case study 21 acute asthma management quizlet

Case of Acute Severe Asthma

Kane guthrie.

• Dec 2, 2022

A 25-year-old lady Miss. Poor Compliance is rushed into your Emergency Department as a Priority 1. She is a brittle asthmatic and has been given 3x 5mg salbutamol nebs, and 0.5mg of adrenaline IM prehospital. On arrival Miss PC is sitting forward in the tripod position , using her accessory muscles to breath. She is tachypnoeic, agitated and unable to talk.

Vital signs: Pulse 143, BP 138/95, RR 42, Sp02 91% on neb, GCS 14/15.

Past Medical and Medication History

• Smoker. Severe asthmatic. Intubated twice in past 2 years
• Currently taking seritide 250/50mg, salbutamol MDI PRN and prednisolone 50mg PRN

Asthma Epidemiology

• Over 2.2 million Australians have currently diagnosed asthma
• 406 deaths attributed to asthma in 2006
• Highest risk of dying from asthma is in the elderly over 70
• The emergency clinician’s goal in treating acute severe asthma is preventing intubation
• Severe/Critical asthma is a life threatening condition

Asthma Pathophysiology

• Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role, in particular, mast cells, eosinophils, T lymphocytes, macrophages, neutrophils, and epithelial cells.
• Smooth muscle hypertrophy and hyperplasia
• Inflammatory cell infiltration and oedema
• Goblet cell and mucous gland hyperplasia with mucous hypersecretion
• Protein deposition including collagen
• Epithelial desquamation
• Most common, responsible for 80-85% of all fatal events is characterised by eosinophilic inflammation associated with gradual deterioration over days-weeks occurring in patients with severe or poorly controlled asthma, and is slow to respond to therapy.
• The second phenotype, with neutrophilic inflammation, has both rapid onset and response to therapy.

Markers of severe asthma:

• Inability to speak in full sentences
• Use of accessory muscles or tracheal tugging
• Cyanosis and sweating
• Pulsus paradoxus (>15mmHg decreased with inspiration). With severe muscle fatigue might be absent
• Quiet chest on auscultation (The “Silent Chest”)
• Confusion or decreased level of consciousness
• Hypotension or bradycardia
• FEV 1<40% predicted
• PEF <40% of predicted or best (<25% in life threatening asthma)
• Oxygen saturation <90-92%
• PaO2 <60mmHg
• PaCO2 >45mmHg

Complications of Asthma :

• Pneumothorax, Pneumomediastinum, Pneumopericardium and Pneumoretroperitoneum
• Cardiac Arrhythmias, Myocardial ischaemia or infarction
• Electrolyte disturbances (hypokalaemia, hypomagnesaemia, hypophosphataemia)
• Lactic Acidosis
• Hyperglycaemia

Conditions that may mimic acute asthma:

• Upper airway obstruction
• Foreign-body aspiration
• Vocal cord dysfunction syndrome
• Pulmonary oedema
• Acute exacerbations of COPD
• Hysterical conversion reaction
• Munchausen syndrome

Diagnostic Test:

• Hyperinflation 5-10%
• Infiltrate 5%
• Pneumothorax <1%
• Pneumomediastinum <1%
• Respiratory alkalosis typical
• Inaccurate predictor of outcome
• Will seldom alter your treatment plan
• An objective measure of lung function
• Useful to assess response to treatment
• Impossible to obtain in the dying patient
• <25% Severe
• 25-50% Moderate
• 50-70% Mild
• >70% Discharge Goal
• Simple, and less painful than ABG
• Provides continuous oxygenation measurements
• Needs to placed on well-perfused site, difficult to obtain readings if global hypoperfusion or peripheral vasoconstriction present.
• Aim to keep sp02 >92%

Management of Acute Severe Asthma

• Hypoxia is the main cause of death in asthma
• Oxygen should be given to keep Sp02 above 92%
• A slight Pco2 rise may occur with oxygen therapy but this is of no clinical significance.

Beta-agonists:

• Rapid acting inhaled beta-agonists (bronchodilators) are the first line therapy for acute asthma.
• Nebulisers should generally be used in acute severe asthma, as provide easier delivery of medication to patient, multi dose inhalers have a role in mild to moderate asthma.
• IV salbutamol gives you the advantage of hitting the beta 2 receptors from the back door, while continuing nebulizer treatment, and should be trialed in patients not responding to nebulisers.
• Continuous nebuliser therapy appears to be more effective than intermittent nebulisers for delivering beta-agonist drugs to relieve airway spasm in acute severe asthma.  (Cochrane Review, 2009)
• Salbutamol toxicity can caused a lactic acidosis which is often unrecognized in asthma patients, the lactic acidosis has been hypothesized to adversely affect ventilation by increasing ventilatory demand, increasing dead space ventilation, worsening dynamic hyperinflation and intrinsic PEEP. Management is to discontinue salbutamol at the earliest opportunity.
• Dose:  Salbutamol Nebuliser Ampoule 5mg
• Dose: Salbutamol IV 5mg in 500mL of 0.9% sodium chloride or 5% dextrose start at 30mL/hr titrating up to 120mL/hr

Anticholinergics:

• Anticholinergics agents block muscarinic receptors in airway smooth muscles, inhibit vagal cholinergic tone and result in bronchodilation.
• Dose: Ipratropium bromide (Atrovent) 500ug to second dose of salbutamol via neb, can be repeated every 4hours
• Use of corticosteroids within 1 hour of presentation to an ED significantly reduces the need for hospital admission in patients with acute asthma. Benefits appear greatest in patients with more severe asthma, and those not currently receiving steroids
• Dose: Prednisolone 50mg PO
• Dose: IV Hydrocortisone 100-200mg
• Note: Parenteral route is indicated in ventilated patient or patient unable to swallow, eg. Vomiting

Adrenaline:

• Can be give either intravenously or via nebulizer
• Bronchoconstriction is the major pathology in asthma; airway oedema might also make a significant contribution. Both the a-agonist and B-agonist effects of adrenaline might be beneficial, with the alpha effect decreasing oedema and the beta effect responsible for bronchodilation.
• Dose:  IV 6mg in 100mls 5% dextrose start at 1-15mLs/hour
• Dose: Nebulizer 1mg in 3ml normal saline

Aminophylline:

• The popularity of aminophylline in asthma exacerbations has diminished in recent years.
• Systematic reviews have shown that IV aminophylline in severe acute asthma does not produce additional bronchodilation above that achieved with beta-agonist and corticosteroids.
• Side effects; cardiac arrhythmia’s, vomiting, toxicity.
• Dose : 5mg/kg over 20min followed by infusion of 500mg aminophyline n 500mL of 5% dextrose at 0.5mg/kg per hour

Magnesium Sulphate:

• Magnesium potential role is asthma may involve a combination of smooth muscle relaxation, inhibition of histamine release and acetylcholine release from nerve endings.
• Most evidence to support the use of magnesium in asthma is in the acute severe asthmatic were it has been shown to be safe and beneficial.
• Dose : IV 2-4g over 30-60mins
• Heliox Mixture 80% helium/20% oxygen
• There is evidence that helium and oxygen mixtures (heliox) may provide additional benefits to patients with acute asthma.
• Heliox mixtures have the potential to decrease airway resistance, and therefore decrease the work of breathing for the severe acute asthma patient.

Antibiotics:

• Antibiotics are not indicated in the management of severe acute asthma.
• Antibiotics should only be used in the setting of an underlying pneumonia, respiratory tract infection or to aid in the prevention of ventilator-associated pneumonia in ICU.

Airway Management

Non-Invasive Positive Pressure Ventilation:

Good quality evidence and trails to support the use of NPPV in asthma are lacking, however it is worth trying when intubation is not immediately indicated. Remember the goal of the emergency clinician’s in treating asthma is to prevent intubation.

• Positive pressure is generally less than 15cmH2O
• Benefit between CPAP vs BiPAP is unknown
• Tachypnea caused by severe asthma can make it difficult for the patient to coordinate they’re breathing with machine making BiPAP uncomfortable
• Need a large randomised control trial to determine the effectives properly of NIV, in acute severe asthma.

“Asthmatic on BiPAP before being Intubated”

Mechanical Ventilation:

1-3% of acute severe asthma requires intubation. Prevention of intubation and mechanical ventilation are the goals of managing acute severe asthma, this can be achieved by maximising pre-intubation therapy, however you don’t want to wait too long or let the severe asthmatic tire before trying to intubate them. Once an asthmatic is intubated and ventilated their morbidity and mortality increasing dramatically, and it can be difficult to wean from the ventilator.

Criteria for Intubation:

• Cardiac or Respiratory arrest
• Altered mental status
• Progressive exhaustion
• Severe hypoxia despite maximal oxygen delivery
• Failure to reverse severe respiratory acidosis despite intensive therapy
• pH <7.2, carbon dioxide pressure increasing by more than 5mmHg/hr or greater than 55 to 70mm/Hg, or oxygen pressure of less than 60mm/Hg.

Challenges:

• Effective pre-oxygenation impossible
• No margin for error or delay
• Need to be intubated by most experienced person available
• High intrathoracic pressure after RSI

Recommendations:

• Fluid bolus before intubation if possible
• RSI preferred
• Ketamine for bronchodilator effects
• Permissive hypercapnea essential

Initial Ventilator settings in paralysed patients:

• FiO2 1.0, then titrate to keep SpO2 >94%
• Tidal Volume 5-6ml/kg
• Ventilator rate 6-8 breaths/min
• Long expiratory time (I:E ratio >1:2)
• Minimal PEEP < 5cmH2O
• Limit peak inspiratory pressure to <40cmH2O
• Target plateau pressure <20cmH2O
• Ensure effective humidification

• Brenner, B. Corbridge, T. & Kazzi, A. (2009). Intubation and mechanical ventilation of the asthmatic patient in respiratory failure. The Journal of Emergency Medicine. 37(2s), s23-s34.
• Camargo, C. Rachelefsky, G. & Schatz, M. (2009). Managing Asthma Exacerbation in the Emergency Department: Summary of the National Asthma Education and Prevention Program Expert Panel Report 3 Guidelines for the Management of Asthma Exacerbation.The Journal of Emergency Medicine. 37 (2S), S6-S17.
• Camargo, C. Spooner, C. & Rowe, B. (2009). Continuous versus intermittent beta-agonist for acute asthma (Review). http://www.thecochranelibrary.com.
• Chua, F. & Lai, D. (2007). Acute severe asthma: Triage, treatment and thereafter. Current Anaesthesia & Critical Care. 18, 61-68.
• Creagh-Brown, B. & Ball, J. (2007). An under-recognized complication of treatment of acute severe asthma. American Journal of Emergency Medicine. 26, 513-515.
• Hodder, R. et al. (2009). Management of acute asthma in adults in the emergency department: nonventilatory management.  CMAJ. 182(2), E55-E67.
• Holley, A. & Boots, R.(2009). Review article: Management of acute severe and near-fatal asthma. Emergency Medicine Australasia, (21) 259-268.
• Jones, L. & Goodacre, S. (2009). Magnesium sulphate in the treatment of acute asthma: evaluation of current practice in adult emergency departments. Emergency Medicine Journal. 26, 783-785.
• Melnick, E. & Cottral, J. (2010). Current Guidelines for Management of Asthma in the Emergency Department.  http://www.ebmedicine.net. 2(2). 1-13.
• Morris, F. & Fletcher, A. (Ed). (2009). ABC of Emergency Differential Diagnosis. Oxford: Blackwell Publishing
• National Asthma Council of Australia. Asthma management handbook: 2006. Accessed http://www.nationalasthma.org.au/cms/images/stories/amh2006_web_5.pdf, 12/02/2010
• Nowak, R. Corbridge, T. & Brenner, B. (2009). Noninvasive Ventilation. The Journal of Emergency Medicine. 37(2S), S18-S22.
• Peters, S. (2007). Continuous Bronchodilator Therapy. Chest. 131(1),1-5.
• Phipps, P. & Garrard, C. (2003). The pulmonary physician in critical care. 12: Acute severe asthma in the intensive care unit. Thorax. 58, 81-88.
• Ram, F. Wellington, S. Rowe, B. & Wedzicha, J. (2009). Non-invasive positive pressure ventilation for treatment of respiratory failure due to severe acute exacerbations of asthma (Review)
• Rodrigo, G. Pollack, C. Rodrigo, C. Rowe, B. (2010). Heliox for non-intubated acute asthma patents (Review).
• Rowe, B. Spooner, C. Ducharme, F. Bretzlaff, J. Bota, G. (2008). Early emergency department treatment of acute asthma with systemic corticosteroids (Review). http://www.thecochranelibrary.com.
• Rowe, B. et al. (2009). Magnesium sulfate for treating exacerbations of acute asthma in the emergency department (Review). http://www.thecochranelibrary.com.

Emergency nurse with ultra-keen interest in the realms of toxicology, sepsis, eLearning and the management of critical care in the Emergency Department | LinkedIn |

Leave a Reply Cancel reply

This site uses Akismet to reduce spam. Learn how your comment data is processed .

WILLIAM DABBS, MD, MEGAN H. BRADLEY, MD, AND SHAUNTA' M. CHAMBERLIN, PharmD

Am Fam Physician. 2024;109(1):43-50

Author disclosure: No relevant financial relationships.

Asthma exacerbations, defined as a deterioration in baseline symptoms or lung function, cause significant morbidity and mortality. Asthma action plans help patients triage and manage symptoms at home. In patients 12 years and older, home management includes an inhaled corticosteroid/formoterol combination for those who are not using an inhaled corticosteroid/long-acting beta 2 agonist inhaler for maintenance, or a short-acting beta 2 agonist for those using an inhaled corticosteroid/long-acting beta 2 agonist inhaler that does not include formoterol. In children four to 11 years of age, an inhaled corticosteroid/formoterol inhaler, up to eight puffs daily, can be used to reduce the risk of exacerbations and need for oral corticosteroids. In the office setting, it is important to assess exacerbation severity and begin a short-acting beta 2 agonist and oxygen to maintain oxygen saturations, with repeated doses of the short-acting beta 2 agonist every 20 minutes for one hour and oral corticosteroids. Patients with severe exacerbations should be transferred to an acute care facility and treated with oxygen, frequent administration of a short-acting beta 2 agonist, and corticosteroids. The addition of a short-acting muscarinic antagonist and magnesium sulfate infusion has been associated with fewer hospitalizations. Patients needing admission to the hospital require continued monitoring and systemic therapy similar to treatments used in the emergency department. Improvement in symptoms and forced expiratory volume in one second or peak expiratory flow to 60% to 80% of predicted values helps determine appropriateness for discharge. The addition of inhaled corticosteroids, consideration of stepping up asthma maintenance therapy, close follow-up, and education on asthma action plans are important next steps to prevent future exacerbations.

• Immediate, unlimited access to all AFP content
• More than 130 CME credits/year
• AAFP app access
• Print delivery available

Issue Access

• Immediate, unlimited access to this issue's content
• CME credits

Article Only

• Immediate, unlimited access to just this article

The Global Asthma Report 2022. Int J Tuberc Lung Dis. 2022;26(supp 1):1-104.

Centers for Disease Control and Prevention. Most recent national asthma data. Accessed January 17, 2023. https://www.cdc.gov/asthma/most_recent_national_asthma_data.htm

McCoy K, Shade DM, Irvin CG, et al.; American Lung Association Asthma Clinical Research Centers. Predicting episodes of poor asthma control in treated patients with asthma. J Allergy Clin Immunol. 2006;118(6):1226-1233.

Meltzer EO, Busse WW, Wenzel SE, et al. Use of the Asthma Control Questionnaire to predict future risk of asthma exacerbation. J Allergy Clin Immunol. 2011;127(1):167-172.

Schatz M, Zeiger RS, Yang SJ, et al. The relationship of asthma impairment determined by psychometric tools to future asthma exacerbations. Chest. 2012;141(1):66-72.

Loymans RJB, Honkoop PJ, Termeer EH, et al. Identifying patients at risk for severe exacerbations of asthma: development and external validation of a multivariable prediction model [published correction appears in Thorax . 2018; 73(8): 795–796]. Thorax. 2016;71(9):838-846.

National Heart, Lung, and Blood Institute. National Asthma Education and Prevention Program. Expert panel report 3: guidelines for the diagnosis and management of asthma. 2007. Accessed June 15, 2023. https://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.htm

Reddel HK, Taylor DR, Bateman ED, et al. An official American Thoracic Society/European Respiratory Society statement: asthma control and exacerbations: standardizing endpoints for clinical asthma trials and clinical practice. Am J Respir Crit Care Med. 2009;180(1):59-99.

Jackson DJ, Bacharier LB. Inhaled corticosteroids for the prevention of asthma exacerbations. Ann Allergy Asthma Immunol. 2021;127(5):524-529.

Pollart SM, Compton RM, Elward KS. Management of acute asthma exacerbations. Am Fam Physician. 2011;84(1):40-47.

Global Initiative for Asthma. Global strategy for asthma management and prevention. 2023. Accessed June 15, 2023. https://ginasthma.org/wp-content/uploads/2023/07/GINA-2023-Full-report-23_07_06-WMS.pdf

Gibson PG, Powell H. Written action plans for asthma: an evidence-based review of the key components. Thorax. 2004;59(2):94-99.

Abramson MJ, Bailey MJ, Couper FJ, et al.; Victorian Asthma Mortality Study Group. Are asthma medications and management related to deaths from asthma?. Am J Respir Crit Care Med. 2001;163(1):12-18.

Salazar G, Tarwala G, Reznik M. School-based supervised therapy programs to improve asthma outcomes: current perspectives. J Asthma Allergy. 2018;11:205-215.

Cicutto L, To T, Murphy S. A randomized controlled trial of a public health nurse-delivered asthma program to elementary schools. J Sch Health. 2013;83(12):876-884.

Sobieraj DM, Weeda ER, Nguyen E, et al. Association of inhaled corticosteroids and long-acting β-agonists as controller and quick relief therapy with exacerbations and symptom control in persistent asthma: a systematic review and meta-analysis. JAMA. 2018;319(14):1485-1496.

Raymond TJ, Peterson TA, Coulter J. Chronic asthma treatment: common questions and answers. Am Fam Physician. 2023;107(4):358-368.

Cloutier MM, Baptist AP, Blake KV, et al. Expert Panel Working Group of the National Heart, Lung, and Blood Institute administered and coordinated National Asthma Education and Prevention Program Coordinating Committee. 2020 focused updates to the asthma management guidelines [published correction appears in J Allergy Clin Immunol . 2021; 147(4): 1528–1530]. J Allergy Clin Immunol. 2020;146(6):1217-1270.

Szefler SJ. Update on the NAEPPCC asthma guidelines: the wait is over, or is it?. J Allergy Clin Immunol. 2020;146(6):1275-1280.

Kim LHY, Saleh C, Whalen-Browne A, et al. Triple vs dual inhaler therapy and asthma outcomes in moderate to severe asthma: a systematic review and meta-analysis. JAMA. 2021;325(24):2466-2479.

Kew KM, Flemyng E, Quon BS, et al. Increased versus stable doses of inhaled corticosteroids for exacerbations of chronic asthma in adults and children. Cochrane Database Syst Rev. 2022(9):CD007524.

O’Byrne PM, FitzGerald JM, Bateman ED, et al. Inhaled combined budesonide-formoterol as needed in mild asthma. N Engl J Med. 2018;378(20):1865-1876.

Bateman ED, Reddel HK, O’Byrne PM, et al. As-needed budesonide-formoterol versus maintenance budesonide in mild asthma. N Engl J Med. 2018;378(20):1877-1887.

Crossingham I, Turner S, Ramakrishnan S, et al. Combination fixed-dose beta agonist and steroid inhaler as required for adults or children with mild asthma. Cochrane Database Syst Rev. 2021(5):CD013518.

Nwaru BI, Ekström M, Hasvold P, et al. Overuse of short-acting β 2 -agonists in asthma is associated with increased risk of exacerbation and mortality: a nationwide cohort study of the global SABINA programme. Eur Respir J. 2020;55(4):1901872.

Sturdy PM, Victor CR, Anderson HR, et al.; Mortality and Severe Morbidity Working Group of the National Asthma Task Force. Psychological, social and health behaviour risk factors for deaths certified as asthma: a national case-control study. Thorax. 2002;57(12):1034-1039.

Pumphrey RSH, Gowland MH. Further fatal allergic reactions to food in the United Kingdom, 1999–2006. J Allergy Clin Immunol. 2007;119(4):1018-1019.

Alvarez GG, Schulzer M, Jung D, et al. A systematic review of risk factors associated with near-fatal and fatal asthma. Can Respir J. 2005;12(5):265-270.

Chang YL, Ko HK, Lu MS, et al. Independent risk factors for death in patients admitted for asthma exacerbation in Taiwan. NPJ Prim Care Respir Med. 2020;30(1):7.

Roberts G, Patel N, Levi-Schaffer F, et al. Food allergy as a risk factor for life-threatening asthma in childhood: a case-controlled study. J Allergy Clin Immunol. 2003;112(1):168-174.

Nowak RM, Tomlanovich MC, Sarkar DD, et al. Arterial blood gases and pulmonary function testing in acute bronchial asthma. Predicting patient outcomes. JAMA. 1983;249(15):2043-2046.

White CS, Cole RP, Lubetsky HW, et al. Acute asthma. Admission chest radiography in hospitalized adult patients. Chest. 1991;100(1):14-16.

Perrin K, Wijesinghe M, Healy B, et al. Randomised controlled trial of high concentration versus titrated oxygen therapy in severe exacerbations of asthma. Thorax. 2011;66(11):937-941.

Rowe BH, Spooner CH, Ducharme FM, et al. Corticosteroids for preventing relapse following acute exacerbations of asthma. Cochrane Database Syst Rev. 2007(3):CD000195.

Edmonds ML, Milan SJ, Camargo CA, et al. Early use of inhaled corticosteroids in the emergency department treatment of acute asthma. Cochrane Database Syst Rev. 2012(12):CD002308.

Kirkland SW, Vandenberghe C, Voaklander B, et al. Combined inhaled beta-agonist and anticholinergic agents for emergency management in adults with asthma. Cochrane Database Syst Rev. 2017(1):CD001284.

Kew KM, Kirtchuk L, Michell CI. Intravenous magnesium sulfate for treating adults with acute asthma in the emergency department. Cochrane Database Syst Rev. 2014(5):CD010909.

Weber EJ, Silverman RA, Callaham ML, et al. A prospective multicenter study of factors associated with hospital admission among adults with acute asthma. Am J Med. 2002;113(5):371-378.

Grunfeld AF, Fitzgerald JM. Discharge considerations for adult asthmatic patients treated in emergency departments. Can Respir J. 1996;3(5):322-327.

Arnold DH, Gebretsadik T, Minton PA, et al. Assessment of severity measures for acute asthma outcomes: a first step in developing an asthma clinical prediction rule. Am J Emerg Med. 2008;26(4):473-479.

Hasegawa T, Ishihara K, Takakura S, et al. Duration of systemic corticosteroids in the treatment of asthma exacerbation; a randomized study. Intern Med. 2000;39(10):794-797.

Jones AM, Munavvar M, Vail A, et al. Prospective, placebo-controlled trial of 5 vs 10 days of oral prednisolone in acute adult asthma. Respir Med. 2002;96(11):950-954.

Chang AB, Clark R, Sloots TP, et al. A 5- versus 3-day course of oral corticosteroids for children with asthma exacerbations who are not hospitalised: a randomised controlled trial. Med J Aust. 2008;189(6):306-310.

Krishnan JA, Davis SQ, Naureckas ET, et al. An umbrella review: corticosteroid therapy for adults with acute asthma. Am J Med. 2009;122(11):977-991.

Higgins JC. The ‘crashing asthmatic.’. Am Fam Physician. 2003;67(5):997-1004.

Continue Reading

More in AFP

More in pubmed.

Copyright © 2024 by the American Academy of Family Physicians.

This content is owned by the AAFP. A person viewing it online may make one printout of the material and may use that printout only for his or her personal, non-commercial reference. This material may not otherwise be downloaded, copied, printed, stored, transmitted or reproduced in any medium, whether now known or later invented, except as authorized in writing by the AAFP.  See permissions  for copyright questions and/or permission requests.

Copyright © 2024 American Academy of Family Physicians. All Rights Reserved.

An official website of the United States government

The .gov means it’s official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

• Publications
• Account settings

Preview improvements coming to the PMC website in October 2024. Learn More or Try it out now .

• Advanced Search
• Journal List
• v.182(2); 2010 Feb 9

Management of acute asthma in adults in the emergency department: nonventilatory management

Associated data.

Peter, a 26-year-old man with chronic, poorly controlled asthma, presents to a walk-in clinic reporting increasing asthma symptoms over a period of one week. He has been needing up to 20 puffs of salbutamol per day. An acute exacerbation of asthma is diagnosed, and the patient is immediately referred to the emergency department.

Acute asthma is a common medical emergency, which, despite repeated review 1 – 6 and the publication of international 7 and national 8 guidelines, including the Canadian Asthma Consensus Guidelines, 9 – 11 often remains poorly managed. 12 – 20 Although there are some signs that evidence-based management of this disorder is improving, 17 , 21 – 23 a recent survey of the management of asthma in children and adults in the emergency department revealed wide variations in care and substantial gaps in management in certain key areas. 19 These included poor adherence to published guidelines on the management of asthma, infrequent measurement of peak expiratory flow, infrequent use of systemic corticosteroids and poor rates of referral to asthma educational services.

Exacerbations of asthma account for about 25% of the total costs of asthma care in Canada. 24 Most exacerbations treated in the emergency department resolve within two hours after presentation. Only about 6%–13% of affected patients require admission to hospital, 17 , 25 and far fewer require admission to a critical care unit.

The most common triggers of exacerbations are viral infections and environmental allergens. Exposures in the workplace (to allergens, sensitizers or irritants) can also trigger exacerbations. 26 The onset and duration of symptoms and the worsening of airflow obstruction before presentation are variable, but these problems usually occur over several hours. 2 , 27 Even in fatal or near-fatal attacks, this means there is potential for early recognition and aggressive treatment. Rarely, a patient has rapid, catastrophic onset of acute asthma, which can be fatal. Whether this reflects a separate phenotype of asthma is unclear. 2 , 6 , 28 – 33

Although the prevalence of asthma is increasing, the overall rate of death from asthma has been falling in Canada, from 400–500 deaths in 1995 34 to 268 deaths in 2004. 35 Asthma mortality rates increase with age. 35 Overall mortality from acute exacerbations is low (< 0.1%), and most deaths related to asthma occur before arrival at a hospital. There are many risk factors for death or near death from acute asthma ( Table 1 ), but a key contributor is failure of patients or physicians to appreciate the severity of the exacerbation, which leads to delayed and insufficiently aggressive treatment. 40 , 47 , 75 – 77 Of note, both heightened and blunted perception of asthma symptoms have been implicated in excess morbidity and mortality related to asthma. 27 , 51 , 62 , 64 , 78 – 81 Patients with blunted perception of their symptoms do not recognize that an exacerbation is occurring and therefore permit the exacerbation to progress before seeking help. Patients with heightened sensitivity to symptoms may exhibit overreliance on short-acting β 2 -adrenergic bronchodilators, which can also result in delays in seeking definitive treatment.

Risk factors for potentially fatal asthma

Effective and efficient treatment of acute asthma in the emergency department requires prompt recognition of the signs and symptoms that indicate a potentially fatal asthma attack ( Table 2 ). Appropriate management of patients whose distress persists despite aggressive initial therapy also requires an awareness of conditions that may mimic an acute attack of asthma ( Box 1 ).

Box 1. Conditions that may mimic acute asthma

• Upper airway obstruction
• Foreign-body aspiration
• Vocal cord dysfunction syndrome 85 – 87
• Pulmonary edema
• Acute exacerbation of chronic obstructive pulmonary disease
• Hysterical conversion reaction
• Munchausen syndrome

Signs and symptoms that may suggest a potentially fatal asthma attack

Once the acute exacerbation has been managed, most patients will be well enough for discharge from the emergency department. In both Canada and the United States, however, relapse rates remain unacceptably high, ranging from 12% to 16% within two weeks after treatment in the emergency department in one recent study. 17 To reduce the risk of relapse, optimizing management after discharge should be a high priority, but observations suggest that discharge planning in this setting is poor. 23 This may reflect an underappreciation of the important role of patient education in the emergency department. 20 , 23 , 88 – 90 Most patients, but especially those with frequent or severe exacerbations and those who meet other high-risk criteria ( Table 1 ), will benefit from formal referral to an asthma specialist or an asthma educator. 91 , 92

Sources of information

In this article, we present the Canadian Thoracic Society’s updated evidence-based key messages for the nonventilatory management of acute asthma. A separate article in this series addresses assisted ventilation for acute asthma. 93 In collating evidence for this update, we did not undertake a formal meta-analysis. Instead, we used the comprehensive PubMed search that was used by the Global Initiative for Asthma group, 7 extending it to August 2009. This search strategy used the following criteria: “asthma,” “adults,” “all fields,” “only items with abstracts,” “clinical trial,” “human” and “all dates.” We included the following additional criteria: “status asthmaticus,” “near fatal asthma,” “acute disease” and “all languages.” We used the same terms to search the database of the Cochrane Airways Group. We also searched for review articles in the Evidence-Based Medicine Reviews from the Cochrane (CENTRAL), MEDLINE, CINAHL and EMBASE databases using the search criteria “acute severe asthma,” “life-threatening asthma” and “status asthmaticus.” We searched the bibliographies of all identified reviews for additional relevant publications. We also reviewed three recent evidence-based guidelines (the Global Initiative for Asthma, 7 the British Guideline on the Management of Asthma 8 and the report of a joint task force of the American Academy of Asthma, Allergy and Immunology, the American Academy of Emergency Medicine and the American Thoracic Society 94 ) and their respective bibliographies. At least two members of the Canadian Thoracic Society Asthma Committee who were also authors of the current report verified relevant references and assigned the recommendation grades and levels of evidence.

We based our grades of evidence on those of the Canadian Task Force on Preventive Health Care, 95 as detailed in a previous article in this series. 96 Because of the difficulty of conducting randomized controlled trials of potentially fatal asthma, some of the key messages presented later in this article represent only grade I recommendations based on level II-3 or level III evidence.

Overview of managing acute asthma in the emergency department

Optimum management of acute asthma in the emergency department requires rapid access to facilities and personnel capable of delivering bronchodilators appropriately, obtaining objective assessment of the severity of the episode (by measurement of lung function), appropriately monitoring oxygen delivery and ensuring safe disposition and referral of patients with asthma.

The general approach to caring for a patient with acute asthma in the emergency department starts with an initial quick assessment to determine whether the patient has any of the risk factors for ( Table 1 ) or signs or symptoms of ( Table 2 ) potentially fatal asthma. Patients meeting these criteria should be immediately triaged to a closely monitored setting within the emergency department for at least one to two hours after arrival. Because acute asthma is an inherently unstable and unpredictable condition, an intravenous line should be inserted and oxygenation continuously assessed and recorded by pulse oximetry. It is important to obtain objective measurements of lung function in this setting; therefore, all patients should undergo either baseline spirometry (to determine forced expiratory volume in 1 second [FEV 1 ]) or measurement of peak expiratory flow rate, and these measurements should be repeated every 30–60 minutes to help guide therapy. Following the principles of concurrent management, 97 treatment with supplemental oxygen and inhaled β 2 -adrenergic bronchodilators should begin simultaneously with the initial assessment, and consideration should also be given to administering an oral or intravenous dose of corticosteroids immediately. Subsequent care will be determined in part by the response to initial therapy and should follow the recommendations outlined below. All health care professionals treating patients in the emergency setting should be skilled in crisis resource management, which involves good communication, delegation of tasks and frequent re-evaluation and reassessment of the patient. 97

Most of the recommendations for treating acute asthma that appeared in the 1996 guidelines of the Canadian Association of Emergency Physicians and the Canadian Thoracic Society 9 and in the 1999 Canadian Asthma Consensus Guidelines 10 , 11 remain unchanged. Here, we summarize new evidence on the potential role of inhaled corticosteroids in the management of acute asthma. The recommendations presented here either extend or do not differ substantially from other recently published national 8 , 9 and international 7 guidelines for the management of acute asthma.

Although initial attention should focus on acute treatment, management of acute asthma begins with assessing the severity of the attack and determining whether the patient is at risk of potentially fatal asthma.

The case continued

The patient is immediately started on supplemental oxygen 40% by mask and is given inhaled bronchodilators. Fifteen minutes later, he is breathing somewhat more easily and is able to provide additional history. He reports that as a child he had numerous allergies. Now, he is living in a mouldy basement apartment with a roommate who owns a cat. Although he has prescriptions for salmeterol and fluticasone combined in a single inhaler, he is unemployed and unable to afford this medication. The last time he took inhaled cortico steroids was three weeks ago, when he finished a physician’s sample of budesonide. Since then, he has been relying on salbutamol, which he has been getting from several walk-in clinics. In addition, he has received two short courses of oral corticosteroids in the past three months.

Assessment and monitoring

Meta-analyses and systematic reviews 2 , 7 , 8 , 38 , 55 , 56 , 58 , 76 , 98 , 99 and case–control 27 , 29 , 36 , 39 , 42 , 46 , 51 , 54 , 64 , 65 , 73 and observational 37 , 40 , 66 , 68 , 100 studies have identified clinical and historical features that can be used to identify patients at high risk for fatal or near-fatal asthma ( Table 1 ). An evaluation for these risk factors is important because when stable, patients who have survived a near-fatal episode of asthma are indistinguishable from other patients with asthma, at least on clinical grounds. 31 The strongest predictor of potentially fatal asthma is a history of previous admission to hospital or intensive care for asthma. 6 , 27 , 38 Patients with such a history should be identified and monitored closely during the first one to two hours after arrival in the emergency department, regardless of apparent stability or improvement in response to initial therapy. Prior history of unstable or poorly controlled asthma or recent need for aggressive management (e.g., systemic corticosteroids) should also alert the treating health care professional to the possibility that the patient’s asthma could be resistant to first-line treatment and therefore might escalate in severity and become life-threatening. Obtaining a thorough history of the patient’s use of prescription and nonprescription medications and recent adherence with therapy is important, because this will affect planned initial and long-term management. Psychosocial factors may be associated with poorly controlled and potentially fatal asthma. 36 , 37 , 46 , 68 , 69 Patients with a poor perception of dyspnea have been identified in some 62 , 64 , 79 but not all 27 , 36 , 63 studies of risk factors for potentially fatal asthma, but there is no simple, validated way to test for this factor in a primary care setting. 101 Failure of the treating physician to appreciate the severity of the acute asthma attack and to initiate appropriately aggressive therapy has also been shown to be a risk factor for a fatal outcome. 40 , 47 , 75 – 77

There is some consensus about the signs and symptoms that may assist in the recognition of a potentially fatal exacerbation of asthma ( Table 2 ). 2 , 5 – 7 , 82 – 84 , 102 , 103 For example, diaphoresis and an inability to lie in the supine position have been correlated with severe airflow obstruction as measured by peak expiratory flow rate. Increasing heart rate is closely correlated with increasing severity of asthma, 104 and it is incorrect to assume that tachycardia is caused by use of a β 2 -adrenergic bronchodilator. 1 There is little correlation among the signs listed in Table 2 , which develop independently, and their presence is not generally predictive of adverse outcomes. 2 , 13 , 102 , 103 , 105

The absence of these symptoms and signs does not guarantee that the exacerbation is unimportant, as patients who appear well may have severe airflow obstruction. 2 Although pulsus paradoxus may correlate with the degree of obstruction, 106 it can diminish as the patient becomes fatigued and loses the ability to generate strong inspiratory efforts. Absence of pulsus paradoxus may therefore be wrongly interpreted as a sign of improvement. Measuring pulsus paradoxus in acute exacerbations is difficult and of limited prognostic use. 107 Similarly, the nature of wheeze has limited correlation with objective measures of airway obstruction and is a poor predictor of the need for admission to hospital. 2 , 5 , 108 However, the absence of wheeze in a patient with dyspnea or altered level of consciousness is an ominous sign. 50 Wheeze may return as airflow improves in response to therapy. The physical examination should also include assessment for stridor, which could indicate obstruction of the upper airway mimicking asthma. Asymmetric breath sounds and subcutaneous emphysema may indicate the presence of barotrauma, such as pneumothorax.

Measuring airflow obstruction

Both patients and physicians tend to inaccurately gauge the level of airflow obstruction, which can lead to undertreatment and hence an unacceptable risk of relapse. 62 , 78 – 81 , 102 , 105 , 109 Therefore, airflow obstruction must be measured objectively when-ever possible, using either FEV 1 or peak expiratory flow. Peak expiratory flow is an integral component of the Canadian Triage and Acuity Scale, a reliable and valid complaint-based triage tool developed by Canadian emergency nurses and physicians to prioritize the severity of a patient’s condition and the timing of care in the emergency department. 110 , 111 Measurements of airflow obstruction can help to guide therapy for acute asthma but are generally underutilized, 12 – 16 despite their ease of performance. In one prospective study, more than 90% of patients presenting to the emergency department with acute asthma had valid spirometry measurements when the test was administered by trained personnel. 112 Peak expiratory flow below 200 mL or less than 30% of predicted or FEV 1 below 1.0 L or less than 25% of predicted at any time during an exacerbation of asthma indicates a high degree of obstruction and suggests the presence of elevated partial pressure of carbon dioxide ( P CO 2 ) and the potential for fatigue of the respiratory muscles in particular and of the patient more generally. 1 , 2 , 83

Monitoring oxygen saturation

Oxygen saturation should be continuously monitored by pulse oximetry, because cyanosis is a late sign reflecting severe hypoxemia (arterial partial pressure of oxygen [ P O 2 ] < 40 mm Hg). For several reasons, oximetry is generally preferred over arterial blood gas analysis to assess oxygenation. Oximetry provides real-time, continuous measurements, whereas blood gases are monitored only intermittently and the samples take time to process. Oxyhemoglobin saturation is more meaningful than P O 2 in assessing arterial oxygen content. Finally, oximetry is much easier to perform and is less painful for the patient. Nonetheless, there are some caveats to the use of pulse oximetry. 113 To obtain reliable readings, the oximeter must be placed at a well-perfused site, and the pulse recorded by the oximeter should match the patient’s pulse determined manually, as a sign that the oximeter signal is strong. Pulse oximeters may not provide reliable data for patients with global hypoperfusion or peripheral vasoconstriction or in rare cases in which car-boxyhemoglobinemia or methemoglobinemia is a possibility. In the setting of acute asthma, determining arterial blood gas levels is indicated if there is concern that the patient is not improving and there are no oximetry data or if the data are thought to be unreliable.

Arterial blood gas analysis is rarely needed for optimum management of acute asthma. However, blood gas levels, either arterial or venous, should be determined if the treating physician wishes to know the P CO 2 and the pH, or if spirometry or peak expiratory measurements are either not available or not possible for a patient whose condition is not improving or is deteriorating. Venous pH and venous P CO 2 closely parallel arterial values and are adequate for identifying major acid–base disturbances. 114 – 116 Venous gas measurement may be preferred over arterial blood gas analysis because the venous sample can be drawn by anyone skilled at venipuncture and is less painful for the patient. However, the venous P O 2 and venous oxygen saturation should be ignored, as they are not representative of arterial values. The presence of hypercapnia can be inferred 112 if the FEV 1 is less than 25% of predicted or peak expiratory flow is less than 30% of predicted. 83 , 84 Hypercapnia during an acute asthma attack is a sign of severe airflow obstruction, but it does not always predict the need for assisted ventilation. 49 , 50 Because most exacerbations of asthma are associated with hyperventilation causing hypocapnia and respiratory alkalosis, the finding of rising or normal arterial or venous P CO 2 in the setting of acute asthma should be interpreted as a sign of impending respiratory failure and the possible need for assisted ventilation if it persists or worsens.

Additional investigations

Chest radiography should be performed if there is no response to therapy or if there is suspicion of an infectious cause, to identify or exclude unrecognized pneumothorax, pneumome-diastinum or pneumonia. 117 Obtaining an electrocardiogram is unnecessary for patients with acute asthma unless an acute coronary syndrome is suspected. Because most exacerbations of asthma are triggered by viral infections, sputum culture is not warranted unless the exacerbation is complicated or caused by obvious pneumonia.

Patients with combinations of the risk factors, signs and symptoms listed in Tables 1 and ​ and2 2 are at high risk of death and should be monitored closely, particularly during the first one to two hours after arrival in the emergency department, even if their condition seems to improve with initial therapy. The early response of FEV 1 or peak expiratory flow at 30 to 60 minutes after initial treatment is the best predictor of outcome. 3 , 103 , 105

At this point, a venous sample for blood gas analysis is obtained, and the patient attempts bedside peak flow measurement. The peak expiratory flow rate is about 25% of predicted. The venous pH is 7.32, and the venous P CO 2 is 50 mm Hg. Furthermore, his bicarbonate level is 25 mmol/L, which indicates that the hypercapnia is mostly acute (in relation to the current attack).

Because the patient has severe hypoxemia and is still in distress, despite initial treatment, a portable chest radiograph is ordered. Additional bronchodilator treatments (eight puffs each of salbutamol and ipratropium through a metered-dose inhaler with a valved holding chamber) are administered, along with 2 g of magnesium sulphate, given intravenously over 20 minutes. Next, eight puffs of fluticasone propionate are given by metered dose inhaler and chamber. The chest radiograph shows extreme hyperinflation, but no signs of pneumothorax, mediastinal or subcutaneous emphysema, or pneumonia.

Therapy for acute asthma

The rapidity of response to initial therapy, as defined by changes in symptoms, signs and FEV 1 or peak expiratory flow, may be a more useful measure of severity and the need for more aggressive therapy than the clinical status at presentation. 2 , 3 Definitions of the terms “status asthmaticus,” “life-threatening” or “near fatal,” and a “severe” episode of asthma are imprecise and should not be used to determine the level of therapy for acute asthma. Here, we use the term “moderate to severe asthma,” by which we mean patients who have no clinical improvement with initial standard therapy and those whose presenting FEV 1 or peak expiratory flow is less than 25%–30% of predicted.

The use of structured management plans and care maps for acute asthma has been shown to improve the use of objective measurements of airflow obstruction, increase the frequency of re-evaluation and reassessment, and reduce admission rates and length of stay in both the emergency department and the hospital. 1 , 21 , 23 , 118 – 122 A structured management plan, the emergency department asthma care pathway, 123 was recently prepared as part of the Asthma Plan of Action of the Ontario Ministry of Health and Long-Term Care 124 and has been endorsed by the Canadian Thoracic Society and the Canadian Association of Emergency Physicians (Appendix 1, available at www.cmaj.ca/cgi/content/full/cmaj.080072/DC1 ). It was modelled in part on a similar plan in an earlier Canadian guideline 9 and other successful care maps for asthma. 21 , 23 Based on clinical criteria, including objective indices of airflow obstruction, this care map classifies the severity of acute asthma in four categories: mild, moderate, severe and life-threatening. Each category is linked to the appropriate level in the Canadian Triage and Acuity Scale 111 to guide the timing and nature of both initial assessment and therapy.

Hypoxia is the main cause of death in cases of acute asthma. Therefore, oxygen should be titrated to achieve oxygen saturation of at least 92%. In general, supplemental oxygen will not suppress the drive to breathe in patients with acute asthma. Even though a slight rise in P CO 2 may occur in response to oxygen therapy, this is of no clinical consequence. 125

Bronchodilators

Rapid-acting inhaled β 2 -adrenergic bronchodilators are first-line therapy for acute asthma. Because the optimal doses necessary to achieve maximal bronchodilation have not been defined, dosing is empiric and should be titrated using an objective measure of airflow obstruction, such as FEV 1 or peak expiratory flow and clinical response. Recommended starting doses for bronchodilators and corticosteroids are unchanged from previous guidelines 9 – 11 and are listed in Appendix 1. These drugs are safe for patients with acute asthma, and the heart rate usually falls with successful response to high doses of β 2 -adrenergic bronchodilators in this setting. 126 Furthermore, these drugs remain effective for patients who have self-treated unsuccessfully with the same agents before arrival in the emergency department. 127 For patients with acute asthma, the inhaled route for bronchodilators is as good as or better than giving the same drugs intravenously. 128 – 131 Concerns have been raised about the safety of intravenously administered epinephrine for acute asthma, 132 but additional research is warranted. Intravenous administration of β 2 -adrenergic bronchodilators or intramuscular or subcutaneous administration of epinephrine 133 should be reserved for patients who are unable to use or who are unresponsive to the inhaled route. Such patients may require intubation and assisted ventilation.

Use of a pressurized metered-dose inhaler, preferably with a valved holding chamber or spacer, is at least as effective as wet nebulization in acute asthma 134 – 136 and has the advantages of lower cost and ability to provide sequential doses more quickly (four to eight puffs in 2 minutes v. 10–20 minutes for a single nebulization). It also provides an opportunity for health care professionals to demonstrate correct use of the inhaler to the patient. When nebulization is used in severe asthma, continuous nebulization appears superior to intermittent nebulization for improvements in airflow obstruction and reduction in the need for admission to hospital. 126 , 137 , 138

Although ipratropium bromide, a short-acting anticholinergic bronchodilator, has a slower onset of action than the β 2 -adrenergic bronchodilators, randomized controlled trials and a meta-analysis have shown that combining these two agents results in greater improvements in lung function and a significant reduction in the need for admission to hospital than use of β 2 -adrenergics alone, particularly for patients with severe airflow obstruction (FEV 1 ≤ 30% of predicted). 139 , 140 As with β 2 -adrenergic bronchodilators, multiple dosing from a metered-dose inhaler with a valved holding chamber or delivery by multiple wet nebulizations is recommended (Appendix 1, available at www.cmaj.ca/cgi/content/full/cmaj.080072/DC1 ).

Corticosteroids

A dose of systemic corticosteroids should be administered within the first hour of treatment for acute asthma for all but patients with the mildest form of the disease. 141 This therapy is particularly important for patients with severe asthma and those already receiving systemic corticosteroids, as recently confirmed by a large prospective study of asthma care that clearly demonstrated an inverse relation between need for hospital admission for acute asthma and time to administration of systemic corticosteroids. 19 There is no evidence from controlled trials of an advantage for the intravenous over the oral route for corticosteroids in moderate to severe asthma. 141 , 142 However, for patients with severe asthma who are too breathless to swallow an oral medication, who are experiencing nausea and vomiting, who have been intubated or who are unable to absorb oral medications, the intravenous route is preferred, at least initially. 143 Optimal doses of systemic corticosteroids for acute asthma have not been determined, but a meta-analysis and two systematic reviews suggested that doses equivalent to 30–80 mg prednisone or methylprednisolone per day (150–400 mg hydrocortisone) are adequate and that higher doses do not seem to confer added advantage. 142 , 144 , 145 Conventional doses for corticosteroids in acute asthma are listed in Appendix 1 (available at www.cmaj.ca/cgi/content/full/cmaj.080072/DC1 ).

Short-term administration of high-dose inhaled corticosteroids appears to accelerate recovery from acute asthma relative to systemic corticosteroids alone, particularly for patients with prolonged attacks and severe airflow obstruction. 146 – 148 The rapid effect of inhaled corticosteroids in acute asthma may reflect a mechanism of action different from their traditional anti-inflammatory effects. It has been postulated that high-dose inhaled corticosteroids have topical non-genomic effects on the airway epithelium, including vasoconstriction and mucosal decongestion. 147 Although it is possible that the addition of early, high-dose inhaled corticosteroids to systemic corticosteroids may confer additional benefit over the use of systemic corticosteroids alone, this has not yet been demonstrated, 149 and additional research is required. There is, however, insufficient evidence to suggest that inhaled corticosteroids should replace systemic corticosteroids for the treatment of severe acute asthma. 150

Other therapies

There is no support for the routine use of intravenous magnesium sulphate for acute asthma, but there is evidence that it is effective for patients with no response to first-line initial therapy and those with initial, severe airflow obstruction (FEV 1 or peak expiratory flow < 25%–30% predicted). 151 The need for admission to hospital can be reduced and measurements of airflow improved with a single bolus dose (2 g intravenously for adults), which has only minor and infrequent adverse effects. The authors of one systematic review suggested that the combination of aerosolized, rather than intravenous, magnesium sulphate with standard care (systemic corticosteroids and inhaled β 2 -adrenergic bronchodilators) lessened airflow obstruction and reduced admissions to hospital, 152 but additional research is required before this route of delivery can be widely adopted.

Aminophylline is not recommended for acute asthma, as systematic reviews have consistently concluded that it confers no additional benefits over β 2 -adrenergic bronchodilators alone. In addition, this drug has a narrow therapeutic margin and can cause substantial toxic effects, especially among hypoxemic patients. 153 , 154

Despite the biological plausibility of modulation of turbulent airflow, systematic reviews have concluded that there is no role for the routine use of helium–oxygen mixtures in the initial treatment of acute asthma. 155 , 156 There may, however, be benefit for patients with more severe airflow obstruction in whom aggressive first-line therapy has failed.

Acute wheezing and breathing distress may be caused by conditions other than asthma, some of which are listed in Box 1 . These conditions should be considered if reassessment indicates no response to initial first-line therapy.

Treatment in pregnancy

Exacerbations of asthma in pregnancy occur primarily in the late second trimester, the major triggers being viral infection and nonadherence with inhaled corticosteroid therapy. 157 Pregnant women with acute asthma appear to be treated less often with systemic corticosteroids than nonpregnant patients and are more likely to report continuing asthma exacerbation after discharge from the emergency department. 158 Because a severe asthma attack during pregnancy poses a greater risk to the fetus than do the adverse effects of asthma therapy, management of acute asthma in pregnancy should be no different than for nonpregnant patients.

Outcome of the case

The patient continues to receive additional bronchodilator therapy and gradually begins to improve. After two hours of therapy, he is breathing much more comfortably and is able to lie back, relax and sleep intermittently. Oxygen saturation is 92% with oxygen (4 L/min) administered by nasal cannulae, and he is no longer relying on his accessory muscles of breathing. Repeat spirometry and venous blood gas analysis reveal FEV 1 70% of predicted, peak expiratory flow 75% of predicted, pH 7.36 and venous P CO 2 46 mm Hg. He asks to be discharged home, stating that he will take his inhaled corticosteroid more regularly in the future. However, despite the strong response to treatment, this patient is clearly at very high risk for fatal asthma, and an urgent consultation with the internist on call is arranged. After the consultation, the patient agrees to a short admission.

Decision to admit

Both clinical and lung function data are used in making the decision to admit a patient to hospital. Patients who continue to exhibit indications of severe asthma despite two to three hours of aggressive treatment should probably be admitted. Several studies have identified factors associated with relapse after discharge from the emergency department. 159 , 160 The response to initial treatment is a better predictor of the safety of discharge from the emergency department or the need for hospital admission than is the apparent severity of an asthma exacerbation at presentation. 3 , 103 , 105 Patients who present with pretreatment FEV 1 or peak expiratory flow less than 25%–30% of predicted and those with values after treatment that are less than 40% of predicted should usually be admitted to hospital. 1 , 2 , 84 , 161 Patients who achieve FEV 1 or peak expiratory flow of at least 60% of predicted can usually be discharged safely, 84 , 162 , 163 provided adequate postdischarge care and follow-up are assured. For patients with intermediate FEV 1 or peak expiratory flow values (i.e., 40%–60% of predicted) after treatment, decision-making must be individualized on the basis of the examining physician’s knowledge of the patient’s previous ability to manage an exacerbation, the likelihood that the patient will be adherent with medications and instructions, and the home or environmental circumstances to which the patient will return. If there are concerns about adherence, particularly historical features suggesting that the patient has a high risk of fatal asthma ( Table 1 ), a cautious approach is prudent and a short admission (one or two days) may be indicated.

Prevention of relapse

To reduce the risk of relapse, most patients with moderate to severe asthma exacerbations and almost all patients who were previously taking inhaled corticosteroids should have a course of oral corticosteroids added at the time of discharge 164 , 165 (Appendix 1, available at www.cmaj.ca/cgi/content/full/cmaj.080072/DC1 , for dose and duration). Gradual tapering of the dose is unnecessary if the duration of oral corticosteroid use is less than one to two weeks. 164 , 166

In a randomized controlled trial, the addition of high-dose inhaled corticosteroids to a course of oral corticosteroids at discharge was associated with a lower risk of relapse of the asthma exacerbation at 21 days than the use of oral corticosteroids alone. 167 In a recent prospective study of asthma care in the emergency department, the risk of relapse at 28 days was inversely correlated with new prescriptions for inhaled corticosteroids at the time of discharge from the emergency department. 19 Studies comparing the effectiveness of high-dose inhaled and oral corticosteroids alone at the time of discharge from the emergency department for preventing relapse have not demonstrated any significant differences between these two management strategies, but additional studies are required. 168 , 169 The effect of combinations of a long-acting β 2 -adrenergic bronchodilator with an inhaled corticosteroid 170 or an inhaled corticosteroid with a leukotriene receptor antagonist in reducing rates of relapse after discharge have also been studied, 171 but there is currently insufficient evidence to recommend these approaches.

Adherence with medical advice after a hospital stay is reportedly poor among patients with acute asthma. 160 , 172 For example, 12% to 22% of patients leaving the emergency department do not fill their prescriptions. 173 , 174 Reasons for poor adherence are complex and include the cost of medications, a poor understanding of asthma and its therapy, limited access to health care professionals and psychological influences, including depression. 175 , 176 If the risk of relapse is considered high and the likelihood of adherence with the postdischarge asthma management plan is thought to be low, options include a short stay in hospital or an intramuscular dose of corticosteroid at discharge (see Appendix 1 for details). 177 – 179 The second of these approaches has been associated with a lower rate of relapse than placebo 178 but appears equivalent to a short course of oral corticosteroids. 164 , 177 , 179 The potential for adverse effects with corticosteroids does not appear to be higher with the intramuscular route than with oral administration. 177

There are no clinical markers to identify individuals at risk for sudden onset of a near-fatal asthma exacerbation, but any patient who survives such an attack should be referred to an asthma specialist for a thorough investigation, including occupational and allergy assessment. Furthermore, it seems prudent to give an autoinjector for epinephrine to these individuals and to anyone with a history of anaphylaxis or angioedema.

The majority of patients who experience an asthma exacerbation will have had poor asthma control preceding the exacerbation. Whether the patient is discharged from the emergency department or admitted to hospital, health care professionals treating the exacerbation should review with the patient what is meant by control of asthma and any barriers to achieving asthma control that may have existed before the exacerbation. Patient education should include the role of medications (especially the importance of anti-inflammatory therapy and the proper use of inhalers) and the importance of avoiding allergens, irritants and workplace exposures if appropriate. 26

Action plans

There is strong evidence to support the role of action plans detailing how to prevent and manage future exacerbations. 99 , 180 , 181 Written action plans specifying an increase in inhaled corticosteroid dose and a concurrent course of oral corticosteroids are effective in reducing admissions to hospital for acute asthma. 99 In contrast, verbal action plans are inadequate: in one study, the odds ratio for death from asthma was four times lower with a written action plan than with a verbal action plan. 73 In general, written action plans contain four essential elements: when to increase therapy, how to increase therapy, the duration of increased therapy and the point at which to cease self-management and seek medical help. 180 Canadian data have confirmed that simply handing out an action plan, without educational discussion, is ineffective in improving asthma control. 182 For some patients, the provision of an action plan based on use of a peak flow meter and asthma education can significantly reduce the risk of relapse, 183 but for most patients, action plans based on self-monitoring of symptoms seem to be just as efficacious as plans based on peak flow. 184 Many examples of asthma action plans are available (see, for example, www.asthmaguide-lines.com or www.lung.ca , or the sample action plan presented as an appendix to an earlier article in this series 185 ).

Reassessment and re-evaluation are crucial elements in achieving and maintaining control of asthma. Therefore, optimal management of an asthma exacerbation includes referral to the patient’s primary care physician, if possible, and/or to an asthma educator or asthma specialist, if available. In one randomized controlled trial, a scheduled appointment with a primary care provider, initiated in the emergency department, was associated with a higher prevalence of primary care follow-up (65%) than either advice alone (42%) or telephone reminders to seek follow-up (48%). 92 However, at one year, there were no differences among groups in terms of use of inhaled corticosteroids, visits to the emergency department or quality of life. Facilitated referral to an asthma specialist after treatment of acute asthma in the emergency department reduced the likelihood of relapse during the ensuing six months. 91

Inpatient treatment of acute asthma

The principles of inpatient treatment of acute asthma are the same as those outlined for therapy in the emergency department. Several studies have demonstrated that the use of structured care plans and observation units is associated with reduced rates of hospital admission and reduced lengths of stay. 119 , 121 , 186

Patients who require admission to hospital for asthma exacerbation have clearly demonstrated poor asthma control and should be referred to an asthma specialist. 91 , 99 , 187 The goals of such referral are to enhance the prospects for success of education related to self-management, which will involve development of a written action plan, to review any barriers to asthma control and to improve the likelihood of adherence with follow-up. If possible, such consultation should take place before the patient is discharged.

Gaps in knowledge and care

The key messages for the nonventilatory management of asthma in adults in the emergency department are presented in Box 2 , Box 3 and Box 4 .

Box 2. Key messages for assessment and monitoring of acute asthma *

• Historical features that identify patients at risk for potentially fatal asthma should be sought as part of the initial assessment of every acute exacerbation of asthma (grade B recommendation; level II-2 evidence).
• Features of the physical examination that characterize a severe and potentially fatal asthma attack should be sought as part of the initial assessment of every acute exacerbation of asthma (grade B recommendation; level II-2 evidence).
• Objective measurement of airflow obstruction, by means of spirometry or measurement of peak expiratory flow, is recommended for optimal management of acute asthma (grade B recommendation; level II-1 evidence).
• Measurement of arterial or venous blood gases is recommended in the presence of severe airflow obstruction, particularly if the forced expiratory volume in 1 second (FEV 1 ) or the peak expiratory flow is less than 40% of predicted or if the patient has had suboptimal response to first-line therapy (grade B recommendation; level II-2 evidence).
• Continuous monitoring of oxyhemoglobin saturation by transcutaneous pulse oximetry should be undertaken for all patients with acute exacerbation of asthma.
• Patients deemed at high risk for potentially fatal asthma should be closely monitored in a critical care area.
• Routine chest radiography is not required, especially if there is an appropriate response to bronchodilator therapy.
• Electrocardiography is not routinely required unless there is a high degree of suspicion for ischemic heart disease that might be aggravated by the exacerbation or its treatment.
• Routine examination and culture of sputum is not required.

Box 3. Key messages for treatment of acute asthma *

• The aggressiveness of treatment should be based on the degree of airflow obstruction and symptoms.
• The use of structured management plans, including care maps, is recommended for the treatment of acute asthma in the emergency department (grade A recommendation; level I evidence).
• Oxygen should be administered to all patients with acute asthma, with the goal of maintaining oxygen saturation at 92% or above.
• Rapid-acting inhaled β 2 -adrenergic bronchodilators are first-line therapy for acute asthma.
• Bronchodilators should be administered by inhalation and are equally effective with administration by nebulizer or by pressurized metered-dose inhaler, preferably with a valved holding chamber (grade A recommendation; level I evidence).
• The combined use of short-acting anticholinergic and β 2 -adrenergic bronchodilators is recommended for patients with moderate to severe acute asthma (grade A recommendation; level I evidence).
• A single dose of systemic corticosteroids within one hour of presentation to the emergency department is recommended for patients with moderate to severe acute asthma (grade A recommendation, level I evidence).
• Early, frequent use of high doses of inhaled corticosteroids, in addition to systemic corticosteroids, may be considered for patients with moderate to severe acute asthma.
• Intravenous administration of magnesium sulphate is recommended for patients with severe acute asthma that is unresponsive to therapy with bronchodilators and systemic corticosteroids (grade B recommendation; level II-I evidence).
• Intravenous administration of aminophylline is not recommended during the first four hours of treatment (grade E recommendation; level I evidence).
• Helium–oxygen mixtures should be reserved for patients with acute asthma that is unresponsive to standard first-line therapy who are likely to require assisted ventilation (grade C recommendation; level I evidence).
• Exacerbations of asthma during pregnancy should be treated aggressively in the same manner as for nonpregnant individuals.
• Patients whose acute asthma is not responding to appropriate therapy should be reviewed for the adequacy of current therapy and for conditions that may mimic or complicate asthma.

Box 4. Key messages for subsequent care of patients with acute asthma *

Decision to admit or discharge.

• Measurement of peak expiratory flow or forced expiratory volume in 1 second (FEV 1 ) is recommended to help in the decision to admit a patient with acute asthma to hospital or to safely discharge him or her from the emergency department (grade B recommendation; level II-1 evidence).
• Any patient with persisting signs and symptoms of severe asthma after two to three hours of appropriate and aggressive treatment should be admitted to hospital.

Prevention of relapse after discharge

• For patients with moderate to severe acute asthma, a short course of oral corticosteroids is recommended upon discharge from the emergency department to help reduce the risk of relapse of the asthma exacerbation (grade A recommendation; level I evidence).
• The combined use of high-dose inhaled corticosteroids and oral corticosteroids at the time of discharge from the emergency department is recommended to reduce the risk of relapse of the asthma exacerbation (grade A recommendation; level I evidence).
• If the risk for nonadherence with oral corticosteroid therapy after discharge from the emergency department and the risk of relapse are thought to be high, consideration may be given to administering an intramuscular dose of corticosteroid, instead of a course of oral corticosteroid (grade B recommendation; level II-2 evidence).
• People who survive sudden-onset, near-fatal exacerbations should be identified, their history should be studied for risk factors, and they should be given an autoinjector for epinephrine.
• Health care professionals should take the opportunity provided by an exacerbation of asthma to educate the patient about the definition of and how to achieve control of asthma.
• Upon discharge from the emergency department or hospital, every patient should have a written management plan (action plan) detailing how to prevent and manage future exacerbations (grade B recommendation; level II-1 evidence).
• Efforts should be directed at ensuring follow-up with a health care professional after a visit to the emergency department for management of an exacerbation of asthma (grade A recommendation; level I evidence).
• Consultation with an asthma specialist is recommended for patients who have been admitted to hospital for asthma.

Gaps in knowledge exist in several areas, representing opportunities for future research in the assessment and management of acute asthma.

Research is needed into ways of identifying the specific phenotype of asthma that is associated with high risk for potentially fatal asthma. 31 Sudden asphyxic asthma 30 may represent a particular phenotype, and efforts are needed to better characterize this relatively rare occurrence and its risk factors. Although it is known that poor preventive management of asthma predisposes people to poor asthma control and heightens the risk of death from asthma, novel methods for monitoring the adequacy of anti-inflammatory control of asthma should be developed and simplified for widespread use. 188 This might entail the development of serologic markers, simplified management of cytologic examination of induced sputum, or reliable and practical methods of analyzing exhaled breath condensate.

Wider use of structured management plans or care maps and observation units would help to standardize care and should be incorporated into the criteria for accreditation of hospitals. Strategies should be developed to increase the use of spirometry and the measurement of peak expiratory flow in the emergency department. 19 , 20 Educational strategies to improve the early recognition of potentially fatal exacerbations and to promote appropriate and timely aggressive intervention should also be developed.

The combination of inhaled β 2 -adrenergic and anticholinergic bronchodilators is useful in the management of acute asthma 139 , 140 but is currently not available in metered-dose inhaler format in Canada. Development of such a combination inhaler should be pursued as a means of making inhaled therapy of acute asthma more efficient. Research is needed on the role of early use of high-dose inhaled corticosteroids in addition to systemic corticosteroids for acute asthma, 147 as is research on the potential roles of aerosolized magnesium 152 and intravenous administration of leukotriene receptor antagonists 189 in this setting. Additional research is also needed on the role of helium–oxygen to improve the delivery of inhaled asthma medications, 155 as is research to develop novel ways of controlling airway inflammation in asthma, through low-dose theophylline 190 and the new phosphodiesterase inhibitors 191 and through the development of newer anti-inflammatory agents.

This article is the fifth in a seven-part case study series that was developed as a knowledge translation initiative of the Canadian Thoracic Society Asthma Committee. The series aims to educate and inform primary care providers and nonrespiratory specialists about the diagnosis and management of asthma. The key messages presented in the cases are not clinical practice guidelines but are based on a review of the most recent scientific evidence available. Financial support for the publication of this series has been provided, in part, by the Canadian Thoracic Society.

• A patient with a history of severe asthma exacerbations is at risk for potentially fatal asthma and will need close monitoring and aggressive therapy.
• Continuous monitoring of oxyhemoglobin saturation and objective measurement of airflow obstruction (by spirometry) or peak expiratory flow are necessary for optimal management of acute exacerbations of asthma.
• Bronchodilators should be administered by inhalation, with administration by nebulizer and by pressurized metered-dose inhaler (preferably with a valved holding chamber) being equally effective.
• Combined use of high-dose inhaled corticosteroids and oral corticosteroids at the time of discharge from the emergency department is recommended to reduce the risk of relapse of the asthma exacerbation.
• Upon discharge from the emergency department or the hospital, every patient should have a written management (action) plan detailing how to prevent and manage future exacerbations.

Articles to date in this series

• Subbarao P, Mandhane PJ, Sears MR. Asthma: epidemiology, etiology and risk factors. CMAJ 2009. DOI:10.1503/cmaj.080612.
• Kaplan AG, Balter MS, Bell AD, et al. Diagnosis of asthma in adults. CMAJ 2009. DOI:10.1503/cmaj.080006.
• Balter MS, Bell AD, Kaplan AG, et al. Management of asthma in adults. CMAJ 2009. DOI:10.1503/cmaj.080007.
• Chapman KR, McIvor RA. Asthma unresponsive to usual care. CMAJ 2009. DOI:10.1503/cmaj.090089.

Supplementary Material

Competing interests: Diane Lougheed has served on GlaxoSmithKline’s National Respiratory Epidemiology Advisory Board. She has received research grants from AllerGen NCE, Ception Therapeutics, Topigen Pharmaceuticals, the Ontario Ministry of Health and Long-Term Care, the Ontario Thoracic Society and the Queen’s University William M. Speare Endowment/Start Memorial Fund. Brian Rowe has received research funding and speaker fees from GlaxoSmithKline and AstraZeneca. He is supported by the 21st Century Canada Research Chairs program through the government of Canada. Mark FitzGerald has served on advisory boards for GlaxoSmith-Kline, AstraZeneca, Novartis, Pfizer, Boehringer-Ingelheim, Altana, Merck and Topigen. He has also been a member of speakers’ bureaus for Glaxo-SmithKline, AstraZeneca, Boehringer-Ingelheim, Pfizer and Merck. He has received research funding paid directly to the University of British Columbia from the Canadian Institutes of Health Research, AstraZeneca, Glaxo-SmithKline, Boehringer-Ingelheim, Merck, Wyeth, Schering, Genentech and Topigen. Mark FitzGerald is a member of the Global Initiative for Asthma (GINA) and is chair of the GINA Science Committee. Alan Kaplan has received honoraria for talks from AstraZeneca, GlaxoSmithKline, Nycomed, Boehringer-Ingelheim and Pfizer. He has served on advisory boards for Merck Frosst, Nycomed, AstraZeneca and Boehringer-Ingelheim. He has received travel reimbursement to meetings of the European Respiratory Society from Merck and AstraZeneca. Andrew McIvor and Rick Hodder have attended advisory board meetings and provided continuing medical education for which they have received honoraria from pharmaceutical companies involved in asthma management: AstraZeneca, Boehringer-Ingelheim, Graceway, GlaxoSmithKline, Novartis, Merck Frosst and Pfizer.

Funding: The Canadian Thoracic Society has received funding to facilitate the knowledge translation activities of the CTS Asthma Committee from AstraZeneca Canada, GlaxoSmithKline Inc., Merck Frosst Canada and Novartis Pharmaceuticals. None of the sponsors played a role in the collection, review, analysis or interpretation of the scientific literature or in any decisions regarding the key messages presented in the case studies.

Contributors: All authors contributed to the development and editing of the publication, and all approved the final version submitted for publication.

* All grade I recommendations, based on level II-3 or level III evidence, unless indicated otherwise.

This article has been peer reviewed.