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Asthma for Ambos


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

Asthma is such a common condition, affecting one in ten Australians.  In Victoria alone, approximately 17.2% of all children have been told by a doctor that they have asthma. The incidence in Aboriginal or Torres Strait Islanders is higher at around 20% . Whilst many of these will never need to go to the hospital, 18824 children in NSW were taken to hospital. Of these, 43% need admission – much higher than their adult counterparts. Many can be safely managed at home with their pre-written asthma action plan (though only 41% of kids under 15 have one), but some children are more at risk of critical or life-threatening asthma than others. In 2009 (the latest dataset from AIHW), there were 411 asthma-related deaths. Fortunately, the death rate in the under-15-year-old sub-population is around 0.2 per 100,00 people. It is hard to tease the data as National Mortality Database lumps all deaths between 5-34 years.

Risk factors for a more severe attack in children include:-

  • Previous severe asthma attacks especially ICU admission
  • Two or more hospital stays due to 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 peak in ED visits for asthma in late summer and autumn in children, whereas more adults present in the winter, possibly due to the increased incidence of viral upper respiratory tract infections among adults at this time of year. Another hypothesis for the increased incidence in the summer months is decreased compliance with preventative medication.

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

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

Because asthma is such a common condition, the ambulance service is very experienced in managing it. Still, I wanted to focus on areas where what should happen and what does happen might diverge.

Are oxygen saturations useful in the management of asthma?

The pathophysiological basis of an acute exacerbation is bronchospasm, increased mucosal oedema and hypersecretion of mucus.  This leads to hypoxic vasoconstriction and decreased blood flow to the under-ventilated lung to match pulmonary perfusion with alveolar ventilation.

In the hospital setting SpO2<91% may be a helpful predictor of prolonged frequent bronchodilator therapy more than 4 hours, and SpO2 of <89% is associated with a need for bronchodilator therapy over 12 hours.

Hypoxaemia and hypocarbia only occur in the presence of life-threatening asthma. Considering the haemoglobin-oxygen dissociation roller-coaster it is easy to see how many children may teeter on the precipice before critical desaturation occurs. Whilst low oxygen saturations mean that a patient is unwell it should be clinically obvious.  On the flip-side normal oxygen sats do not mean the patient is fine.  Concerns have been raised that oxygen administration may lead to potential 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 and intra-pulmonary shunting with subsequent reduction in cardiac output. Once the 78% nitrogen in the patients’ alveoli gets replaced with increasing amounts of supplemental oxygen, this is resorbed, leading to the subsequent reduction in alveolar volume and collapse.

Are nebulizers better than spacers?

A recent Cochrane review comparing the use of nebulizers with spacers found no difference in hospital admission rates with either mode of delivery. There also appeared to be no difference in lung function or oxygen saturation when either device was used. What was different, however, was the adverse effects profile. The common salbutamol side effects of tremors and tachycardia were more prevalent in those using a nebulizer device.

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 40mcg of salbutamol via a 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 are as effective as conventional devices in resource-poor settings.

Can you give too much salbutamol?

Inhaled B2 agonists are given to relieve bronchospasm and improve oxygenation.  Minor side effects that we have all seen include tremors, anxiety, headache, dry mouth and palpitations. They have been shown to cause or worsen hypoxaemia if given without oxygen. The mechanism behind this is pulmonary vasodilation leading to a worsening ventilation-perfusion mismatch.

Metabolic acidosis has been seen as a direct result of inhaled salbutamol due to lactic acidosis. Even when the mechanical work of breathing has been improved with paralysis and ventilation this still holds true. The body compensates for this metabolic acidosis in the non-paralysed patient by increasing the respiratory rate.  This may be mistaken as worsening respiratory function, so escalating doses of beta-agonists are provided.

So how does one recognise potential salbutamol toxicity in the pre-hospital setting? It should be considered in all children who are wheezy, restless, and tachycardic with increasing doses of beta-agonist.

Even normal doses of inhaled salbutamol have been shown to cause hypokalemia, but the clinical significance of this is unknown. Theoretically, hypokalemia and worsening respiratory and metabolic acidosis may have catastrophic cardiac effects.

Is adrenaline dangerous in asthma?

One of the 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 from 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. There may also be some alpha effects via a reduction in localized oedema and a reduction in microvascular leakage. Small studies have shown no difference between nebulized adrenaline and nebulized salbutamol in terms of increased peak expiratory flow. There 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, salbutamol or nebulized adrenaline are likely to benefit, so alternative routes 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.

Do all children with wheezing have asthma?

Around 17% of infants experience wheezing within 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%, almost double the incidence of asthma (11.5%) in this population. By the school years, the incidence of wheeze and asthma are nearly 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, some clinical entities 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 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 wheezing does not guarantee that the child has asthma. It is also worth mentioning that the absence of a wheeze does not rule it out. If there is severe bronchospasm and mucosal oedema not enough air entry will occur to cause a wheeze.


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



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1 thought on “Asthma for Ambos”

  1. Hi Andrew,

    I thoroughly enjoyed your talk about paediatric respiratory conditions at Werribee the other week.

    As a Graduate paramedic, something that I’m constantly trying to grapple with distinguishing exacerbations of COPD from CHF in patients with conflicting past medical histories.

    Any chance you could provide some insight into assessments of this patient cohort and specific signs and symptoms used to distinguish them? Or perhaps where to find some further resources where I could do some further reading?

    Thanks in advance!