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1. 2. 3. 4. 5. 6. 7. 8. 9. Guide to the Essentials in Emergency Medicine, 3rd Edition Chapter 46: Asthma Irwani Ibrahim; Goh Ee Ling; Malcolm Mahadevan DEFINITION Asthma is a chronic inflammatory disorder characterised by variable airway obstruction with recurrent or chronic wheeze and/or cough. Because the underlying pathophysiology is that of bronchial hyperreactivity due to airway inflammation, the cornerstone of therapy is steroids. CAVEATS “Wheezing is not always asthma”. Differentials to consider include the following: 1. Congestive cardiac failure 2. Upper airway obstruction 3. Bronchogenic carcinoma with obstruction 4. Bronchiectasis 5. Metastatic carcinoma with lymphangitic metastasis 6. Gastrooesophageal reflux (GERD) 7. Chronic obstructive pulmonary disease (COPD) Physical signs may be absent at the time of examination as symptoms are often transient but this does not exclude the diagnosis of asthma. Absence of rhonchi on auscultation may indicate a silent chest in severe, lifethreatening asthma. CLINICAL ASSESSMENT The aims of clinical assessment are as follows: 1. Determine the severity of acute asthmatic attack and treat accordingly (see Table 1). 2. Identify patients who are at high risk of dying from asthma (see Table 2). 3. Establish the patient’s current treatment and level of asthma control (see Table 3). The Global Initiative for Asthma (GINA) assessment of asthma control can be used to quantify and objectively monitor control, and guide therapy for both doctors and patients. History 1. Presenting symptoms: Triad of asthma symptoms are dyspnoea, wheezing and cough 2. Precipitating factors, e.g. dust and upper respiratory tract infection 3. Risk factors for asthmarelated deaths (see Table 2) 4. Current medications including recent dose changes and compliance Physical examination 1. General appearance: Mental state (agitated or drowsy), signs of respiratory distress and cyanosis 2. Vitals signs: Especially oxygen saturation levels (SpO2 ) 3. Respiratory: Prolonged expiratory phase, rhonchi, crepitations and air entry Investigations Not indicated in most cases and guided by clinical assessment. 1. Chest Xray: Indicated in patients not responding to initial therapy. Look for pneumothorax, pneumonia or congestive cardiac failure. 2. Arterial blood gas: During an asthma exacerbation, PaCO2 is often below normal (<40 mmHg). A normal PaCO2 is already a cause for concern, and a raised PaCO2 suggests a lifethreatening exacerbation. 3. Others: Full blood count and renal panel (especially for hypokalaemia due to nebulised salbutamol). TABLE 1 Classifying severity of asthma exacerbations Mild Moderate Severe Respiratory arrest imminent Speech Speak in sentences Speak in short phrases Speak only a few words Hardly able to talk Activity While walking Can lie down While talking Prefer to sit While at rest Sit upright Exhausted Feeble respiratory effort Mental state May be agitated Usually agitated Usually agitated Drowsy or confused Wheeze Moderate, often only end expiratory Loud, throughout exhalation Usually loud, throughout inhalation and exhalation No wheeze (“silent chest”) Respiratory rate Increased Increased Often >30/min Decreased Accessory muscles use Usually not Commonly Usually Paradoxical thoracoabdominal movement Pulse/minute <100 100–120 >120 Bradycardia SpO2% (room air) >95% 91–95% <91% Clinically cyanosed Peak expiratory flow (PEF) after initial bronchodilator OR % predicted or % personal best >80% 60–80% <60% or response lasts <2 hours TABLE 2 Factors that increase the risk of asthmarelated death A history of nearfatal asthma requiring intubation and mechanical ventilation Hospitalisation or emergency care visit for asthma in the past year Currently using or having recently stopped using oral corticosteroids (a marker of event severity) Not currently using inhaled corticosteroids Overuse of shortacting B agonists, especially use of more than one canister of salbutamol (or equivalent) monthly A history of psychiatric disease or psychosocial problems Poor adherence to asthma medications and/or poor adherence to (or lack of) a written asthma action plan Food allergy in patients with asthma TABLE 3 Global Initiative for Asthma (GINA) assessment of asthma control Asthma symptom control Controlled Partly controlled Uncontrolled In the past 4 weeks, has the patient had: Daytime asthma symptoms more than twice a week? Yes □ No □ None of these 1–2 of these 3–4 of these Any night waking due to asthma? Yes □ No □ Shortacting B agonist reliever for symptoms more than twice a week? Yes □ No □ Any activity limitations due to asthma? Yes □ No □ SPECIAL TIPS FOR GPs All asthmatics should be on a preventer inhaler. Daily use of a lowdose inhaled corticosteroid will reduce the risk of severe exacerbations and thus reduce asthma deaths in highrisk patients very cost effectively. During an acute asthma attack, the early use of an oral corticosteroid will reduce the risk of asthma death. Thus, nearly all patients who need nebulised treatment for acute severe asthma in the clinic need a course of oral prednisolone approximately 0.5 mg/kg/day for 5 to 7 days without the need to tail down. Patients who need frequent (more than once in 6 to 12 months) nebulisations for acute asthma are at high risk of asthmarelated death. MANAGEMENT The aims of emergency department therapy for asthma are as follows: 1. Ensure adequate oxygenation. 2. Reverse airflow obstruction. 3. Relieve inflammation. See Figure 1 for the asthma management flowchart. Supportive measures 1. The patient should be placed in at least a monitored area. In the presence of severe asthmatic attack, the patient should be managed in the critical care area. 2. Monitoring: Electrocardiogram, pulse oximetry and vital signs. 3. Support airway, breathing and circulation: a. Secure airway in patients with imminent respiratory arrest or severe asthma that is worsening despite appropriate treatment in the ED. Ketamine is the preferred induction agent. b. Administer supplemental oxygen. c. Obtain intravenous access (not necessary in mild attacks). d. The use of noninvasive ventilation in asthma is controversial and not routine. Drug therapy 1. Bronchodilators a. Continuous inhaled shortacting betaagonist salbutamol in combination with ipratropium via nebulisation every 20 minutes for 1 hour. b. Addition of ipratropium has been shown to produce additional bronchodilation with minimal side effects. c. Pressured metereddose inhaler (pMDI) with a spacer can be used if aerosolisation with nebulisers is a cause for concern. 2. Steroids a. It reduces inflammation and also has an acute bronchodilator effect. b. Give oral prednisolone 0.5–1 mg/kg or intravenous hydrocortisone 100 mg. It should be administered within 1 hour of presentation. c. Steroids administered via the oral route are as rapid in onset and effective as that given via the intravenous route. 3. Magnesium sulphate a. Indicated in poor responders to bronchodilator therapy with moderate to severe asthma. b. Its mechanism of action is likely to inhibit smooth muscle contraction, decrease histamine release from mast cells and inhibit acetylcholine release. c. Give 1–2 g as an infusion over 30 minutes. Watch out for hypotension. Disposition 1. Patients who are intubated and require mechanical ventilation will be admitted to a medical intensive care unit. Note: Use low tidal volumes with slow respiratory rate of 6–8/min for patients that get intubated, keeping plateau pressure <30 mmHg, as with COPD; about 35 mmHg is when risk for barotrauma increases significantly. 2. Admit the following patients to a general ward under Respiratory Medicine or an observation unit if available in the emergency department. a. Patients who only respond partially and/or whose PEFR is <50% of predicted within 60 minutes. b. Patients who require secondline therapy with magnesium sulphate. c. Patients who respond to treatment but have risk factors for asthmarelated deaths. 3. Patients who improve symptomatically may be able to be discharged. Do the following: a. Check inhaler technique to ensure adequacy. b. Ensure a clear written asthma action plan. c. Advise patients to avoid precipitating factors, e.g. dust and fumes. d. Emphasise the importance of compliance with regard to followup and taking medications. e. Arrange for early followup with a respiratory specialist outpatient clinic. f. Initiate inhaled corticosteroids (if not previously prescribed) and prescribe 5 to 7 days’ course of oral corticosteroids. FIGURE 1 Flowchart showing the management of asthma REFERENCES/FURTHER READING Emerman CL, Cydulka RK, McFadden ER. Comparison of 2.5 mg vs 7.5 mg inhaled albuterol in the treatment of acute asthma. Chest. 1999;115(1):92– 6. [PubMed: 9925067] Brenner B, Kohn MS. The acute asthmatic patient in the ED: to admit or discharge. Am J Emerg Med. 1998;16(1):69–75. [PubMed: 9451319] McFadden ER, Casale TB, Edwards TB, et al. Administration of budesonide once daily by means of turbuhaler to subjects with stable asthma. J. Allergy Clinical Immunol. 1999;104(1):46–52. Quadrel M, Lavery RF, Jaker M, et al. Prospective randomized trial of epinephrine, metaproterenol and both in the prehospital treatment of asthma in the adult patient. Ann Emerg Med. 1995;26(4):469–73. [PubMed: 7574130] Lin RY, Rehman A. Clinical characteristics of adult asthmatics requiring intubation. J Med. 1995;26(5–6):261–77. [PubMed: 8721903] Global Initiative for Asthma. Global Strategy for Asthma Management and Prevention. Revised 2020. Available from: www.ginasthma.org Nathan RA, Sorkness CA, Kosinski M, et al. Development of the asthma control test: a survey for assessing asthma control. J Allergy Clin Immunol. 2004;113(1):59–65. [PubMed: 14713908] Silverman RA, Osborn H, Runge J, et al. IV magnesium sulfate in the treatment of acute severe asthma. Chest. 2002;122:489–97. [PubMed: 12171821] MOH Clinical Practice Guidelines 1/2008. Management of Asthma. 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