocclusion is suggestive of a midfacial Le Fort fracture.

It is important to exclude an associated skull fracture which may be indicated by the presence of clear fluid in the nasal cavity. A fracture through the cribriform plate can result in a CSF leak. In an ideal world you can test for beta-2-transferrin (present only in CSF, perilymph, and aqueous humor), but I have yet to hear of EDs which offer this.

The signs and symptoms of nasal septal injury may evolve during the 24 to 72 hours after injury. Children with nasal trauma should be safety-netted to return if anything changes after they go home.

Investigations

A history and clinical examination should more than suffice in guiding the management of children with nasal injuries. In simple nasal injuries, imaging adds very little. Plain radiographs are of very limited benefit as the majority of the nose in children in cartilaginous and therefore poorly visualised on x-rays.

In injuries associated with more worrying features i.e. CSF leak or malocclusion, CT imaging is the modality of choice due to the risk of a Le Fort fracture or a base of skull injury.

Classification

A number of classifications systems have been proposed for nasal injuries. The first and most widely quoted was based on the pattern of injury sustained and the direction of force applied. More recently, a classification system based on pathological findings was proposed. This second classification system has been adapted, to incorporate clinical findings as opposed to the  pathologic patterning of injury.

Table showing 6 types of nasal injury
Classification of nasal injuries

A complicated fracture is classified as a Type II to Type IV  fracture with CSF rhinorrhea, airway obstruction, septal haematoma, crush injury, numbness, severe displacement or midface involvement.

Treatment

The management of nasal trauma in infants and children depends upon their age, the degree of nasal obstruction, and associated injuries. Children with nasal trauma should maintain upright posture to prevent the formation and facilitate the resolution of any associated oedema and hematoma. Patients who have no symptoms, minimal swelling, and no septal deviation or hematoma do not need specific follow-up.  Ensure adequate analgesia is given and appropriate advice when to return (on-going bleeding, evolving nasal obstruction, worsening pain).

Epistaxis – Most acute nasal bleeds respond to direct pressure over the anterior nose. Encourage the child to pinch their own nose but if they are unable, asking a parent to perform this has the added benefit of helping reduce the patient’s anxiety. During simple compression, position the child upright and sit them forward. This will help avoid possible aspiration of blood. Distraction and play therapy during compression are useful. In the majority, bleeding is controlled within 5 – 10 minutes.

If direct pressure fails to control bleeding, a number of management options are available but are rarely needed in the emergency department. These include:

  • Nasal packing. Tamponading the bleeding point can be very effective but can be very distressing to children. Sedation is often required to facilitate the procedure. It is advisable to seek an ENT opinion before packing a child’s nose, especially if this is traumatic.
  • Topical vasoconstrictors. These can be very effective but are not without risks. They are most commonly used in the theatres by the ENT surgeons. Options include topical phenylephrine or oxymetazoline. After application of a vasoconstrictor, direct pressure should be applied for at least 5 minutes before reassessing for further bleeding.
  • Tranexamic acid.
  • Cautery. In the emergency department, chemical cautery is commonly used, predominately in the adult population. Typically 75% silver nitrate is used to arrest bleeding. Cauterisation is undertaken around the bleeding point. Cautery works most effectively on dry areas so direct cautery of a bleeding point is often unsuccessful until the surrounding area has been treated. Care must be taken to avoid the skin and it is paramount the child is calm and cooperative, which may necessitate sedation. Make sure you don’t cauterise both sides of the septum.

Children presenting with possible fractures or obvious deformity should be reviewed by an ENT specialist; generally this can wait a few days. In the very young, injuries resulting in nasal obstruction should be referred urgently as young children are obligate nasal breathers.

As mentioned previously, swelling and oedema can make an accurate assessment difficult. As such, an immediate referral of a child with a broken nose but no features of airway compromise may not be needed. Children can be referred to an outpatient clinic for review but should be seen within in five to seven days. Short delays in definitive management of up to a week have been shown to have little impact on long term outcome. However, delays over seven days can make reduction of fractures more challenging, largely due to the active growth centres in a child’s nasal bones promote rapid healing.

Potential complications of nasal injuries

A number of potential complications can arise as a result of nasal trauma, particularly if there is a fracture. The most common complication is obstruction. This is often due to either soft tissue swelling or a deviation of the septum following an injury. Persistent obstruction following an injury is more likely due to septal deviation and therefore requires assessment by an ENT surgeon.   

Poor cosmesis following healing is a common problem reported by patients and is a valid concern for many parents. Recent work has shown that those sustaining fractures at a younger age compared to those that had none, had no differences in functional outcomes but were likely to suffer with deviations of the septum, bumps or humps in the nasal bridge and saddle formation.  Ensuring a timely referral to a surgeon may help reduce the incidence of a poor aesthetic result for the patient.

A septal haematoma that is not promptly dealt with can result in a septal abscess or necrosis (and a future flat nose). Though infection can remain localised, cases of intracranial infection via tracking through the cavernous sinus have been reported. Cavernous sinus thrombosis is also a recognised complication of septal haematomas. Damage to the cribiform plate with a resulting CSF leak is also a potential avenue for intra-cranial infection.

Rarer complications but still clinically important include:

  • Lacrimal duct obstruction
  • Maxillary hypoplasia
  • Naso-oral fistula
  • Anosmia. If this occurs following trauma, it very rarely returns.

Take homes

A clever history and examination are key.

Ensure you examine the inside of the nose especially for a septal haematoma

Adequate analgesia and distraction will make examination much easier

Radiological investigations have little use in simple injuries.

Direct pressure for at least 10 minutes should stop most cases of epistaxis.

Make sure, if referring to clinic, the child is seen within a week.

You have examined Freya and she has no signs of obstruction, no septal haematoma and her bleeding as stopped. She does seem to have a deviated septum however, so you discharge her with advice for simple analgesia, safety-netted and referred her for rapid access ENT clinic within seven days.

References

Baek HJ, Kim DW, Ryu JH, Lee YJ. Identification of Nasal Bone Fractures on Conventional Radiography and Facial CT: Comparison of the Diagnostic Accuracy in Different Imaging Modalities and Analysis of Interobserver Reliability. Iran J Radio. 2013 Sep; 10(3): 140–147.

Beck R, Sorge M, Schneider A, Dietz A. Current approaches to epistaxis treatment in primary and secondary care. Dtsch Arztebl Int. 2018 Jan; 115(1-2): 12–22

Béquignon E, Teissier N, Gauthier A, Brugel L, De Kermadec H, Coste A, Prulière-Escabasse V. Emergency Department care of childhood epistaxis. Emerg Med J. 2017;34(8):543

Burnius M, Perlin D Pediatric ear, nose, and throat emergencies. Pediatr Clin North Am. 2006;53(2):195

Caglar B, Serin S, Akay S, Yilmaz G, Torun A, Adibelli ZH, Parlak I. The accuracy of bedside USG in the diagnosis of nasal fractures. Am J Emerg Med 2017 Nov;35(11):1653-1656.

Calder N, Kang S, Fraser L, Kunanandam T, Montgomery J, Kubba. A double-blind randomized controlled trial of management of recurrent nosebleeds in children. Otolaryngol Head Neck Surg. 2009;140(5):670

Elden LM, Potsic WP. Otolaryngology trauma. In: Textbook of Pediatric Emergency Medicine, 5th, Fleisher GR, Ludwig S, Henretig FM (Eds), Lippincott Williams & Wilkins, Philadelphia 2006. p.1663.

Hester TO Campbell JP. Diagnosis and management of nasal trauma for primary care physicians. J Ky Med Asoc. 199795(9):386

Higuera S, Lee E I, Cole P, Hollier L H, Jr, Stal S. Nasal trauma and the deviated nose. Plast Reconstr Surg. 2007;120(7, Suppl 2):64S–75S

Hoppe IC, Kordahi AM, Paik AM, Lee ES, Granick MS (2014) Age and sex-related differences in 431 pediatric facial fractures at a level 1 trauma center. J Craniomaxillofac Surg 42(7):1408–1411

Joseph J, Martinez-Devesa P, Bellorini J, Burton MJ. Tranexamic acid to help treate nosebleeds. Cochrane review. 2018

Lkas Anschuetz B, KaiserN, Dubach P, Caversaccio M lun nasal trauma in children:a frequent diagnostic challenge. Euro Arch Oto-Rhin-Larng.2019. 276; :85-91

Lopez MA, Liu JH, Hartley BE, Myer CM. Septal hematoma and abscess after nasal trauma. Clin Pediatr (Phila). 2000;39(10):609

Precious DS, Delaire J, Hoffman CD. The effects of nasomaxillary injury on future facial growth. Oral Surg Oral Med Oral Pathol. 1988; 66:525-530.

Puricelli MD, Zitsch RP. Septal Hematoma Following Nasal Trauma. J Emerg Med. 2016 Jan;50(1):121-2.

Rohrich RJ, Adams WPJr, Nasal fracture management: minimizing secondary nasal deformities, Plast. Reconstr. Surg. 2000, 266-273

Schlosser RJ, Bolger WE. Nasal cerebrospinal fluid leaks: critical review and surgical considerations.Laryngoscope. 2004;114(2):255

Stucker FJ Jr, Bryarly RC, Shickley WW. Management o nasal trauma in children. Arch Oolaryngol. 1984: 110 (3): 90

Thomson CJ, Berkowitz RG. Extradural frontal abscess complicating nasal septal abscess in a child. Int J Pediatr Otorhinolaryngol. 1998;45(2):183

Wu KH, Tsai FJ, Li TC, Tsai CH, Peng CT, Wang TR. Normal values of inner canthal distance, interpupillary distance and palpebral fissure length in normal Chinese children in Taiwan. Acta Paediatr Taiwan. 2000;41(1):22. 

Yoon HY, Han DG. Delayed Reduction of Nasal Bone Fractures Arch Craniofac Surg. 2016 Jun; 17(2): 51–55

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/

Ultrasound Guided Peripheral Vascular Access

Cite this article as:
Trent Calcutt. Ultrasound Guided Peripheral Vascular Access, Don't Forget the Bubbles, 2021. Available at:
https://doi.org/10.31440/DFTB.23253

One of my favourite things in paediatrics is the expanding role of ultrasound guided vascular access.

When I started as a paediatric registrar, I’d just finished an adult ICU term where I’d become spent a majority of time supporting provision of a vascular access service, and as part of this had become a PICC line insertion instructor. Eventually, I got to the point where I dreamt of abstract grey shapes. But then I started a paediatric job in a regional hospital where it seemed that ultrasound was used for vascular access rarely if at all. Initially, I thought there must have been something different about paediatric vascular access that I was unaware of. One day, when looking after a young lady with Rett’s who was known to be difficult to cannulate, I reached for the ultrasound. In the five years since, ultrasound has been a standard part of my practice in achieving vascular access in children, with technique adapted to fit the age of the patient.

Ultrasound-guided vascular access and paediatrics seem like such a natural partnership. The concept of a DIVA (“difficult IV access”) patient is receiving increasing interest and research. Criteria for a DIVA can include prematurity, inability to see or feel a vessel, or an episode of multiple prior attempts. These criteria would be met by a huge number of the kids we care for, in particular toddlers or the previously premature infant. 

Chonky baby arm
Spot the veins

Why is ultrasound not the first-line adjunct in these tricky kids? It’s probably multifactorial, but certainly, ultrasound is more difficult in children than adults. Its utility is varied in the NICU context and for infants under 2.5kg, although can still have a role with a modification to technique. It’s also harder to learn ultrasound in a population who are scared, angry, impatient and poorly tolerant of a prolonged period of needle-through-skin. For these reasons, I think that there is less appeal to replace the familiar (cannulating without an ultrasound), with the unfamiliar (cannulating with an ultrasound). As I’d experienced, this also leads to a culture where ultrasound is infrequently utilized, decreasing the likelihood of implementation by new or more junior staff.

Once the learning investment is made to reach a proficient level of ultrasound competency (about 20 cannulas in adults) the potential benefits are significant. Decreased time spent performing a procedure, decreased number of attempts and subsequent patient trauma, and increased cannula longevity are all achievable.

I’ve spent a lot of time thinking success optimisation in paediatric ultrasound guided cannulation, both during my own development of proficiency and then in an effort to verbalize this skill when educating others. Below are my 5 top tips to enhance your ultrasound-guided cannulation skills:

I’m hoping that some of these words may help avoid some bits of the inevitable trial and error process that comes with learning a new skill.

There is sometimes a general impression of both practical and personal inconvenience in using ultrasound for vascular access. An ultrasound may not be nearby. There is the fear of “looking silly” in front of other people, as turning on, adjusting, and then physically coordinating the use of the ultrasound may be unfamiliar. During the period of establishing proficiency, an approach to decreasing this sense of unfamiliarity is to get in the habit of bringing the ultrasound with you do a cannula. Turn on and optimize the ultrasound to view vessels, and spend a period mapping out candidates for cannulation using your non-cannulating hand. Draw on the patient with a skin pen if you want to keep track of the best sites. Then, discard the ultrasound and cannulate using whatever technique is most familiar to you, but with the added knowledge of vessel location, depth, size, and direction. If this becomes a routine and almost ritualistic process, the mental barrier created by a lack of familiarity with ultrasound settings and holding the transducer should decrease over time. It is a relatively small step from performing vascular mapping to placing a cannula under real-time ultrasound guidance.

The preparation otherwise is quite straightforward. In addition to the set up that you use for all other cannulas, you need the following four things:

  • An ultrasound with a linear array probe (the smaller the footprint and the higher the frequency, the better)
  • Sterile lubricating gel and some form of sterile barrier to cover your probe (this varies institutionally)
  • Cavilon wipe or skin prep (securement devices / dressings / tape doesn’t like to stick to ultrasound gel so will need some encouragement)
  • An extra person (one of your hands is out of action, so you need an additional person to perform the task that your non-dominant hand would normally do; this is typically stabilization of the distal limb)

The ultrasound sits on the opposite side of the bed to the operator, so as to minimize truncal movement in looking from the puncture site to screen. Aside from making sure the correct probe is selected, the only 3 settings you need to know how to adjust are depth (typically as shallow as possible), gain (similar to a ‘brightness’ setting to highlight blood-filled vessels), and a midline marker (for physical-digital landmark referencing).

As alluded to above, pre-scanning is a useful skill even in the absence of cannulating under real-time ultrasound guidance. It’s a good idea to scope out the most appropriate vessels and puncture sites prior to picking up your cannula. Essentially the objective is to place a cannula within a vessel with as few attempts as possible, as quickly as possible, with as little pain as possible, and in a site that will provide the greatest longevity. Characteristics of vessels that tend to correlate with these outcomes are:

  • long and straight stretches
  • vessel 6mm or less below the surface
  • vessels greater than 2mm in diameter
  • vessels that don’t cross a joint (provides freedom of movement and less extravasation)
  • vessels without upstream thrombosis or obstruction

Mid-forearm vessels often meet the above criteria.

The greater length of cannula able to be placed within the vessel can correlate with longevity, however larger cannula diameter may increase the phlebitis and decrease longevity. This requires consideration of the balance between length and diameter of device. Of the commonly available devices, a good balance is a blue cannula (22G). There are several specialised less widely available devices that are longer versions of small diameter cannulae (24G and 22G).

In practical terms, to find these vessels you can start in the antecubital fossa (more familiar area for most of us) and track them down, or plonk down on the forearm and pan circumferentially. Scanning in the short axis / transverse axis / cross-sectional view tends to work best in kids. To assess suitability, translate the probe up and down along a vessel to get an idea of the direction. If it’s running diagonally, rotate your probe until it’s running along the same plane as the vessel to act as a mental reminder of the angle/direction that you need to insert your cannula. Pick the specific spot on the vessel that you’d like to puncture, bearing in mind that you will be puncturing the skin millimetres back from that point. Pick the patch of the vein that is the longest, straightest, shallowest, and biggest. Have a second fallback site planned out elsewhere for if required. Lastly, make sure to track the vein proximally as far as you can to ensure that it doesn’t run into a large thrombosed/occluded/recannalizing patch of vessel.

Obscure angles make things more challenging, in my experience. Right angles and parallel lines are your friends because they assist in mental unburdening and allow you to devote energy to troubleshooting issues. As mentioned above, map the vessel prior to puncture. Part or all of a vein will often wander diagonally along its journey, so approaching from the wrong direction increases the likelihood of punching through the side of the vessel. The centre of the image corresponds to the arrow/marker along the long edge of the probe, so you have a reference point between digital (screen) and physical (skin). Use the ultrasound as a mental reminder of your plane of approach; rotate the probe until the vessel is consistently sitting in the very centre of your image as you plane up and down. In other words, the ultrasound image is perfectly perpendicular to the plane of the vessel.

Speaking of right angles, I prefer to keep the ultrasound at right angles to the surface that you’re scanning. Angling back and forth creates a loss of contact and a distorted image as the ultrasound bounces of structures and does not return to the transducer. This creates a less clear image where vessels artificially look larger. If you need to change your view, translate/glide the probe along the skin, rather than introducing angle. It can be useful to temporarily angle the transducer perpendicular to the shaft of the cannula if you lose sight of it as this will light it up more clearly.

This is a big one. Thinking of your cannulation as a two-phase puncture process is something that I find extremely helpful. Your objective is not to puncture the skin and end up inside the vessel in a single action, and in fact, attempting to do this seems decrease the likelihood of success. 

 

Puncture Phase 1

Puncture 1 is the process from skin puncture to positioning the tip of your cannula on the superficial wall of the vessel. To achieve this, align your probe to achieve a view with the vessel in the centre of the image. Puncture the skin with the cannula a few millimetres distal to the probe. This bit is painful, so do this with a decisive action so that 2-3 mm of the cannula is within the soft tissue. Increase your angle of insertion to 30-45°. Your next objective is to find the tip of the cannula. Moving your non-dominant (ultrasound) hand, translate/slide the probe towards the puncture site until a glimmering white dot becomes apparent in your image. Once you are convinced that you are viewing your cannula, you need to ensure that you are viewing the tip at all times.

The most important thing to remember is the only way to be certain that you are viewing the tip of your cannula is when the glimmering dot disappears when you move the probe 1mm proximally (away). It is frustratingly easy to think that you are viewing your cannula tip when instead you are halfway along the shaft, with the tip out the deep wall of the vessel. Maintain this view via a “walking” approach. For each 1-2mm advancement (step) of the cannula, make an equivalent proximal movement with your ultrasound probe (step). Move the ultrasound away so that you cannot see cannula tip anymore, and then advance the cannula into view. If needed, intermittently stop advancing your cannula and check your tip position as described above. I find advancing at 30-45° until you reach the vessel works well as minimal cannula is wasted on the journey there.

If you find yourself wandering off track, keep the ultrasound focused around the vessel as the centre of your image (as this is your target). Correcting if off centre is slightly counterintuitive. Move your cannulating hand away from the direction that you want to move your cannula tip (ie- moving right will move the tip left). Continue inserting until your cannula tip is sitting at 12 o’clock on top of your vessel. As you reach this point, the tip of the cannula may gently tent the roof of the vessel, turning an “O” shape into a “❤️” shape. This is a good test of correct positioning. Once you’ve reached this point, you’re ready for puncture phase 2!!

 Puncture Phase 2

Puncture 2 is the process of entering the vessel to feeding your cannula fully in. With the tip of your cannula in view and the roof of the vessel tented (❤️), continue incrementally advancing your cannula with tiny movement, walking the ultrasound forward to ensure the tip remains in view (as above). Gently decrease your angle of insertion so that the superficial wall is not tenting towards the deep wall but rather into the potential space of the proximal vessel. Eventually, your tented vessel (❤️) will suddenly encompass the cannula and return to a circular shape (O). This may be associated with a tactile pop. You can check for flashback for additional confirmation of vessel puncture, but I prefer to not take my eyes off the ultrasound screen at this point.

Continue decreasing your angle of insertion to maintain the tip of the cannula in the top 50% of the vessel (keep the sharp bevel away from the deep wall). This may eventually require you be pushing the cannula into the skin, which really requires your assistant to get out of the way. Don’t lose site of your tip! Continue to step forward; cannula then ultrasound. To check whether you are in the vessel and not in soft tissue or dragging on the vessel wall, waggle the tip of the cannula around gently (left, right, up, down). There should be absolutely no distortion of the soft tissue surrounding the vessel; completely free cannula tip movement. I tend to leave the metal stylet in until the plastic catheter is fully inserted to the hub because of greater visibility and added rigidity. This does, however, carry the risk of puncturing the back or sidewall of the vessel if you don’t keep a close eye on your cannula tip. At the very least, ensure 3-4mm of the cannula is inside the vessel lumen prior to gliding the plastic catheter off (to avoid tissuing / tearing the vessel roof). Once this is done, you’ve just successfully place a real-time ultrasound-guided cannula! Well done!

I think it’s reasonable with each healthcare interaction to measure success both in the resolution of issue (beneficence) and in minimization of harm / traumatic experience (non-maleficence). Vascular access is our commonest painful procedure, hence representing a significant potential burden of pain, anxiety, and trauma. Undertaking steps to minimize vascular access attempts, maximize speed/efficiency, and maximize cannula longevity are important considerations in the healthcare interaction. Even if we manage to achieve the elusive goal of a single puncture hospital admission, this still requires a single puncture. 

This discussion is not really directed towards addressing the specifics of analgesia and sedation but suffice to say that time permitting these should be used and optimized readily. A topical anaesthetic is valuable, although in the case of an ultrasound-guided cannula application by the operator is useful in ensuring good placement. Evidence is increasingly suggesting that topical anaesthetic is appropriate in all ages including neonates.

The power of social stories, rehearsal, music therapy, and just general distraction cannot be undervalued. There is a multitude of approaches to this. 

Unfortunately, it is not an uncommon experience to be in a situation where vascular access is required with a degree of clinical urgency. In this circumstance, oral/intranasal/topical medication may have not had time to work, and a specialist in distraction may not be readily available.

In this circumstance, I have found that playing calm and quiet music more useful than positioning a video in front of a child. Maintaining a minimum of people speaking, and using quiet calm voices is valuable. I have had some success using the ultrasound itself as a distraction modality while telling the child a story of the “doughnut that has lost its hole” (vein and cannula tip respectively) as the tip tracks toward the vessel. A variant is the “star that fell from the sky into the lake” (cannula tip and vein respectively). There are many approaches to pain reduction through distraction.

It is my sincere hope that these tips are of some practical and clinical value in your cannulating endeavours. If it makes a difference for a single child, then surely it’s worth it. Good luck!