Steroids in Wheeze: Meredith Borland at DFTB18

Cite this article as:
Team DFTB. Steroids in Wheeze: Meredith Borland at DFTB18, Don't Forget the Bubbles, 2019. Available at:
https://doi.org/10.31440/DFTB.17716

This talk was recorded live at DFTB18 in Melbourne, Australia. With the theme of ‘Science and Story’ we pushed our speakers to step out of their comfort zones and consider why we do what we do. Caring for children is not just about acquiring the scientific knowhow but also about taking a look beyond a diagnosis or clinical conundrum at the patient and their families. Tickets for DFTB19, which will be held in London, UK, are now on sale from www.dftb19.com.

Asthma for ambos HEADER

Asthma for Ambos

Cite this article as:
Andrew Tagg. Asthma for Ambos, Don't Forget the Bubbles, 2016. Available at:
https://doi.org/10.31440/DFTB.9592

Tonight I had the privilege to talk to the team at the Werribee branch of Ambulance Victoria. I was given the brief to talk on something to do with paediatric respiratory problems so I thought I would focus on one of their most common presentations – asthma.

Asthma is a common condition and affects one in ten Australians. Approximately 17.2% of all kids in Victoria have been diagnosed with it. The incidence in Aboriginal or Torres Strait Islanders is higher at around 20%. Whilst a large number of these will never need to go to hospital, of those that do go, 43% per cent need admission. This is much higher than their adult counterparts. A large number can be safely managed at home with their pre-written asthma action plan (though only 41% of kids under 15 years of age have one) but some children are more at risk of critical or life-threatening asthma than others. Fortunately, the death rate in the under 15-year-old sub-population is around 0.2 per 100,00 people.

Risk factors for a more severe attack include:-

  • A previous severe asthma attack requiring an ICU admission
  • Two or more hospital stays because of asthma in the last year
  • Use of more than two reliever inhalers in the last month
  • Exposure to tobacco smoke
  • Previous allergic rhinitis, food allergies or hay-fever

There is a seasonal peak in ED visits in late summer and autumn for children, whereas more adults present in the winter. This may possibly be due to the increased incidence of viral upper respiratory tract infections among grown-ups at this time of year.

Some people are more likely to call an ambulance than others. They include those with :-

  • Poor knowledge about asthma
  • No asthma action plan
  • Poor self-management skills
  • Limited access to primary care

Paramedics are very experienced in managing it because asthma is such a common condition. I want to focus on some areas where what should happen and what does happen might diverge.

Myth – Oxygen saturations are useful in the management of asthma

An acute attack is characterised by bronchospasm, coupled with mucosal oedema and hypersecretion of mucus. This leads to aV/Q mismatch as there is hypoxic vasoconstriction and decreased blood flow to the under-ventilated lung in order to match pulmonary perfusion with alveolar ventilation.

In the hospital setting, oxygen saturations of less than 91% may predict the need for prolonged bronchodilator therapy.

Hypoxaemia and hypocarbia only occur in the presence of life-threatening asthma. If you take into account the haemoglobin-oxygen dissociation roller-coaster it is easy to see how many children may teeter on the precipice of collapse before critical desaturation occurs. Whilst low oxygen saturations mean that a patient is unwell it should be clinically obvious at this point.  On the flip side, normal oxygen sats do not mean the patient is fine.  There is a concern that oxygen administration may lead to a delay in recognising clinical deterioration. Low oxygen saturations may also represent a degree of mucus plugging that may be helped with repositioning.

Hyperoxia can lead to absorption atelectasis as well as intra-pulmonary shunting with a subsequent reduction in cardiac output. As the 78% nitrogen in the alveoli gets washed out with increasing amounts of supplemental oxygen, tt is resorbed. This leads to a reduction in alveolar volume and collapse.

Myth – Nebulizers are better than spacers

A recent Cochrane review comparing nebulizers with spacers found that there was no real difference in hospital admission rate with either mode of delivery. Lung function tests and oxygen saturations were also unaffected by the mode of medication delivery. What was different, however, was the adverse effect profile. If you used a nebulizer you were much more likely to see tremor and tachycardia.

Old British Thoracic Society guidelines suggested using up to 50 puffs of salbutamol via spacer but this is probably a bit excessive.  The current recommendation is that 400mcg of salbutamol via spacer is probably equivalent to 2.5mg via nebulizer.

So do you know how to use a spacer? I took the Werribee team through the procedure.  If you are not sure then take a look at this great instructional video from Asthma Australia:-

Whilst spacers are cheap, those of you with the MacGyver instinct may want to make your own.

These jerry rigged spacers have certainly been shown to be as effective as conventional devices in resource poor settings.

Myth – You can never give enough salbutamol

Inhaled B2 agonists relieve bronchospasm and improve oxygenation.  The minor side effects that we have all seen include tremor, anxiety, headache, dry mouth and palpitations. If given, without oxygen, they have also been shown to cause or worsen hypoxaemia. Pulmonary vasodilation leads to a worsening ventilation-perfusion mismatch.

Inhaled salbutamol may also cause metabolic acidosis even when the mechanical work of breathing has been improved with paralysis and ventilation this still occurs. In the non-paralysed patient, the body compensates for this acidosis by increasing the respiratory rate to blow off the CO2. Be mindful that the tachypnoea in your asthmatic patient may be due to excess beta-agonist and not their asthma.

So how does one recognise potential salbutamol toxicity in the pre-hospital setting? Consider it in all children who are wheezy, restless, tachycardic and have had large doses of beta-agonist.

Normal doses of inhaled salbutamol have been shown to cause hypokalaemia but the clinical significance of this is unknown. Hypokalemia, coupled with worsening respiratory and metabolic acidosis can have catastrophic cardiac effects.

Myth – Adrenaline is dangerous in asthma

One of the most most obvious reasons for using adrenaline in the setting of apparent severe or life threatening asthma is that the diagnosis may be in doubt.  Asthma and atopy often co-exist. Patients with known food allergies and asthma are much more likely to die due to anaphylaxis than those without asthma.  A child with severe anaphylaxis may initially have no more signs than a wheeze and worsening air hunger that is mistakenly treated as asthma. The diagnosis of anaphylaxis should be considered in all who fail to respond to initial therapy.

Nebulized adrenaline may be helpful in acute asthma via direct beta adrenoceptor mediated bronchodilatation. It is possible that there are also some alpha effects via reduction in localized oedema and reduction in microvascular leakage. Small studies have shown no difference between nebulized adrenaline and nebulized salbutamol in terms of increased peak expiratory flow. The may also be less of a drop off in PaO2 due to the V/Q mismatch seen with salbutamol use due to alpha action.  In younger children, bronchospasm may be less of an issue than mucosal oedema.
Remember all inhaled therapies are ineffective if they don’t go anywhere. If the child is so tight that they can barely inhale then salbutamol or nebulized adrenaline are likely to be of benefit and so alternative route should be sought.  IM adrenaline can be given quickly to the critically ill asthmatic whilst IV access is obtained.  At the time of writing a clinical trial into the potential benefit of IM adrenaline as an adjunct to inhaled B2 agonists is recruiting in the US

Myth – If the child is wheezing, they have asthma

Around 17% of infants experience wheeze with the first three years of life. Not all of these end up with a diagnosis of asthma. By the age of 4-5 the incidence of wheeze is around 21.7% which is almost double the incidence of asthma (11.5%) in this population. By the school years, the incidence of wheeze and asthma are near identical.
Wheeze is characterized by “a continuous whistling sound during breathing that suggests narrowing or obstruction in some part of the respiratory airways.” With that definition in mind, there are a number of clinical entities that may cause a wheeze. There is a grey area between those children with obvious asthma and obvious bronchiolitis. Whilst bronchodilators would be appropriate in asthma a large Cochrane review found them to be ineffective in bronchiolitis.  Most clinicians would give a one-off trial of salbutamol as long as it did not interfere with other management.  There is also no evidence of benefit for the use of systemic corticosteroids in pre-school wheeze.  Other potential diagnoses to consider include inhaled foreign bodies, pneumonia or pneumonitis, tracheomalacia or complications of congenital conditions.

So the presence of wheeze does not guarantee that the child has asthma. It is also worthwhile mentioning that the absence of a wheeze does not rule it out either. If there is severe bronchospasm and mucosal oedema not enough air entry will occur to cause a wheeze

Selected References

Asthma in Australia: with a focus chapter on chronic obstructive pulmonary disease. 2011 Full text

Oxygen saturations are useful in the management of asthma

Mehta SV, Parkin PC, Stephens D, Schuh S. Oxygen saturation as a predictor of prolonged, frequent bronchodilator therapy in children with acute asthma. The Journal of pediatrics. 2004 Nov 30;145(5):641-5.

Inwald D, Roland M, Kuitert L, McKenzie SA, Petros A. Oxygen treatment for acute severe asthma. British Medical Journal. 2001 Jul 14;323(7304):98.

Helmerhorst HJ, Schultz MJ, van der Voort PH, de Jonge E, van Westerloo DJ. Bench-to-bedside review: the effects of hyperoxia during critical illness. Critical Care. 2015 Aug 17;19(1):1.

Nebulizers are better than spacers

Zar HJ, Brown G, Donson H. Are spacers made from sealed cold-drink bottles as effective as conventional spacers?. Western Journal of Medicine. 2000 Oct;173(4):253.

Castro-Rodriguez JA, Rodrigo GJ. β-Agonists through metered-dose inhaler with valved holding chamber versus nebulizer for acute exacerbation of wheezing or asthma in children under 5 years of age: a systematic review with meta-analysis. The Journal of pediatrics. 2004 Aug 31;145(2):172-7.

You can never give enough salbutamol

Tomar RP, Vasudevan R. Metabolic acidosis due to inhaled salbutamol toxicity: A hazardous side effect complicating management of suspected cases of acute severe asthma. medical journal armed forces india. 2012 Jul 31;68(3):242-4.

Yousef E, McGeady SJ. Lactic acidosis and status asthmaticus: how common in pediatrics?. Annals of Allergy, Asthma & Immunology. 2002 Dec 31;89(6):585-8.

Udezue E, D’Souza L, Mahajan M. Hypokalemia after normal doses of nebulized albuterol (salbutamol). The American journal of emergency medicine. 1995 Mar 31;13(2):168-71.

Starkey ES, Mulla H, Sammons HM, Pandya HC. Intravenous salbutamol for childhood asthma: evidence-based medicine?. Archives of disease in childhood. 2014 Jun 17:archdischild-2013.

Adrenaline is dangerous in asthma

Coupe MO, Guly U, Brown E, Barnes PJ. Nebulised adrenaline in acute severe asthma: comparison with salbutamol. European journal of respiratory diseases. 1987 Oct;71(4):227-32.

If the child is wheezing they have asthma

Ducharme FM, Tse SM and Chauhan B. Asthma 2: Diagnosis, management, and prognosis of preschool wheeze. Lancet. 2014. 383:1593-604.

Okpapi A, Friend AJ, Turner SW. Acute asthma and other recurrent wheezing disorders in children. American family physician. 2013 Jul;88(2):130-1.

Goldstein H, Tagg A, Lawton B, Davis T. Easing the wheeze. Emergency Medicine Australasia. 2015 Oct 1;27(5):384-6.

Gadomski AM, and Scribani MB. Bronchodilators for bronchiolitis. Cochrane Database of Systematic Reviews. 2014;6:CD001266

Salbutamol – When to give the next dose?

Cite this article as:
Henry Goldstein. Salbutamol – When to give the next dose?, Don't Forget the Bubbles, 2016. Available at:
https://doi.org/10.31440/DFTB.9553

Salbutamol is one of the most frequently used medicines in the paediatric pharmacopeia. Most of us can say that it’s a short acting beta agonist delivered by nebuliser or more commonly via an MDI with spacer. Some might recall that the half life is between 2.7 and 5.5hrs.

And, most perplexing of all, once we’ve used it in the acute situation, how best to use it next? I’m talking here about the post-burst, pre-discharge phase of asthma or an exacerbation of a reactive airway picture.

Pierce is 5yo, he presents at 2300 to your ED. His Mum says he can’t sleep due to the coughing and she thinks his asthma is playing up. He receives a burst and another dose an hour later; he looks like he’s coping another hour later. He takes a 2mg/kg dose of Prednisolone. You come to review Pierce and his mum asks “So, what happens next?”

We’re talking here about the frequency of salbutamol usage. If you had asked me this question a month ago, I’d have been certain of my answer. My mental model for how to manage a presentation like this (especially out of hours) was rock solid with experience, but light on evidence.

I’ve had a suspicion I’ve been doing things differently and hence decided to review my practice, first by talking to peers, then looking at some guidelines and finally my reviewing the literature.

My practice, overnight, had been to be quite prescriptive with salbutamol – a slow, regular, wean and then not less than q2h until the sun came up (0500 in the Queensland summer), before aiming for q3h, consultant review if indicated, education and discharge during the morning ward/short-stay round.

This is not the practice of my peers; “You just wean them and then send them home.” Or, “Just review them regularly and give it as you need to.”, were the common answers – hopefully what most folk reading this are thinking –  and certainly what I aim to do before the sun goes down.

The RCH Melbourne guidelines suggest only dosing salbutamol when symptoms return.

The experimental literature around this question and reducing the frequency of salbutamol dosing is surprisingly sparse, but here are a few of the highlights:

Chandra, 2005

Chandra undertook a small study of 62 adults with the aim compare regular (q4h) salbutamol plus symptomatic vs symptomatic treatment alone. Patients in the pro re nata only arm used less salbutamol and had less use of salbutamol overall but there was no significant difference in the length of stay or rate of improvement. Patients were randomised 6 hours into their treatment, which seems to expunge most of the external validity for this paper to our clinical question.

Karpel et al., Chest 1997

Karpel et al. performed an elegant study with 100 adults presenting to NY emergency departments in which the patients were dosed every 30 minutes with salbutamol or placebo inhaler such that the groups essentially became dosed at q30mins or q60mins or q90mins or q120minutes – all after an initial load of 6 puffs of salbutamol. At each time point, FEV1 was recorded. They concluded that q60mins was the optimal dose, with minimal side effects.

This study didn’t utilise a ‘burst’ / salbutamol load, which is now standard (and first described in 1988), and may alter the conclusions, as the outcomes seemed to identifying number of patients who responded well initial dosing, and noted that these early responders benefitted comparably from q30,60 and 120 minutely dosing.

Admittedly, the frequent, regular dosing of salbutamol, once loaded, doesn’t make pharmacological sense; although it’s worth noting that only 15% of the dose makes it to the lung surface, whilst the other 85% is swallowed and undergoes first-pass metabolism, there are negligible levels of salbutamol in serum. These of course, are pharmacologic parameters, rather than clinical ones.

On reflection, my prescriptive style required minimal reviews and developed from working jobs as a solo Paeds Reg on nights. The perceived benefits were that with a high patient load and variable nursing experience, I was able to reduce decision making and cognitively offload all whilst keeping patients safe (I’ve not seen salbutamol toxicity from q2h dosing.) I’ve previously suggested other arguments for this, including the predictability for parents, although I’m not so sure about this part.

There are some merits in this shape of care, but it’s not “evidence based” nor “what most doctors would do.” So, is it safe? Is it wrong? How best to change practice?

 

References:

Product Information Salbutamol CFC-free MDI – https://au.gsk.com/media/223609/ventolin_cfc_free_inhaler_pi_004_approved.pdf

Acute Asthma – RCH Melbourne Guidelines –  https://www.rch.org.au/clinicalguide/guideline_index/asthma_acute/

Karpel JP, Aldrich TK, Prezant DJ, et al. Emergency treatment of acute asthma with albuterol metered-dose inhaler plus holding chamber: how often should treatments be administered? Chest. 1997 Aug;112(2):348-56. – https://www.ncbi.nlm.nih.gov/pubmed/9266868

Chandra A1, Shim C, Cohen HW, et al. Regular vs ad-lib albuterol for patients hospitalized with acute asthma. Chest. 2005 Sep;128(3):1115-20.

Managing acute asthma in children – Australian Asthma Handbook (Accessed 1/8/1016) – https://www.asthmahandbook.org.au/figure/show/67

DFTB in EMA #3 – Easing the Wheeze

Cite this article as:
Henry Goldstein. DFTB in EMA #3 – Easing the Wheeze, Don't Forget the Bubbles, 2015. Available at:
https://doi.org/10.31440/DFTB.7662

The team at DFTB had our third article published in the series for Emergency Medicine Australasia Journal.

Wheezing children commonly present to the ED. Bronchiolitis, preschool wheeze and asthma are common causes of such presentations. It is important to note that the term ‘wheeze’ is frequently misused by parents to describe a number of respiratory noises, including transmitted upper airway sounds and stridor.[1] Wheeze is, in itself, a symptom manifested by ‘a continuous whistling sound during breathing that suggests narrowing or obstruction in some part of the respiratory airways’.[2] One British study reported that 29.3% of children have had a wheeze by the age of three, and 30% of preschoolers with recurrent wheeze are diagnosed with asthma by 6 years of age.[3, 4] This article briefly reviews the diagnosis and management of preschool wheeze, while considering recent guidelines on bronchiolitis and asthma.

Click here to read the full article – “Easing the wheeze.”

Reference:

Goldstein, H., Tagg, A., Lawton, B. and Davis, T. (2015), Easing the wheeze. Emergency Medicine Australasia, 27: 384–386. doi: 10.1111/1742-6723.12463