Asthma Module

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

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

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

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

What investigations and treatment options should you consider?

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

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

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

The following clinical signs should be recorded:

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

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

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

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

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

Observations

  • Include general observations.

CXR

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

Blood Gas

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

Oxygen 

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

Inhaled β2 agonist 

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

Ipratropium Bromide 

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

Oral steroids 

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

Nebulised Magnesium 

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

Antibiotics 

  • Insufficient evidence to refute or recommend.

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

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

Safe follow up

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

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

An age based approach to wheeze in children

Bronchiolitis

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

Viral Wheeze

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

Asthma

  • Described above. 

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

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

Management

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

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

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

What investigations and treatment options should you consider?

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

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

Do you know how to use a spacer?

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

How would you rate the severity score of this presentation?

What investigations or treatment needs to be considered?

Which IV medications if any should be used? 

Which important differentials need to be considered?

What escalation plans need to be put in place?

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

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

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

So what is the evidence? (Cochrane review)

IV salbutamol 

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

IV MgSO4 

  • Appears to be safe and beneficial in severe asthma

IV aminophylline 

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

IV ketamine 

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

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

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

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

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

Ensuring you have appropriately assessed and optimised their condition

Reassess the patient?

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

Have you exhausted medical management?

  • ? adrenaline ? ketamine ?heliox 

What could be missing? 

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

Escalation options

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

Non invasive ventilation 

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

Does this child need to be intubated?

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

Alternative treatment options

Adrenaline

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

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

Heliox 

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

Ketamine

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

NIV

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

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

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

What are the next steps that need to be taken?

What is the ‘deadly triad’ in asthma?

What are the key ALS modifications in asthma arrest?

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

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

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

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

  1. Intubate Early

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

  1. Ventilate with caution

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

  1. Manual chest deflation

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

  1. Consider tension pneumothorax

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

  1. Rehydrate

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

  1. GIVE ADRENALINE! – Utilise its bronchodilator effect. 

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

A: Hypoxaemia is an early sign of clinical deterioration 

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

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

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

The correct answer is C.

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

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

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

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

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

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

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

C: After two sets of 3hrly

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

The correct answer is B.

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

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

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

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

C: If the pMDI is ineffective

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

The correct answer is B.

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

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

When is intubation indicated in paediatric asthma presentations?

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

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

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

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

The correct answer is C.

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

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

A: Burst therapy with salbutamol. 

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

C: Humidified air nebuliser and antipyretics for fever. 

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

The correct answer is B.

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

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

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

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

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

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

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

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

DFTB – Managing acute asthma, Simon Craig (2017)

DFTB – Asthma for ambos (2016)

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

DFTB – The curious incident of the wheeze in the night

PEMBLOG – Heliox in the emergency department (2017)

EMCases – Management of acute paediatric exacerbations (2016)

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

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

RCEMLearning – Arrest in asthma

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



Please download our Facilitator and Learner guides

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

Asthma – medical management

Cite this article as:
Tessa Davis. Asthma – medical management, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.2815

A 9 year old boy is rushed into ED with what is clearly a severe exacerbation of his asthma. His sats are 80%, his RR is 60-70 and he is not looking great. You can hear some air entry with a bit of wheeze. He clearly needs some good treatment and he needs it quickly. Which drugs you choose?