On-line version ISSN 2078-5135
SAMJ, S. Afr. med. j. vol.103 n.3 Cape Town Mar. 2013
U G LallooI; G M AinslieII; M S Abdool-GaffarIII; A A AwoteduIV; C FeldmanV; M GreenblattVI; E M IrusenVII; R MashVIII; S S NaidooIX; J O'BrienX; W OttoXI; G A RichardsXII; M L WongV (Official Working Group of the South African Thoracic Society)
IDepartment of Pulmonology and Critical Care, University of KwaZulu-Natal, Durban, MB ChB, FCP, MD, DOH, FCCP, FRCP
IIRespiratory Clinic, Groote Schuur Hospital and University of Cape Town, MB ChB, FRCP
IIIPulmonologist in private practice, Amanzimtoti, KwaZulu-Natal, MB ChB, FCP
IVDepartment of Medicine, Walter Sisulu University, Mthatha, Eastern Cape, MB BS, FMCP, FWACP, FRCP (Lond), FCP (SA)
VDivision of Pulmonology, University of the Witwatersrand, Johannesburg, MB BCh, DSc, PhD, FRCP, FCP (SA) M L Wong, MB BCh, FCP (SA), FCCP, FRCP (Lond)
VICentre for Chest Diseases, Milpark Hospital, Johannesburg, MB BCh, FCP (SA), FCCP
VIIDivision of Pulmonology, Department of Medicine, Stellenbosch University, MB ChB, FCP (SA), PhD
VIIIDepartment of Family Medicine and Primary Care, Stellenbosch University, MB ChB, MRCGP, FCFP (SA), PhD
IXFaculty of Health Sciences, Durban University of Technology, MB ChB, MFamMed, FCFP (SA), PhD
XPulmonologist in private practice, Cape Town, MB ChB, FCP (SA)
XIDepartment of Internal Medicine, University of the Free State, Bloemfontein, MB ChB, MMed (Int)
XIIDivision of Intensive Care, University of the Witwatersrand, MB BCh, PhD, FCP (SA), FRCP
Acute asthma attacks (asthma exacerbations) are increasing episodes of shortness of breath, cough, wheezing or chest tightness associated with a decrease in airflow that can be quantified and monitored by measurement of lung function (peak expiratory flow (PEF) or forced expiratory volume in the 1st second) and requiring emergency room treatment or admission to hospital for acute asthma and/or systemic glucocorticosteroids for management. The goals of treatment are to relieve hypoxaemia and airflow obstruction as quickly as possible, restore lung function, and provide a suitable plan to avoid relapse. Severe exacerbations are potentially life-threatening and their treatment requires baseline assessment of severity, close monitoring, and frequent reassessment using objective measures of lung function (PEF) and oxygen saturation. Patients at high risk of asthma-related death require particular attention. First-line therapy consists of oxygen supplementation, repeated administration of inhaled short-acting bronchodilators (beta-2-agonists and ipratropium bromide), and early systemic glucocorticosteroids. Intravenous magnesium sulphate and aminophylline are second- and third-line treatment strategies, respectively, for poorly responding patients. Intensive care is indicated for severe asthma that is not responsive to first-line treatment. Antibiotics are only indicated when there are definite features of bacterial infection. Factors that precipitated the acute asthma episode should be identified and preventive measures implemented. Acute asthma is preventable with optimal control of chronic asthma.
The prevalence of asthma is increasing worldwide, and surveys indicate that the majority of patients in developed and developing countries do not receive optimal care and are therefore not well controlled. The aim of this guideline is to promote an optimal standard of management of acute asthma in order to facilitate rapid recovery and transition to chronic care. It is intended as a companion to the management of chronic persistent asthma, as adherence to the latter plays a pivotal role in reducing acute asthma morbidity and mortality.
The South African Thoracic Society first published a guideline for the management of acute asthma in 1994. This 2013 update of the guideline was prompted by the need for:
- incorporation of advances in the pharmacological treatment of acute severe asthma
- early recognition and objective assessment of acute severe asthma
- optimal management and rapid transition to chronic care
- prevention of acute attacks
- harmonisation with international guidelines (e.g. Global Initiative for Asthma (GINA)).
The guideline was developed following meetings with a working group of pulmonologists and primary care/family medicine practitioners constituted by the South African Thoracic Society and chaired by Professor U G Lalloo. The initial meeting was held with the working group on 2 - 3 July 2005. Subsequently the editorial board was convened and met on several further occasions to develop and finalise this guideline document. The meetings were sponsored by the National Asthma Education Program (NAEP) of the South African Thoracic Society. This was made possible through unrestricted educational grants to the NAEP from the SA Thoracic Society, Altana Madaus (now Nycomed), AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline and MSD.
The strategies recommended in this guideline are classified according to the evidence categories in Table 1 and denoted as evidence A, B, C and D.
4. Acute asthma symptoms, acute asthma and exacerbations
The cardinal symptoms of asthma are cough, tightness of chest, wheeze and shortness of breath. There is remarkable variation in the perception of asthma symptoms and therefore concern for patients who have a blunted perception of the severity of their asthma symptoms.
Acute symptoms are episodic and are managed by self-medication with a reliever medication (inhalation of beta-2 (β2)-agonists). The frequent use of reliever medication indicates suboptimal control and demands attention to controller treatment.
Asthma exacerbations, also referred to as acute asthma or asthma attacks, result from frequent and progressive asthma symptoms and require early recognition to prevent morbidity and mortality. In some patients acute exacerbations may be of abrupt onset and progress rapidly to respiratory failure and death. An asthma exacerbation may be defined for practical purposes as a progressive (usually) or abrupt worsening in asthma symptoms, with increased use of bronchodilators (rescue medication) with progressively decreasing response and/or a decrease in pulmonary function as measured by PEF or spirometry.[1,2] The term status asthmaticus is used less often and refers to an asthma exacerbation that is severe and continuous.
The features of acute asthma are due to widespread narrowing of the airways. The pathophysiology of airway narrowing is complex, and smooth-muscle constriction, hypersecretion of mucus and mucus plugging of small airways, oedema of the airway wall with infiltration with inflammatory cells (e.g. neutrophils and eosinophils), and disruption of the airway epithelium are all involved.
5. Management of acute asthma
The management of acute asthma is summarised in Fig. 1. The key steps are:
5.1 Initial assessment and classification of severity
A brief history and physical examination should be conducted immediately the patient presents and at the same time as treatment is initiated. A detailed history may follow once the patient is stable and should include the duration and severity of symptoms, exercise tolerance, sleep disturbance, all current medications (including devices and doses prescribed and taken, time of onset and cause of the present attack, possible triggers, and presence of high-risk factors (see below)). The examination should assess the presence of any complications (e.g. pneumonia, lobar collapse or atelectasis, pneumothorax and pneumomediastinum). Objective functional assessments such as baseline PEF or FEV1 and arterial oxygen saturation (SpO2) measurements (by pulse oximetry) before starting treatment should be routine[1,3-7] (evidence C). PEF measurement is preferred in emergency units, hospital wards, primary care clinics and general practitioner surgeries because it is widely available, simple, inexpensive, portable and safe. A baseline PEF measurement should be made before treatment is initiated (see Appendix I, 'How to measure peak expiratory flow (PEF)'), but may not be possible in patients with severe respiratory distress. Arterial blood gas measurements are required if the SpO2 is <92% or the attack is responding poorly to treatment.[6,7] The measurement should be made while the patient is on supplemental oxygen. A chest radiograph is not routine but should be done if a complication or other disease (e.g. tuberculosis, lung cancer) is suspected or if there is poor response to treatment, but its acquisition must not compromise ongoing monitoring and treatment.
Acute asthma may be conveniently classified as mild, moderate or severe (life-threatening) based on symptoms, signs, and lung function and laboratory data. Table 2 summarises the features of acute asthma and criteria used to classify the severity of acute asthma.
5.2 Identification of patients at high risk
In addition to patients who are classified as having acute severe asthma, patients must also be considered as at high risk if they have any of the features listed in Table 3.[9,10] Such patients are at risk of rapid deterioration.
The goals of treating acute asthma are to:
- prevent worsening
- relieve airway obstruction (rapidly improves symptoms)
- treat hypoxia
- restore lung function to normal or previous best
- prevent relapse.
There are several classes of bronchodilators for acute asthma, each with a different mode of action and used sequentially depending on the response to treatment. They are presented in order of importance with a view to a stepwise approach to treatment.
Short-acting inhaled β2-agonists (SABAs), e.g. salbutamol and fenoterol, are the cornerstone of bronchodilator treatment for acute asthma exacerbations[1,11,12] (evidence A). They act by stimulating β2 receptors in the airways. When the patient responds well to SABAs (usually 2 or 3 doses given by nebulisation or metered dose inhalation) there is no need for any other bronchodilator treatment for acute asthma. The following are the key properties of SABAs:
- They are administered by inhalation, most commonly by nebulisation in acute asthma.
- They rapidly improve airway obstruction.
- They may be repeated as frequently as necessary depending on the patient's response: clinical improvement and improvement in peak flow to >60% predicted or >60% of previous best. Some experts propose 75%. β2-agonists may be administered continuously (every 20 minutes) in acute asthma.[13,14]
- In severe acute asthma, it is recommended that whenever possible they should be administered using an oxygen-driven nebuliser.
- They are relatively safe even in high doses when administered by nebulisation.
- They may be given by intravenous infusion in exceptional circumstances when nebulisation is not possible or is considered unreliable.
How to administer?
SABAs are administered repeatedly as the best way of achieving rapid reversal of airflow obstruction (Table 4)[11,12] (evidence A). If the attack is severe or life-threatening, delivery via an oxygen-driven nebuliser is mandatory. In mild to moderate exacerbations a metered dose inhaler (MDI) together with a large-volume spacer (LVS) produces at least an equivalent improvement in lung function and is more cost-effective. If using an MDI plus an LVS, put 2 puffs (100 µg/puff) into the LVS and advise the patient to take several deep breaths from the spacer, repeating the procedure for up to 20 puffs over 20 minutes for 1 hour. For nebulisation administer 5 mg salbutamol or 1 mg fenoterol, available in premixed unit dose vials (UDVs), initially. If a rapid response is not obtained, repeat the nebulisation every 20 minutes (continuously) for 1 hour. After the first hour, the frequency will depend on the severity of the attack and the response to initial treatment. No additional bronchodilator medication is necessary if the SABA produces a complete response (PEF returns to >60% of predicted or personal best) and the response is sustained for several hours. Consider continuous nebulisation (3 UDVs per hour) in patients with severe acute asthma (PEF or FEV1 <50% of previous best or predicted) and those poorly responsive to initial intermittent β2-agonist therapy[13,14] (evidence A).
Intravenous salbutamol is rarely used. It is given as an initial dose of 0.5 mg intravenously slowly, followed by a maintenance dose of 3 - 20 µg/min (5 mg diluted in 500 ml dextrose water or normal saline). It should be continued until there is sustained improvement (ideally <24 hours). Serum potassium and lactate should be monitored.
Inhaled ipratropium bromide is the only anticholinergic agent for the treatment of acute asthma. It achieves bronchodilation by a vagal pathway through inhibition of muscarinic receptors. Its bronchodilator effect in asthma is inferior to that of SABAs. The key properties of ipratropium bromide are:
- It is administered by inhalation only - most commonly by nebulisation or with an MDI with an LVS.
- There is no evidence that it provides significant additional bronchodilator effect to optimal doses of SABAs in mild to moderate acute asthma. It is therefore reserved as a second-line bronchodilator treatment for severe acute asthma.
- Combination with a SABA produces better bronchodilation than either drug alone[17,18] (evidence B) and is associated with lower hospitalisation rates in severe acute asthma[17,19] (evidence A). It is usually added to SABA nebulisation solution when there is poor or inadequate response to repeated doses of inhaled SABAs.
How to administer?
Ipratropium bromide may be administered in combination with a SABA every 20 minutes via a nebuliser at a dose of 0.5 mg in UDVs. It may also be administered via an MDI and LVS (20 µg/puff, up to 20 puffs).
18.104.22.168 Magnesium sulphate
Magnesium sulphate has recently been demonstrated to have bronchodilator effects and is of value (reducing hospital admission) in severe acute asthma when other bronchodilators fail[20-22] (evidence A). It probably works by inhibiting smooth-muscle contraction, decreasing histamine release from mast cells, and inhibiting acetylcholine release. The properties of magnesium sulphate are:
- It is mainly used intravenously (can be used by nebulisation with SABAs but with much less benefit[22-24]).
- It is not recommended routinely in acute asthma, but is of value in severe acute asthma (patients with FEV1 <25%) and those not responsive to other bronchodilators.
- It is generally safe, but may be associated with side-effects of flushing, sweating, hypotension, nausea, muscle weakness and central nervous system depression.
How to administer?
Intravenous magnesium sulphate may be given as a 1 - 2 g infusion over 20 minutes. It should be given as a single-dose infusion and may be repeated once, but not sooner than 12 hours.
Nebulised magnesium sulphate should be administered at a dose of 135 - 1 150 mg together with a SABA, but this is far less effective than intravenous administration.[23,24]
Intravenous aminophylline is the only theophylline recommended in acute asthma. It is a theophylline with ethylenediamine to render it water-soluble. It is thought to act by phosphodiesterase inhibition and non-selective adenosine receptor antagonism. Selective phosphodiesterase inhibitors such as roflumilast are not registered for use in acute asthma. The properties of aminophylline are:
- It has a very narrow therapeutic range, and toxicity is common (cardiac arrhythmias, nausea and vomiting, convulsions, hypotension and coma).
- It is not routinely given in acute asthma, as no synergism has been demonstrated. Only recommended when there is no response to SABAs, ipratropium bromide and magnesium sulphate (i.e. severe refractory asthma).
How to administer?
A loading dose of 5 mg/kg is infused over 30 minutes (withhold or give only half the dose to patients already on oral theophylline), followed by a maintenance infusion of 0.5 mg/kg/h (approximately 1000 mg/24 h). This should be increased by one-third (0.9 mg/ kg/h) in smokers and patients taking phenytoin and decreased by one-third in the elderly and those with congestive cardiac failure or liver disease, or taking a macrolide, ciprofloxacin or cimetidine. Blood levels should be monitored daily and the dose adjusted accordingly.
Adrenaline has been replaced by the β2-agonists and is rarely indicated for acute asthma attacks. It may, however, be used if no intravenous access is immediately available and the patient is moribund. Subcutaneous adrenaline (0.3 ml of 1/1000 solution, repeated every 20 minutes if no response) has been successful and side-effects are not significant even when given intravenously under emergency circumstances. It has also been administered via an endotracheal tube if a patient is unable to take inhaled medication and/or there is no intravenous access. It may also be used if there is associated anaphylaxis or angio-oedema. Special care must be taken in the elderly and those with or at risk of cardiovascular disease.
Glucocorticosteroids are recommended routinely for the treatment of acute asthma (evidence A).[26,27] They are the most important antiinflammatory agents in asthma. The key properties of CS are:
- They prevent relapse.[26,27]
- Onset of action is within hours of administration, and the first dose should be given orally or intravenously immediately, treatment for acute asthma is commenced.
- Oral CS are usually as effective and work as quickly as those given intravenously, and are preferred because they are cheaper and less invasive.[28,29]
- CS need to be continued for 7 - 14 days.
- CS have been shown to be effective when administered by MDI or nebulisation in acute asthma,[31,32] but the inhaled route is not cost-effective or as reliable as systemic administration in acute asthma. There is insufficient evidence that the inhaled route can replace systemic CS in acute asthma.[33,34]
- They result in resolution of the airway inflammation that contributes significantly to the airway obstruction in acute asthma and is not reversed with bronchodilators such as β2-agonists, anticholinergics, magnesium sulphate and theophylline.
How to administer?
CS are usually given in the form of oral prednisone (0.5 - 1 mg/kg or equivalent per day, usually 30 - 50 mg daily) in all patients with acute asthma attacks[26,27] (evidence A) and continued for 7 - 14 days. There is no advantage in using a higher dose (evidence B) or in tapering the dose when administered for this duration (evidence B). Intravenous CS (hydrocortisone 100 - 200 mg or equivalent, 6-hourly) can be used if the patient is vomiting or unable to take oral medication. Highly potent CS such as dexamethasone and betamethasone are not recommended in acute asthma.
Standard-dose inhaled CS should be started during the admission and continued on discharge as part of chronic therapy[31-34,36-38] (evidence A).
Supplemental oxygen must be administered whenever possible in patients with moderate to severe acute asthma. Also, nebulised bronchodilators should whenever possible be delivered by oxygen-driven nebulisers. Most patients with moderate to severe acute asthma have hypoxia that is readily corrected by supplemental oxygen.
How to administer?
Oxygen is generally administered by facemask and response monitored with pulse oximetry to maintain an O2 saturation over 92%[1,6,39] (evidence C). Lack of pulse oximetry should not prevent oxygen being administered. There is usually no need to administer more than 40% oxygen. The flow rates are determined by the recommendations on the specific facemasks. If inhaled bronchodilator therapy is given by nebulisers, they should preferably be driven by oxygen at a flow rate of at least 6 l/min to prevent hypoxaemia[6,40] (evidence A).
5.3.4 Miscellaneous treatments
Antibiotics are not routinely indicated in acute asthma and should only be given if there is definite evidence of infection such as fever, purulent sputum and clinical and/or radiological signs of pneumonia.[41,42] Note that yellowish sputum is frequent in acute asthma and is due to the high eosinophil content and not a sign of infection on its own.
Intravenous fluids are administered in acute severe asthma based on the clinical setting, taking into account maintenance and replacement requirements and the need for calorie intake in patients unable to take oral fluids. There are no formal studies of routine fluid administration in acute asthma.
Heliox is a mixture of helium and oxygen. It has the advantage of reducing airway resistance and has been used in desperate circumstances in non-responsive severe acute asthma.[43-45] It is not available in most centres.
5.3.5 Treatments for which there is no evidence of benefit and/or that should be avoided
Leukotriene modifiers are not currently recommended in acute asthma.[1,46]
Antihistamines have no role in acute asthma.
Mucolytics, given either systemically or by nebulisation, are contraindicated as they may worsen cough and bronchospasm and only serve to complicate the treatment regimen.
Sedatives should be strictly avoided during asthma attacks because of their respiratory depressant effect. Their use in non-intubated patients has been associated with asthma deaths.[42,47,48]
Physiotherapy may provoke bronchospasm and worsen the attack. It is only indicated if there is lobar collapse that persists despite initial bronchodilator and CS therapy.
5.3.6 Stepwise treatment of acute asthma
The stepwise treatment of acute asthma is set out in Table 4.
5.4 Assessment of response to treatment
Measurements of pulse rate, respiratory rate, PEF or FEV1 and arterial oxygen saturation should be made at 15 - 30-minute intervals until a clear response to treatment is achieved.[3-5,42-49] Measurement of the change in PEF in response to initial therapy is one of the best ways to assess response to treatment for acute asthma.[1,42,49] Early response to treatment (PEF at 30 minutes) is the most important predictor of outcome and need for hospitalisation.[42,4'1 Criteria for endotracheal intubation and/or intensive care unit (ICU) admission are listed in Table 5. ICU management of acute asthma is described below. Once a satisfactory response is obtained the patient may:
- be discharged on a course of oral prednisone for 7 - 14 days together with controller medication
- continue to receive bronchodilator treatment in the emergency room, ward, high-care unit or ICU at a frequency of 4 -8-hourly based on the attending physician's discretion. Ongoing monitoring of baseline parameters such as clinical status, PEF, SpO2, arterial blood gas, etc. is at the attending physician's discretion.
5.5 Mechanical ventilation
- Intubation should be performed with a large-diameter tube by the most experienced person available. The induction agent is a matter of personal preference. Benzodiazepines cause respiratory depression, so the initial attempt must be rapidly successful. Etomidate (0.2 -0.4 mg/kg), propofol (2 - 2.5 mg/kg) and ketamine (1 - 2 mg/kg) are other options. The latter has sedative, analgesic and anaesthetic properties without respiratory depression, but increases bronchial secretions and causes hallucinations. Succinylcholine remains the agent of choice for acute paralysis despite histamine release. Volume modes ensure delivery of a tidal volume (TV) that exceeds physiological dead space (usually 5 - 6 ml/kg ideal body weight or 250 - 300 ml).
- Set the peak pressure alarm such that the desired volume is actually delivered. The pressure required to deliver an adequate TV may be quite high when airflow resistance is very high. Considerable expertise is required to manage ventilation in these patients.
- Auto-PEEP (positive end-expiratory pressure). Auto-PEEP causes hyperinflation and haemodynamic compromise and should be minimised. Auto-PEEP is influenced by respiratory rate, TV, and the inspiratory-to-expiratory time ratio and inspiratory flow rates. Ventilator graphics make the monitoring of PEEP much simpler.
- Start with a respiratory rate of 8 - 12 breaths per minute with no or minimal external PEEP.
- Permissive hypercapnia, a higher CO2 than normal, is acceptable provided the pH is >7.2. If the pH is less than this, increase the respiratory rate cautiously as this may increase auto-PEEP.
- Short-duration paralysis may sometimes be necessary. Non-depolarising agents such as vecuronium bromide, rocuronium bromide, cisatracurium besilate and pancuronium bromide may all be used and do not induce bronchospasm. Atracurium besilate and mivacurium chloride cause dose-dependent histamine release, but it is not certain whether this causes clinical deterioration. Stop paralysis as soon as possible, as the combination of steroid and neuromuscular blocking agents is particularly likely to cause critical illness myopathy.
- When the patient improves, convert to pressure support modes. A trial of external PEEP is warranted as this may decrease work in spontaneously breathing patients. Non-invasive ventilation remains controversial and is not routinely recommended. Criteria for endotracheal intubation/ICU admission are listed in Table 5, and suggested criteria for discharge from the emergency unit in Table 6.[49,56-59] If the pretreatment FEV1 or PEF is <25% predicted or personal best, or the post-treatment FEV1 or PEF <40% predicted or personal best, admission is usually required.[1,59]
Once admitted for poor response, the optimal duration of hospital stay is unclear. There is often major bed pressure to discharge patients too early, but this increases the risk of early relapse. Readmission may occur in the next 2 - 3 months, particularly if the diurnal variation in PEF is >20%, and a course of oral CS and optimisation of long-term controller treatment are essential to reduce relapse.
5.6 Prevention of relapses
The factors that precipitated the attack should be identified and attempts made to avoid them.[60-631
5.7 Discharge plan
- Provide a 7 - 14-day course of oral CS (20 - 40 mg daily of prednisone or equivalent). No tapering required if used for this duration.
- Instruct the patient to use their inhaled bronchodilator (SABA) as required for both symptomatic and objective improvement (PEF if available) until they are stable and return to their baseline.
- Review the patient's use of controller therapy during the exacerbation. Patients should commence or continue inhaled CS (frequently in the form of a combination inhaler with long-acting β2-agonists). If the patient was already on inhaled CS, careful attention should be paid to reviewing the dose. Consider providing a short course of oral CS to be taken in the event of subsequent exacerbations for frequent exacerbators.
- The patient's inhaler technique and use of a peak flow meter to monitor therapy at home should be reviewed.
- A follow-up appointment with the patient's usual primary care provider or an asthma specialist should be made within 2 weeks of discharge to ensure that treatment is continued to achieve control. Ideally, patients discharged from the emergency unit should be referred to specialist care as they do better than those returned to routine care.
- The patient's response to the attack should be evaluated. A written asthma action plan should be reviewed or provided. Hospitalised patients are more receptive to information and advice about their illness. Healthcare providers should take the opportunity to review patient understanding of the causes of asthma attacks, trigger avoidance (including smoking cessation), the purpose and correct use of treatment, and the action to take in response to worsening symptoms or peak flow values[60-63] (evidence A).
2. Chan-Yeung M, Chang JH, Manfreda J, Ferguson A, Becker A. Changes in peak flow, symptom score, and the use of medications during acute exacerbations of asthma. Am J Respir Crit Care Med 1996;54(4):889-893. [ Links ]
3. Emerman CL, Cydulka RK. Effect of pulmonary function testing on the management of acute asthma. Arch Intern Med 1995;155(20):2225-2228. [http://dx.doi.org/10.1001/archinte.1995.00430200117015] [ Links ]
5. Geelhoed GC, Landau LI, Le Souef PN. Evaluation of SaO2 as a predictor of outcome in 280 children presenting with acute asthma. Ann Emerg Med 1994;23(6):1236-1241. [ Links ]
6. British Thoracic Society. Guideline for emergency oxygen use in adult patients. Thorax 2008;63:1-68. [ Links ]
7. Carruthers DM, Harrison BD. Arterial blood gas analysis or oxygen saturation in the assessment of acute asthma? Thorax 1995;50(2):186-188. [ Links ]
8. Findley LJ, Sahn SA. The value of chest roentgenograms in acute asthma in adults. Chest 1981;80(5):535-536. [ Links ]
9. Suissa S, Blais L, Ernst P. Patterns of increasing beta-agonist use and the risk of fatal or near-fatal asthma. Eur Respir J 1994;7(9):1602-1609. [http://dx.doi.org/10.1183/09031936.94.07091602] [ Links ]
10. Harrison BDW, Slack R, Berrill WT, et al. Results of a national confidential enquiry into asthma deaths. Asthma J 2000;5:180-186. [ Links ]
11. Rudnitsky GS, Eberlein RS, Schoffstall JM, Mazur JE, Spivey WH. Comparison of intermittent and continuously nebulized albuterol for treatment of asthma in an urban emergency department. Ann Emerg Med 1993;22(12):1842-1846. [http://dx.doi.org/10.1016/S0196-0644(05)80411-1] [ Links ]
12. Reisner C, Kotch A, Dworkin G. Continuous versus frequent intermittent nebulisation of albuterol in acute asthma: A randomized, prospective study. Ann Allergy Asthma Immunol 1995;75(1):41-47. [ Links ]
13. Rodrigo GJ, Rodrigo C. Continuous vs intermittent beta agonists in the treatment of acute adult asthma: A systematic review with meta-analysis. Chest 2002;122(1):160-165. [ Links ]
14. Bradding P, Rushby I, Scullion J, Morgan MD. As-required versus regular nebulized salbutamol for the treatment of acute severe asthma. Eur Respir J 1999;13(2):290-294. [ Links ]
15. Travers A, Jones AP, Kelly K, Barker SJ, Camargo CA, Rowe BH. Intravenous beta2-agonists for acute asthma in the emergency department. Cochrane Database Syst Rev 2001;(2):CD002988. [http://dx.doi.org/10.1002/14651858.CD002988] [ Links ]
16. Cates CJ, Crilly JA, Rowe BH. Holding chambers (spacers) versus nebulisers for beta-agonist treatment of acute asthma. Cochrane Database Syst Rev 19;(2):CD000052. [http://dx.doi.org/10.1002/14651858.CD000052.pub2] [ Links ]
17. Rodrigo G, Rodrigo C, Burschtin C. A meta-analysis of the effects of ipratropium bromide in adults with acute asthma. Am J Med 1999;107(4):363-370. [http://dx.doi.org/10.1016/S0002-9343(99)00243-0] [ Links ]
18. Rodrigo GJ, Rodrigo C. First-line therapy for adult patients with acute asthma receiving a multiple-dose protocol of ipratropium bromide plus albuterol in the emergency department. Am J Respir Crit Care Med 2000;161(6):1862-1868. [ Links ]
19. Lanes SF, Garrett JE, Wentworth CE 3rd, Fitzgerald JM, Karpel JP. The effect of adding ipratropium bromide to salbutamol in the treatment of acute asthma: A pooled analysis of three trials. Chest 1998;114(2):365-372. [ Links ]
20. Rowe BH, Bretzlaff JA, Bourdon C, Bota GW, Camargo CA Jr. Magnesium sulfate for treating exacerbations of acute asthma in the emergency department. Cochrane Database Syst Rev 2000;(2):CD001490. [http://dx.doi.org/10.1002/14651858.CD001490] [ Links ]
21. FitzGerald JM. Magnesium sulfate is effective for severe acute asthma treated in the emergency department. West J Med 2000;172(2):96. [ Links ]
22. Mohammed S, Goodacre S. Intravenous and nebulised magnesium sulphate for acute asthma: A systematic review and meta-analysis. Emerg Med J 2007;24(12):823-830. [http://dx.doi.org/10.1136/emj.2007.052050] [ Links ]
23. Blitz M, Blitz S, Beasely R, et al. Inhaled magnesium sulfate in the treatment of acute asthma. Cochrane Database Syst Rev 2005;(4):CD003898. [http://dx.doi.org/10.1002/14651858.CD003898.pub4] [ Links ]
25. Parameswaran K, Belda J, Rowe BH. Addition of intravenous aminophylline to beta2-agonists in adults with acute asthma. Cochrane Database Syst Rev 2000;(4):CD002742. [http://dx.doi.org/10.1002/14651858.CD002742] [ Links ]
26. Manser R, Reid D, Abramson M. Corticosteroids for acute severe asthma in hospitalised patients. Cochrane Database Syst Rev 2001;(1):CD001740. [http://dx.doi.org/10.1002/14651858.CD001740] [ Links ]
27. Rowe BH, Spooner C, Ducharme FM, Bretzlaff JA, Bota GW. Early emergency department treatment of acute asthma with systemic corticosteroids. Cochrane Database Syst Rev 2000;(2):CD002178. [http://dx.doi.org/10.1002/14651858.CD002178] [ Links ]
28. Ratto D, Alfaro C, Sipsey J, Glovsky MM, Sharma CP. Are intravenous corticosteroids required in status asthmaticus? JAMA 1988;260(4):527-529. [http://dx.doi.org/10.1001/jama.1988.03410040099036] [ Links ]
29. Harrison BD, Stokes TC, Hart GJ, Vaughan DA, Ali NJ, Robinson AA. Need for intravenous hydrocortisone in addition to oral prednisolone in patients admitted to hospital with severe asthma without ventilatory failure. Lancet 1986;1(8474):181-184. [http://dx.doi.org/10.1016/S0140-6736(86)90654-9] [ Links ]
30. 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. [http://dx.doi.org/10.2169/internalmedicine.39.794] [ Links ]
31. Rodrigo G, Rodrigo C. Inhaled flunisolide for acute severe asthma. Am J Respir Crit Care Med 1998;157(3):698-703. [ Links ]
32. Rodrigo GJ. Comparison of inhaled fluticasone with intravenous hydrocortisone in the treatment of adult acute asthma. Am J Respir Crit Care Med 2005;171(11):1231-1236. [http://dx.doi.org/10.1164/rccm.200410-1415CC] [ Links ]
33. Lee-Wong M, Dayrit FM, Kohli AR, Acquah S, Mayo PH. Comparison of high-dose inhaled flunisolide to systemic corticosteroids in severe adult asthma. Chest 2002;122(4):1208-1213. [ Links ]
35. C'Driscoll BR, Kalra S, Wilson M, Pickering CA, Carroll KB, Woodcock AA. Double-blind trial of steroid tapering in acute asthma. Lancet 1993;341(8841):324-327. [http://dx.doi.org/10.1016/0140-6736(93)90134-3] [ Links ]
36. FitzGerald JM, Shragge D, Haddon J, et al. A randomized controlled trial of high dose, inhaled budesonide versus oral prednisone in patients discharged from the emergency department following an acute asthma exacerbation. Can Respir J 2000;7(1):61-67. [ Links ]
37. Edmonds ML, Camargo CA, Saunders LD, Brenner BE, Rowe BH. Inhaled steroids in acute asthma following emergency department discharge. Cochrane Database Syst Rev 2000;(3):CD002316. [http://dx.doi.org/10.1002/14651858.CD002316.pub2] [ Links ]
38. Rowe BH, Bota GW, Fabris L, Therrien SA, Milner RA, Jacono J. Inhaled budesonide in addition to oral corticosteroids to prevent asthma relapse following discharge from the emergency department: A randomized controlled trial. JAMA 1999;281(22):2119-2126. [http://dx.doi.org/10.1001/jama.281.22.2119] [ Links ]
39. Rodrigo GJ, Rodriquez Verde M, Peregalli V, Rodrigo C. Effects of short-term 28% and 100% oxygen on PaCO2 and peak expiratory flow rate in acute asthma: A randomized trial. Chest 2003;124(4):1312-1317. [ Links ]
40. Gleeson JG, Green S, Price JF. Air or oxygen as driving gas for nebulised salbutamol. Arch Dis Child 1988;63(8):900-904. [ Links ]
41. Graham VA, Milton AF, Knowles GK, Davies RJ. Routine antibiotics in hospital management of acute asthma. Lancet 1982;1(8269):418-420. [ Links ]
43. Colebourn CL, Barber V, Young JD. Use of helium-oxygen mixture in adult patients presenting with exacerbations of asthma and chronic obstructive pulmonary disease: A systematic review. Anaesthesia 2007;62(1):34-42. [http://dx.doi.org/10.1111/j.1365-2044.2006.04897.x] [ Links ]
44. Rodrigo G, Pollack C, Rodrigo C, Rowe BH. Heliox for non-intubated acute asthmatic patients. Cochrane Database Syst Rev 2006;(4):CD002884. [http://dx.doi.org/10.1002/14651858.CD002884.pub2] [ Links ]
45. Rodrigo GJ, Rodrigo C, Pollack CV, Rowe BH. Use of helium oxygen mixtures for the treatment of acute asthma: A systematic review. Chest 2003;123:891-896. [ Links ]
46. Iverman RA, Nowak RM, Korenblat PE, et al. Zafirlukast treatment for acute asthma: Evaluation in a randomized, double-blind, multicenter trial. Chest 2004;126(5):1480-1489. [http://dx.doi.org/10.1378/chest.126.5.1480] [ Links ]
48. Joseph KS, Blais L, Ernst P, Suissa S. Increased morbidity and mortality related to asthma among asthmatic patients who use major tranquillisers. BMJ 1996;312(7023):79-82. [ Links ]
49. Rodrigo GJ, Rodrigo C, Hall JB. Acute asthma in adults: A review. Chest 2004;125(3):1081-1102. [ Links ]
51. Cddo M, Feihl F, Schaller MD, Perret C. Management of mechanical ventilation in acute severe asthma: Practical aspects. Intensive Care Med 2006;32(4):501-510. [http://dx.doi.org/10.1007/s00134-005-0045-x] [ Links ]
52. Bellomo R, McLaughlin P, Tai E, Parkin G. Asthma requiring mechanical ventilation. A low morbidity approach. Chest 1994;105(3):891-896. [ Links ]
53. Blanch L, Bernabé F, Lucangelo U. Measurement of air trapping, intrinsic positive end-expiratory pressure, and dynamic hyperinflation in mechanically ventilated patients. Respir Care 2005;50(1):110-123. [ Links ]
54. Behbehani NA, Al-Mane F, Dyachkova Y, Paré P, FitzGerald JM. Myopathy following mechanical ventilation for acute severe asthma: The role of muscle relaxants and corticosteroids. Chest 1999;115(6):1627-1631. [ Links ]
55. Petrof BJ, Legaré M, Goldberg P, Milic-Emili J, Gottfried SB. Continuous positive airway pressure reduces work of breathing and dyspnea during weaning from mechanical ventilation in severe chronic obstructive pulmonary disease. Am Rev Respir Dis 1990;141(2):281-289. [http://dx.doi.org/10.1164/ajrccm/141.2.281] [ Links ]
56. Ram FS, Wellington S, Rowe B, Wedzicha JA. Non-invasive positive pressure ventilation for treatment of respiratory failure due to severe acute exacerbations of asthma. Cochrane Database Syst Rev 2005;(3):CD004360. [http://dx.doi.org/10.1002/14651858.CD004360.pub2] [ Links ]
57. Phipps P, Garrard CS. The pulmonary physician in critical care. 12: Acute severe asthma in the intensive care unit. Thorax 2003;58(1):81-88. [ Links ]
58. Pearson MG, Ryland I, Harrison BD. National audit of acute severe asthma in adults admitted to hospital. Standards of Care Committee, British Thoracic Society. Qual Health Care 1995;4(1):24-30. [http://dx.doi.org/10.1136/qshc.4.1.24] [ Links ]
59. Udwadia ZF, Harrison BD. An attempt to determine the optimal duration of hospital stay following a severe attack of asthma. J R Coll Physicians Lond 1990;24(2):112-114. [ Links ]
60. Grunfeld A, FitzGerald JM. Discharge considerations in acute asthma. Can Respir J 1996;3:322-324. [ Links ]
61. Gibson PG, Powell H, Coughlan J, et al. Self-management education and regular practitioner review for adults with asthma. Cochrane Database Syst Rev 2003;(1):CD001117. [http://dx.doi.org/10.1002/14651858.CD001117] [ Links ]
62. Baren JM, Boudreaux ED, Brenner BE, et al. Randomized controlled trial of emergency department interventions to improve primary care follow-up for patients with acute asthma. Chest 2006;129(2):257-265. [http://dx.doi.org/10.1378/chest.129.2.257] [ Links ]
63. Csman LM, Calder C, Godden DJ, et al. A randomised trial of self-management planning for adult patients admitted to hospital with acute asthma. Thorax 2002;57(10):869-874. [http://dx.doi.org/10.1136/thorax.57.10.869] [ Links ]
64. Zeiger RS, Heller S, Mellon MH, Wald J, Falkoff R, Schatz M. Facilitated referral to asthma specialist reduces relapses in asthma emergency room visits. J Allergy Clin Immunol 1991;87(6):1160-1168. [http://dx.doi.org/10.1016/0091-6749(91)92162-T] [ Links ]
U G Lalloo (firstname.lastname@example.org)
Appendix I. How to measure peak expiratory flow (PEF)
As airways narrow, the PEF rate falls. The PEF is usually measured using the mini-Wright peak flow meter (Fig. 2). Careful instruction is required to measure PEF reliably because its measurement is effort-dependent. The maximum rate of flow of air that the patient can forcibly exhale starting from full inhalation, expressed in litres per minute, is measured. It should be explained in simple terms ('take a deep breath in, and then blow out as hard and fast as possible into the meter, like blowing out the candles on a cake'). However, it is much easier and more effective to show a patient how to use a peak flow meter than to explain it to them in words only. PEF should be recorded as the best of three forced expiratory blows from total lung capacity in a standing or sitting position, with a maximum pause of 2 seconds before blowing. The subject does not have to exhale completely.
PEF expressed as a percentage of the patient's previous best value is most useful clinically, but in the absence of a known previous best value, it should be expressed as a percentage of predicted.[1,2] PEF depends on the patient's age, sex and height. The normal reference values sourced from the Nunn and Gregg nomogram are recommended for the calculation of 'percentage predicted' PEF values[2,3] (Fig. 3).