Sensational Solids

Cite this article as:
Annabel Smith. Sensational Solids, Don't Forget the Bubbles, 2020. Available at:

You are a paediatric registrar, discharging a 5-month-old boy (Sam) home after an overnight admission with a respiratory illness. When you check if there are any final questions, Sam’s parents want to know whether they should be commencing solids now, and if so, how they should go about it.

This is a great opportunity for some quick education for the family, made a little more efficient on a busy ward with the provision of some written information (see the resources section for my favourite websites). There have been lots of changes to infant feeding advice over the years, and a plethora of ideas about what comprises a healthy infant diet, so families can easily become confused. Some targeted, sensible advice can get most families on track towards safe and healthy eating for their infants, with positive implications for long term health and wellbeing.


When to introduce solids?

According to the World Health Organisation, all infants should ideally be exclusively breastfed for the first 6 months of life – no food and no extra water (medicines are, of course, allowed) – as introducing solids too early can interfere with this provision of nature’s perfect nutrition. However, the Australasian Society of Clinical Immunology and Allergy (ASCIA) has advised that food exposures can start occurring from (but not before) 4 months and that this is beneficial for allergy prevention. I encourage this for families in my care, explaining that from 4-6 months, these are to be just exposures, not meals – e.g. a lick of nut butter from a parents’ finger, a taste of bolognaise sauce, a finger play with mushy vegetables, and so forth.

From 6 months, babies particularly need sources of iron (as placental-derived stores will have run out), so regular small meals can commence – all solids should be offered AFTER a breastfeed until around 9-10 months of age when this can usually be reversed. Babies will need to be developmentally ready to start solids, with good head and neck control, ability to sit upright with support, showing an interest in food, and opening their mouth when offered a spoon. If not showing these signs by 7 months, the infant should be seen by their GP.

Infants can be fed purees, and/or soft hand-held foods (including foods they can safely suck on, such as a strip of toast or meat). There are different philosophies around the benefits of each method, but practically, it can work best for families to use a mixture of spoon- and finger-feeding. Finger-feeding provides great sensory and developmental experiences, but is messy and time-consuming, and requires a developmental level equivalent to around 8-9 months of age to reliably consume anything, so purees do have their place. Regardless of the feeding method, all meals must be closely and actively supervised by a competent adult.


What foods can be given and what should be avoided?

Infants can and should be exposed to all food groups from as early an age (at least prior to 12 months) as possible, except for honey, due to the risk of botulism (this can be introduced after 12 months if desired). Hard foods pose a choking hazard, so fruit and vegetables should be softened with cooking, and nut butter should be used instead of whole nuts. Home-cooked wholefoods are typically best for health, but there are some healthy commercial preparations. 

To avoid confusion if allergic reactions occur, families should, according to ASCIA, introduce food types one at a time, a couple of days apart. This also gives the infant time to adjust to all the new, exciting textures and flavours.

Water should be offered with all solids from 6 months onwards to encourage good drinking habits. Infants and children shouldn’t drink juice, and cow’s milk shouldn’t be used a drink until after 12 months, although small amounts can be used on cereals or as a component of other meals for dairy exposure. After 12 months, limit cow’s milk to 500ml per day (less or none is fine, especially if still breastfeeding, and/or if having plenty of other calcium sources, such as other dairy products, or green leafy vegetables). ‘Toddler formula’ is almost never needed, and then only on specialist advice.


What happens if Sam has a reaction to a food?

Allergic reactions to food can be immediate or delayed and are highly variable and sometimes controversial. Symptoms may include rashes, respiratory difficulty, or gastrointestinal issues. Any suspected reactions require an immediate cessation of the suspected food(s), and medical review (urgency dependant on the severity of the symptoms) should be sought.


What if the family follows a special diet, like veganism?

Vegetarian and vegan families, or any other families following a relatively restricted diet for any reason, would benefit from an early assessment by a registered dietician. These diets may lack vitamins and minerals critical for the health of the developing infant, but can usually be safely adhered to with support and planning. Restrictive diets do increase the risk for food allergy and intolerance on later exposures, however, and families must be aware of this.

Ultimately, food should be about fun, togetherness, and good health. Families should be encouraged to keep mealtimes positive and family-centred, with everyone eating together at a table whenever possible (with all devices turned off). Parents should evaluate their own diet and ensure they are setting a good example, and empowering and teaching their children how to fuel their amazing, active bodies with a wide variety of healthy, delicious foods. It’s never too early to start forming good habits and positive food relationships.


References and Resources:-

Australasian Society for Clinical Immunology and Allergy (

Useful handouts;

  • Information on how to introduce solid foods to infants (
  • Infant feeding and allergy prevention (

Raising Children’s Network (

The Royal Children’s Hospital Melbourne (

The 38th Bubble Wrap

Cite this article as:
Leo, G. The 38th Bubble Wrap, Don't Forget the Bubbles, 2020. Available at:

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

Surviving Sepsis Campaign International Guidelines

Cite this article as:
Damian Roland. Surviving Sepsis Campaign International Guidelines, Don't Forget the Bubbles, 2020. Available at:

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

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


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


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

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


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


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


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


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


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


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

So the big-ticket items

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

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

2005 definition:

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

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

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

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

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

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

6. Following discussion and debate recommendations would be made:


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


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


‘Screening’ remains in

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

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

Ultimately no one particular screening system is recommended.


There is no target lactate

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

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


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

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


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

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


Broad spectrums antibiotics, but narrow when pathogens available

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

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

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


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

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

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

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


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


Use advanced haemodynamic variables, not bedside clinical signs in isolation

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


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

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

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



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


The 37th Bubble Wrap

Cite this article as:
Leo, G. The 37th Bubble Wrap, Don't Forget the Bubbles, 2020. Available at:

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

Hot Garbage: Mythbusting fever in children

Cite this article as:
Alasdair Munro. Hot Garbage: Mythbusting fever in children, Don't Forget the Bubbles, 2020. Available at:

Juniper is a 3yr old girl brought in with her mother, with a 48hr history of fever. Her mum is particularly concerned because her fever was up to 39.8°C, didn’t come down with paracetamol and she describes an episode which sounds like a rigor. On examination, she has a temperature of 39.3°C, a runny nose and bright red tonsils, and looks otherwise well. You go to discharge her, but your colleague asks if you should wait to see if her temperature comes down with ibuprofen before sending her home?



Febrile illnesses are the most common cause of presentation to acute paediatric medical services. This means that fever is the most common presenting symptom seen by paediatricians, and it is clearly a huge cause of concern for parents. Despite this fact, it is clear that in day-to-day practice that there is a widespread misunderstanding about fever, its purpose, and its clinical interpretation.

Well, no longer! Once you have finished reading, you will be a master of all things related to fevers in children. We will start with some basic understanding of the processes surrounding fever, and finish off with some mega myth-busting!

What is fever?

Fever is an elevated core body temperature, as part of a physiological response to infection regulated by the hypothalamus. This is crucial to understand – your body is in control of your temperature. This is not something an infection is doing to your body; it is something your body is doing to the infection. This is different from pathological hyperthermia, where your temperature is elevated by either hypothalamic dysfunction or external heat. These are extremely rare.

Note: there are other, non-infectious causes of fever, such as cancer, Kawasakis, and autoinflammatory conditions, but these are rare in comparison to infectious fever and are covered elsewhere.


What temperature counts as a fever?

At what threshold do we say a child has an elevated body temperature? This is more controversial than one might think, as actually the data from which we derive “normal” body temperature is extremely poor. The most common cut off for defining a fever is 38°C – but it is important to remember that there is nothing magic about 38°C compared to 37.9°C, and temperature is better taken in context or a trend, if possible.

How do we get fevers?

The process of developing fever is extremely complex, and our understanding is still developing. At present, our best explanation is that the process is triggered by the presence of chemicals referred to as pyrogens. Pyrogens can either be exogenous (such as parts of the microbe itself, like the lipopolysaccharide on the outside of bacteria), or endogenous, such as cytokines like IL1, TNF, Prostaglandin E2 and importantly IL6, which are released by immune cells when they detect an invader. These pyrogens act to increase body temperature peripherally, but importantly also trigger receptors in the preoptic nucleus in the brain. This releases PGE2 into the hypothalamus, which then sets a new target temperature. This target is met by many facets designed to increase heat, including:

  • Release of noradrenaline by the sympathetic nervous system, increasing thermogenesis in brown adipose tissue and causing peripheral vasoconstriction and piloerection (reducing heat loss)
  • Acetylcholine release stimulating muscle myocytes to induce shivering
  • Feeling cold”, inducing heat-seeking behaviours (warm clothes and blankets)

It is important to remember that the body is trying to get hotter. If you intervene with non-medicinal efforts to cool it down, it will work even harder to try to heat up.

Why do we get fevers?

The process of having a fever has been conserved across species from lizards to mammals, and even plants! This is because it is a beneficial response to an infection. The mechanisms by which a fever helps protect you from infection include:

  1. Higher temperatures inhibiting growth/replication of pathogens
  2. Higher temperatures promoting the immune response to infection

It is also worth noting that bacteria are killed more easily by antibiotics at higher temperatures, so there is also a potential third mechanism.



Fever is beneficial. When a pathogen causes infection, pyrogens stimulate the hypothalamus to increase the body temperature through several mechanisms, and this increased temperature helps inhibit the growth of the pathogen AND stimulates the immune system to fight it.

That was a lot of science. Don’t worry – it’s time to get clinical! All this science stuff is lovely, but what does this mean for our patients?

Clinical significance of fever

As we have ascertained, fever is beneficial. For this reason, when a child presents with fever, the fever itself is actually of no concern. What we are interested in is the reason for the fever. Is this fever the result of a benign, self-limiting, childhood infection – or is it associated with a serious bacterial infection? Trying to determine this is enough for its own blog article (the most important thing is the end of the bed assessment – see Andy Tagg’s excellent breakdown of the paediatric assessment triangle).

Ignore the fever itself – what’s important is ascertaining its cause.

Now, let’s get on and bust some myths that persist surrounding fever in children!


Myth 1 – Higher temperature indicates a serious infection

This is one of the most common concerns amongst parents. The particular height of temperature may be what prompts them to come to hospital, or even what prompts the health care provider to initiate more aggressive management or investigations.

The truth is that the relationship between the height of temperature and risk of serious illness is at best complicated, and at worst a dangerous distraction. There is a very poor correlation, with such woeful sensitivity and specificity that it will both grossly over and under-call serious infections (either if the high temperature is used to rule in, or lower temperature to rule out). The caveat to this is in younger infants (particularly under 60 or 90 days), who have a higher baseline risk of serious infections (and more to the point – once they spike a temperature will be managed aggressively regardless of how high it was). Some studies have shown an extremely weak association in older children, but not enough for it to have any meaningful influence on our management. A fever is a fever – higher temperatures should not be managed any differently than lower ones.


Myth 2 – Temperature not relieved by antipyretics indicates a serious infection

Another common misconception also linked to the myth above. Some fevers respond well to antipyretics, and some do not. We do not understand why this is the case, however, studies have not demonstrated that failure to respond to antipyretics is a useful indicator of a more serious infection. It is not very pleasant for the child to remain hot, but it does not mean they are at any higher risk. A child whose temperature does not respond to antipyretics should not be treated any differently to one that does.

Myth 3 – Rigors indicated a serious infection

This has been covered in-depth in a separate blog post – but to summarise; there is extremely weak evidence that rigors are associated with an increased risk of bacterial infection in children, which is irrelevant when factors that are more important are taken into account. There is also evidence of no increased risk. The presence or absence of rigors should not be a deciding factor in the management of febrile children.

Myth 4 – You must wait for a fever to come down before discharge

This may seem common practice for many of you working in acute paediatrics. If a child is febrile on arrival, people often want to wait to see the temperature come down before allowing them to be discharged (this should be differentiated from seeing observations normalize in the absence of fever – which is a more understandable if still slightly questionable practice). As we have seen, a fever merely indicates the presence of an infection. If you have ascertained the cause of the fever, or at least ruled out any red flags for serious causes, the ongoing presence or absence of a fever means nothing for the child. If it comes down before discharge, it will probably just go up again once they are home! There is no need to make them wait around for hours for no reason.

Myth 5 – Fever should be treated with antipyretics

We have established that fever is beneficial. Therefore, there is essentially no reason to treat a fever in and of itself. It will not cause harm, and it is probably helping. Some children tolerate having higher temperatures extremely well, so if they are playing happily or do not seem terribly bothered about their temperature of 39°C then you leave them well alone.

Treat the child, not the fever.

Myth 6 – Fever should not be treated with antipyretics

There is an opposing school of thought, which says that since fevers are beneficial, we should not treat them at all. Given how absolutely dreadful it can feel to have a fever (which many of us adults should be able to vouch for), many of us give medicines to try to bring the temperature down and make the child more comfortable. This is the right thing to do. Despite the potential benefits having a fever confers, there is no evidence of any clinically meaningful harms to treating temperatures in unwell children, or even in adults in ICU. If the child is distressed by the temperature, they should have antipyretics to make them feel more comfortable.


  • Fever helps your body to fight infection and is not dangerous (no matter how high)
  • The fever itself is not important. The cause of the fever is what matters
  • There is little to no evidence that higher temperatures, temperatures that don’t respond to antipyretics, or rigors indicate an increased risk of serious infection
  • Persisting fever on its own is not a reason to postpone discharge
  • Only treat fevers if they are causing distress. Treat the child, not the fever


Postscript: Febrile convulsions

When I posted my initial thread on twitter about fevers, there were many comments asking why I didn’t address febrile convulsions. This was mainly because these are worth a post to themselves (which they have here). In brief, febrile convulsions are extremely distressing for parents to observe, but they are common and they are very benign. We do not advise treating fevers to prevent febrile convulsions, and until recently, this was because there was no evidence that they had any effect in preventing them. A recent study from Japan did demonstrate a decrease in recurrence of febrile convulsions in children who had already had one if given regular PR paracetamol, however, there are major caveats to this study discussed in depth here.


For the more visual oriented, the talented Emma Buxton has created an infographic of the key reminders from this blog post:

The 36th Bubble Wrap

Cite this article as:
Leo, G. The 36th Bubble Wrap, Don't Forget the Bubbles, 2020. Available at:

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

A better discharge summary

Cite this article as:
Beckie Singer. A better discharge summary, Don't Forget the Bubbles, 2020. Available at:

Discharge summaries, often considered the bane of every junior doctor and ED physician’s existence. But what if we took a step back and considered these as a clinical handover to primary care – similar in nature to the clinical handover that occurs in the transfer of care documents that you would send with a patient you are transferring to another hospital? They suddenly take on a whole other level of importance. Studies from the ‘adult medicine world‘ have shown that roughly 20% of patients experience an adverse event during the hospital-to-home transition, many of which could be mitigated by good handover between the hospital and the primary care provider.


Cite this article as:
Andrew Tagg. Decade, Don't Forget the Bubbles, 2019. Available at:

Decade, not just an amazing Duran Duran greatest hits album, but also a unit of time. The last 10 years have seen great changes in all of our lives and whilst the births of various children do rank quite highly, the founding of Don’t Forget The Bubbles is also a highlight in many of our lives.  When we started it back in 2013 we could not have imagined what it has morphed into.


Some key events of the decade

The beginning of the (?) teens saw the introduction of the first iPad. It was not as revolutionary as the iPhone but allowed us to read the paper in bed and engage in a more mobile form of entertainment consumption.

2010 saw the official opening of the tallest building in the world, the Burj Khalifa, and led Tom Cruise to wonder “what would happen if I climbed up this”?

2011 saw the first proper royal marriage in ages as HRH Prince William married Catherine Middleton in front of 22.8 million television viewers.

2012 saw the rise of K-Pop as Gangam Style became the most-watched music video ever reaching over a billion hits on YouTube. It was also the year that the Higgs-Boson, long thought to exist, was finally discovered.

2013 saw the introduction of CRISPR, the gene-editing technology that could change everything and user in a new era of designer babies if some scientists had their way. It also introduced the world to Anna and Elsa and a million children dreamed of building snowmen that would come to life.

2014 was the year we lost some of the greats – Rik Mayall, Casey Kasem (the voice of Shaggy in Scooby Doo), Maya Angelou, Robin Williams.

By June 2015 same-sex marriage had finally become legal in the US. It also saw the release of Star Wars: The Force Awakens, a film that would finally help us rid our memories of those dreadful prequel movies.

Pokemon Go was the flavour of the day in 2016 launching augmented reality into the mainstream and reality became a little more distorted as Donal Trump was elected the 45th President of the United States of America.

2017 was the year of our very first conference in Brisbane, something that we never thought we would be doing when we started the website some years earlier. Now our year seems to revolve around planning the next one.

2018 highlights the deepening climate crisis as Penrith in Sydney hits 47.3 degrees. 2018 also saw the death of one of the world’s finest – Stan Lee – at the age of 95.

In 2019 Rick Deckard hunted down the Nexus-6 replicants and Roy Batty gave that famous speech.


Some of the top papers of the decade

*Not necessarily the most important


Maitland K, Kiguli S, Opoka RO, Engoru C, Olupot-Olupot P, Akech SO, Nyeko R, Mtove G, Reyburn H, Lang T, Brent B. Mortality after fluid bolus in African children with severe infection. New England Journal of Medicine. 2011 Jun 30;364(26):2483-95.

Roberts KB, American Academy of Pediatrics. Subcommittee on Urinary Tract Infection, Steering Committee on Quality Improvement and Management. Urinary tract infection: clinical practice guideline for the diagnosis and management of the initial UTI in febrile infants and children 2 to 24 months. Pediatrics. 2011 Sep;128(3):595-610.


Powell C, Kolamunnage-Dona R, Lowe J, Boland A, Petrou S, Doull I, Hood K, Williamson P, MAGNETIC Study Group. Magnesium sulphate in acute severe asthma in children (MAGNETIC): a randomised, placebo-controlled trial. The Lancet Respiratory Medicine. 2013 Jun 1;1(4):301-8.


Long E, Sabato S, Babl FE. Endotracheal intubation in the pediatric emergency department. Pediatric Anesthesia. 2014 Dec;24(12):1204-11.

Everard ML, Hind D, Ugonna K, Freeman J, Bradburn M, Cooper CL, Cross E, Maguire C, Cantrill H, Alexander J, McNamara PS. SABRE: a multicentre randomised control trial of nebulised hypertonic saline in infants hospitalised with acute bronchiolitis. Thorax. 2014 Dec 1;69(12):1105-12.


Riskin A, Erez A, Foulk TA, Kugelman A, Gover A, Shoris I, Riskin KS, Bamberger PA. The impact of rudeness on medical team performance: a randomized trial. Pediatrics. 2015 Sep 1;136(3):487-95.

Cunningham S, Rodriguez A, Adams T, Boyd KA, Butcher I, Enderby B, MacLean M, McCormick J, Paton JY, Wee F, Thomas H. Oxygen saturation targets in infants with bronchiolitis (BIDS): a double-blind, randomised, equivalence trial. The Lancet. 2015 Sep 12;386(9998):1041-8.

McNab S, Duke T, South M, Babl FE, Lee KJ, Arnup SJ, Young S, Turner H, Davidson A. 140 mmol/L of sodium versus 77 mmol/L of sodium in maintenance intravenous fluid therapy for children in hospital (PIMS): a randomised controlled double-blind trial. The Lancet. 2015 Mar 28;385(9974):1190-7


Cronin JJ, McCoy S, Kennedy U, an Fhailí SN, Wakai A, Hayden J, Crispino G, Barrett MJ, Walsh S, O’Sullivan R. A randomized trial of single-dose oral dexamethasone versus multidose prednisolone for acute exacerbations of asthma in children who attend the emergency department. Annals of emergency medicine. 2016 May 1;67(5):593-601.


Irwin AD, Grant A, Williams R, Kolamunnage-Dona R, Drew RJ, Paulus S, Jeffers G, Williams K, Breen R, Preston J, Appelbe D. Predicting risk of serious bacterial infections in febrile children in the emergency department. Pediatrics. 2017 Aug 1;140(2):e20162853.


Tagg A, Roland D, Leo GS, Knight K, Goldstein H, Davis T, Don’t Forget The Bubbles. Everything is awesome: Don’t forget the Lego. Journal of paediatrics and child health. 2018 Nov 22.


Lyttle MD, Rainford NE, Gamble C, Messahel S, Humphreys A, Hickey H, Woolfall K, Roper L, Noblet J, Lee ED, Potter S. Levetiracetam versus phenytoin for second-line treatment of paediatric convulsive status epilepticus (EcLiPSE): a multicentre, open-label, randomised trial. The Lancet. 2019 May 25;393(10186):2125-34.

Dalziel SR, Borland ML, Furyk J, Bonisch M, Neutze J, Donath S, Francis KL, Sharpe C, Harvey AS, Davidson A, Craig S. Levetiracetam versus phenytoin for second-line treatment of convulsive status epilepticus in children (ConSEPT): an open-label, multicentre, randomized controlled trial. The Lancet. 2019 May 25;393(10186):2135-45.


We’d love to hear what you think are some of the key papers of the last decade. Drop us a line in the comments section.

So what is next for DFTB?

Curriculum mapping

Dani Hall and a team of intrepid data-miners have been working on a curriculum mapping project to get a better idea of what we have in the 850 posts we have already published as well as to guide content creation. With the help of the RLH/DFTB fellows, we are then going to be creating some core modules for clinician-educators. Imagine you want to run a session on, for example, bronchiolitis. We are going to create the package for you, complete with pre-reading, some key papers complete with discussion points and controversies, and some fun activities to match.

Knowledge translation

One of our core aims at DFTB is to make current research more accessible. Whether that is breaking down the latest research with the help of PERUKI and PERN, showcasing original research or busting long-held beliefs we will continue to keep you up to date.

Conferences and beyond

When the idea of holding a DFTB conference was first suggested some years ago we laughed and suggested we’d struggle to fill 50 seats. We’ve gone on to sell out our first three conferences and are well on our way to doing the same in Brisbane for  We love the conferences bringing our community together, raising the profile of the patient, and sharing knowledge and so we are already planning for DFTB21.

We also recognize that the conference cannot be everything and so we are creating some more educational options, an amuse-bouche to the conference main course if you will. Look out for more details in the New Year.

What’s the formula for formula?

Cite this article as:
Annabel Smith. What’s the formula for formula?, Don't Forget the Bubbles, 2019. Available at:

Whilst breastfeeding confers myriad benefits for infants and their mothers, there are many reasons why some infants will require formula, at least at some point in their first 12 months of life. Having a basic understanding of the different products available and the way formula should be prepared and administered is important for all doctors and nurses working with young children. The variety of formulas, bottles and teats available, as well as the complexities of preparation, administration, and storage, confuses the best of us, so here’s my attempt to make it a little clearer.

The 35th Bubble Wrap

Cite this article as:
Leo, G. The 35th Bubble Wrap, Don't Forget the Bubbles, 2019. Available at:

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

Neonatal respiratory distress

Cite this article as:
Jasmine Antoine. Neonatal respiratory distress, Don't Forget the Bubbles, 2019. Available at:

You are the paediatric registrar on shift overnight, your phone rings. “Its Mary in birth suite, can you please review a term baby in room 1, born one hour ago via vaginal delivery is tachypnoeic.

Respiratory distress is common; it affects 7% of term infants. It is the most common reason that term babies are admitted to special and intensive care nurseries. There are several factors that increase the likelihood of respiratory distress to occur in a term neonate, meconium exposure, maternal gestational diabetes, chorioamniotitis, oligohydramnios and delivery by caesarian section.

Common causes of respiratory distress include:

  • Transient tachypnea of the newborn (aka retained fetal lung fluid)
  • Respiratory distress syndrome (aka hyaline membrane disease)
  • Persistent pulmonary hypertension
  • Pneumothorax
  • Meconium aspiration
  • Sepsis


What are the less common ones that we don’t want to miss?

  • Congenital pneumonia
  • Congenital pulmonary airway malformation
  • Pleural effusion
  • Congenital cardiac disease
  • Oesophageal atresia with/out trans oesophageal fistula
  • Congenital diaphragmatic hernia
  • Metabolic problems: hypothermia, hypoglycemia
  • Airway obstruction: choanal atresia, micrognathia, macroglossia, tracheomalacia, subglottic stenosis, airway haemangioma
  • Bony abnormalities: skeletal dysplasia
  • Hypoxic- ischaemic encephalopathy
  • Neuromuscular causes: congenital myotonic dystrophy, spinal muscular atrophy, congenital myopathies, seizures


So what should we be looking for on examination?

  • Is the newborn pink or blue? What are the oxygen saturations? Pre-ductal (taken on the right hand) and post ductal (taken on one of the feet)
  • Is the infant distressed? What is their respiratory effort: subcostal and intercostal recessions, head bob, tracheal tug is often difficult to spot in newborns due to their large head/lack of neck combination. Is the baby grunting?
  • What is the respiratory rate, is it >60?
  • What are the other vital signs: heart rate and temperature?
  • Chest wall movement: is the chest moving adequately and symmetrically?
  • Air entry: is it equal, are there added sounds, are there bowel sounds in the chest?


On your arrival the infant is on the resuscitaire. She is receiving CPAP of 8cm via mask. She has increased work of breathing with subcostal and intercostal recessions, grunt and remains tachypnoeic with a respiratory rate of 80. You continue to administer CPAP of 8cm. What else needs to be undertaken in birth suite?


  • Keep the infant warm: make sure the heater is on and the infant is on the portion of the resuscitaire that the radiant heater impacts. Is she wearing a beanie? Has she been dried off? Is she on warm and dry wraps?
  • Is her position ideal: neutral airway position
  • Does she require any oxygen: what are the oxygen saturations?
  • Are you getting adequate pressures: is the CPAP maintaining 8cm? Is the mask an appropriate size? Is the flow correct? Is the upper airway obstructed? Does she need to be suctioned?


You decide to take the baby to the nursery for further assessment and treatment. What do you need to do to get prepared for the move?


Most rescuitaires cannot maintain enough power to adjust the height of the cot or provide heat whilst transiting. Consider if you have enough warm wraps, enough oxygen and air in the cylinders and appropriate monitoring.


The newborn is admitted to the nursery for ongoing respiratory distress. CPAP is continued at 8cm in 30% oxygen. What investigations should be done?  

  • FBC and Blood culture: respiratory distress can be the first sign of sepsis.
  • Blood glucose
  • Consider a gas: an arterial gas will be the most accurate but can be difficult to obtain without intra arterial access. Venous or capillary gases are more practical. Capillary gases are more prone to error when infants are poorly perfused but are quick and easy to undertake.
  • CXR: with a nasogastric tube insitu, this will help identify an oesophageal atresia.


Why do infants get respiratory distress?

The etiology of respiratory distress is as varied as the causes. Many infants struggle with the transition following birth to neonatal life. Whatever the underlying pathology; surfactant deficiency, meconium aspiration or persistent pulmonary hypertension, these cause atelectasis and ventilation perfusion (V/Q) mismatch. Leading to hypoxemia and hypercarbia and ultimately respiratory acidosis. Tissues then become poorly perfused leading to metabolic acidosis, which furthers pulmonary vasoconstriction, causing endothelial and epithelial injury and respiratory distress syndrome.


What next?

  • Keep the infant warm
  • Positioning of the infant: in an isolette so you can monitor their respiratory distress, head neutral position, consider prone.
  • Respiratory support:
    • start with CPAP 8cm in the oxygen required to maintain saturations >/= 90%
    • indications for intubation are: FiO2 >40%, extreme prematurity, recurrent apnoea that require stimulation or apnoea requiring resuscitation, respiratory failure (pCO2 > 70 and pH < 7.2)
  • IV antibiotics to cover for sepsis: use broad spectrum antibiotics. Your hospital will have a policy. Amoxicillin and gentamicin are a good starting point. Remember to cover for the common pathogens; Group B streptococcus and Escherichia coli.
  • Nutrition: a term baby with significant respiratory distress will find it difficult to suck feed. Consider starting IV dextrose and small amounts of enteral feeds via a nasogastric tube when expressed breast milk is available.
  • Decompress the stomach with an NGT

Just remember there are a few contraindications to CPAP

  • Bilateral choanal atresia and tracheoesophageal fistula, upper airway anomalies can make CPAP unsafe or ineffective
  • Unrepaired gastroschisis
  • Unrepaired congenital diaphragmatic hernia, as CPAP can lead to gastric distension and affect the thoracic organs.


What is the bottom line?

  • Respiratory distress can be the first sign of sepsis
  • Manage respiratory distress early so it does not progress. Start CPAP at 8cm in the oxygen required to maintain saturation.
  • CPAP has been shown to reduce the need and duration of mechanical ventilation 


Selected resources

Reuter S, Moser C, Baack M. Respiratory distress in the newborn. Pediatrics in review. 2014 Oct;35(10):417.

Queensland health clinical guideline Neonatal respiratory distress including CPAP