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This is a 5 year-old boy who came to the ED for an asthma exacerbation in the setting of 3 days of rhinorrhea and sore throat. He has been taking his albuterol with minimal improvement. He has had at least 2 exacerbations in the past month and is only on albuterol. His exam is notable for boggy nasal turbinates and erythematous oropharynx.
How would you classify this child’s asthma?
Asthma treatment in the ED is focused on the acute exacerbation and chronic control. Our patient is having 2 exacerbations per month. This places him in the mild, intermittent category. These patients benefit most from lifestyle modification and rescue inhaler as needed. Click here to see the latest guidelines on classifying asthma and initiating therapy.
There are a few pediatric clinical assessment scores for asthma.[1]
- The Pediatric Respiratory Assessment Measure (PRAM). The PRAM uses 5 variables, (wheezing, air entry, contraction of scalenes, suprasternal retraction, and oxygen saturation) to help determine whether or not a person should be admitted.
- The Pulmonary Index Score (PIS) is an asthma score that is also based on 5 clinical variables (respiratory rate, degree of wheezing, inspiratory to expiratory ratio, accessory muscle use, and oxygen saturation).
- The Pediatric Asthma Severity Score (PASS) consists of three variables (wheezing, prolonged expiration, and work of breathing).
PRAM | PIS | PASS |
Wheezing | Respiratory Rate | Wheezing |
Air Entry | Degree of wheezing | Prolonged Expiration |
Contraction of scalene | I:E ratio | Work of breathing |
Suprasternal retraction | Accessory Muscle Use | |
Oxygen Saturation | Oxygen Saturation |
It is important to note that all risk assessment scores need to have construct validity and reliability. That is, one must check if they measure what they intend to measure and if they are reproducible. Many suggest that asthma severity scores lack validity because there is no gold standard for severe asthma. Additionally, these scores have been criticized[2] for their reliability, as asthma affects many age groups and can manifest differently for each age. Therefore, you should know they exist, but use them cautiously.
Asthma exacerbations have classically been treated acutely with short-acting beta agonist and PO steroids. But these steroid treatments provided short-lived results. Within a short time, the child often has another exacerbation.
The role of systemic steroids has often been challenged because of its potential side effects of immunosuppression, weight gain, and adrenal suppression. Because inhaled corticosteroids (ICS) lack systemic absorption, attempts have been made to replace systemic steroids for acute exacerbation but have failed to show benefits[3]. What these studies neglected was that those with asthma have a chronic underlying process and many require maintenance medications or controllers. In a recent randomized, controlled trial, Sampayo et al.[4] investigated whether or not prescribing a one-month supply of an inhaled corticosteroid would affect symptoms after discharge and follow-up rates with a primary care physician. They found that at 2 weeks, those with ICS had fewer daytime shortness of breath, night-time cough, and required less albuterol but found no significant difference in these outcomes at 8 weeks follow-up. They also found that there was no difference in follow-up with PMD. Now, this study had many limitations. Only 50% of patients actually filled their ICS after discharge or after follow-up with a PMD. There was also no difference in the number of patients in the control group who were either started on ICS by their PMD or maintained on ICS by their PMD after follow-up. Because it was only recommended that patients follow up with their PMD and we don’t know when this “follow-up” actually occurred – presumably at some point both groups received the same rates of ICS making the data hard to interpret. If the point when rates of prescribed ICS became similar was after 2 weeks, that could explain why there was an early benefit (in the first 2 weeks) but not at 8 weeks. Regardless of its limitations, this study attempts to address an interesting future for asthma care in the ED but is clearly not the answer. More research is needed on this topic.
Other interventions should be targeted around asthma triggers. These include reduction in tobacco smoke, dust mites, air pollution, and cockroach allergens. However, in addition to allergic triggers, other overlapping medical conditions should be considered as well.
It is estimated that up to 40% of people with allergic rhinitis have asthma. The exact mechanism is unclear but common hypothesis include include nasal-bronchial reflex, mouth breathing caused by nasal obstruction, and pulmonary aspiration of nasal contents. Some have proposed that given their IgE similarity, that they are really the same disease with different clinical manifestations. Few studies clearly define a benefit with asthma when treating allergic rhinitis; however, though not always significant, most studies have shown some type benefit.[5] Because only 2% of topical nasal corticosteroids are deposited in the lower airways, they have a limited role in acute asthma exacerbation. The Allergic Rhinitis and its Impact on Asthma guidelines (ARIA) recommend treating asthma exacerbations with topical inhaled glucocorticoids and oral non-sedating antihistamines if they were triggered by allergic rhinitis.[6] Some recommend oral decongestants as well although the evidence is limited.[7] Though the data as a while are limited on this subject, the risks from the topical corticosteroids and antihistamines are minimal. Early intervention with these relatively safe medications might be warranted from the ED to help prevent the recurrent acute asthma exacerbation waiting around the corner.
http://blog.clinicalmonster.com/2012/07/staten-island-corner-asthma-enough-with-the-prednisone-make-it-dex/
https://emergencymedicinecases.com/pediatric-asthma/
[1] Sawicki, G. Haver, K. Acute asthma exacerbations in children: Home/office management and severity assessment. In: UpToDate, Post, TW (Ed), UpToDate, Waltham, MA, 2017.
[2] Eggink H, Brand P, Reimink R, Bekhof J (2016) Clinical Scores for Dyspnoea Severity in Children: A Prospective Validation Study. PLoS ONE 11(7): e0157724. doi:10.1371/journal.pone.0157724
[3] Edmonds ML, Milan SJ, Brenner BE, Camargo Jr CA, Rowe BH. Inhaled steroids for acute asthma following emergency department discharge. Cochrane Database of Systematic Reviews 2012, Issue 12. Art. No.: CD002316. DOI: 10.1002/14651858.CD002316.pub2.
[4] Esther M. Sampayo, Maryann Mazer-Amirshahi, Elizabeth A. Camp, Joseph J. Zorc, Initiation of an Inhaled Corticosteroid During a Pediatric Emergency Visit for Asthma: A Randomized Clinical Trial, Annals of Emergency Medicine, Available online 2 March 2017, ISSN 0196-0644, http://dx.doi.org/10.1016/j.annemergmed.2017.01.005.
[5] Taramarcaz P, Gibson PG. Intranasal corticosteroids for asthma control in people with coexisting asthma and rhinitis. Cochrane Database of Systematic Reviews 2003, Issue 3. Art. No.: CD003570. DOI: 10.1002/14651858.CD003570.
[6] Brozek JL, Bousquet J, Baena-Cagnani CE, Bonini S, Canonica GW, Casale TB, van Wijk RG, Ohta K, Zuberbier T, Schünemann HJ, et al. Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines: 2010 revision. J Allergy Clin Immunol. 2010 Sep;126(3):466-76.
[7] Wheatley LM, Togias A. Allergic Rhinitis. The New England Journal of Medicine 2015;372:456–63.
Steven Greenstein
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2 Comments
ablumenberg · March 17, 2017 at 11:12 am
“Asthma treatment in the ED is focused on the acute exacerbation and chronic control”
I don’t agree.
I’m really glad there is a Cochrane review (Citation #3) that addresses this question. It’s a very good meta-analysis which did not show an improvement in outcomes when ICS were prescribed from the ED. After citing this meta-analysis, your next statement reads:
“What these studies neglected was that those with asthma have a chronic underlying process and many require maintenance medications or controllers”
While this is partially true, I disagree with the logic of the argument. I think that pathophysiology is useful ONLY when there is insufficient evidence to address a clinical question. How pathophysiology affects a complex human being is better predicted by a clinical trial than by our understanding of pathophysiology. This is particularly important when clinical data actually exists. In this case, the clinical data refutes the argument that ICS make a difference when prescribed from the ED.
We could speculate for hours as to why this is. Is an ED population somehow different than a primary care population? Is the disease process different? Is compliance different? Is follow up different? I would argue yes to all of these questions, but honestly we won’t reach a conclusion as to WHY there was no improvement with ICS. Still, the data speak for themselves.
An important concept that addresses compliance as a factor is whether studies followed an intention-to-treat model because it takes into account human and social factors. There’s a parable in medicine that goes “The best medication is the one the patient takes.”
It’s true that in the Sampayo paper only about 50% of the study group filled their prescriptions, but at least the study followed an intention-to-treat model. Unfortunately the evidence for symptom control was inconclusive. Looking at the outcomes such as cough, wheeze, shortness of breath the effects were marginal and had broad confidence intervals. In fact, the best statistically significant outcome was less use of rescue albuterol at two weeks – an outcome of dubious significance given 1) the lack of blinding in this study and 2) the confounding variable of daily ICS use (the patient already inhaled something as “asthma treatment” might make them less likely to use a second inhaler medication for the same symptom).
At the end of all this, I disagree for two reasons.
1. It’s been studied. It doesn’t work that great for ED patients.
2. The ER is an acute care setting. To paraphrase a cinematic masterpiece from the late 1990s, we are single serving doctors. It’s not the place to start a medication which needs months of refills.
Ian deSouza · March 17, 2017 at 12:34 pm
Nicely composed response, complete with the quotes and paraphrases I have come to expect! I appreciate the detailed dismantling of an easy target, the Sampayo paper, although it did not seem to be presented as good evidence in the first place.
If you look more closely into the Cochrane review, you’ll find that the majority of the patients analyzed in the ICS+PO steroid vs. PO steroid were ADULTS. So, technically, it appears from this review that the only evidence that we have to attempt to answer the question for pediatric patients its the Sampayo study, lacking as it is. The author of this post concludes appropriately, “…this study attempts to address an interesting future for asthma care in the ED but is clearly not the answer. More research is needed on this topic.”
Since there is no evidence to answer this question in children, then we are left to pathophysiology (as you said) and more importantly, appeal to common sense (which I agree may not always hold water in medicine either). I believe Greenstein attempted to express the importance of categorizing the asthma patient, some of whom may in fact need ICS prescribed as preventative medications. ICS are very benign medications, and without direct evidence against its use, may still be worth prescribing for the frequent ED asthmatic. (In reality, I am more apt to consider adjunctive treatment for allergic rhinosinusitis with nasal steroid and possible anti-histamine.)
And finally, you know as well as I that at least where we work, the ED has not been the “acute care setting” that you see on TV or in your favorite cinematic masterpieces when you consider the complaints of the majority of ED patients and their expectations of us, emergency clinicians. This isn’t going to change anytime soon in the current econopolitical climate.