An 18-year-old known asthmatic presented with a two-day history of increasing shortness of breath on a background of a recent coryzal illness. She had a background of reasonably poor control and had been admitted to the intensive care unit for mechanical ventilation twice as a child. Her current medication included regular inhaled serotide 250, montelukast 10mg and theophylline MR 450mg BD. At presentation she was in extremis; pulse rate was 65 per minute, blood pressure 75/54 mmHg and respiratory rate 14 per minute. Arterial blood gas analysis demonstrated a PaCO2 of 11 kPa and PaO2 of 7.6 kPa with associated respiratory acidosis. Nebulised salbutamol and intravenous magnesium sulphate therapy was administered. along with 200mg of intravenous hydrocortisone. On arrival of the intensive care team, the patient’s respiratory rate deteriorated to a rate of 4 per minute. Assisted ventilation with a self-inflating bag and 100% oxygen was performed; rapid-sequence intubation was performed using ketamine and rocuronium.
Following intubation, immediate difficulties were experienced with mechanical ventilation. High airway pressures in excess of 40 cmH2O with tidal volumes of less than 200 ml were observed. Immediate chest radiography confirmed correct positioning of the endotracheal tube and excluded a pneumothorax. Adequate sedation and neuromuscular blockade were confirmed. Auscultation confirmed severe, widespread wheeze with limited air entry. Further nebulised salbutamol was administered and an aminophylline infusion initiated. The patient was transferred to the intensive care unit where magnesium, ketamine and vecuronium by infusion were added. Various modes of mechanical ventilation were tried including volume and pressure triggered with varying success; this included lengthening the I:E ratio, frequent disconnections to allow deflation and adjustment of PEEP to maximum compliance. Continuous salbutamol was administered via an ultrasonic nebuliser. Airway pressures remained high and there was little improvement in her acidosis. 2 hours after admission the patient suffered a PEA cardiac arrest from which she could not be resuscitated.
What are the difficulties in ventilating severe asthmatics, and what strategies can we use to overcome them?
Approximately 1400 deaths due to asthma occur every year in the United Kingdom, the majority in the those aged over 65.(1) Many deaths occur at home in patients with poor concordance or those unaware of the severity of the attack.(2) Mechanical ventilation is reserved as rescue therapy for severe or life-threatening exacerbations in whom medical therapies have failed or proved partially effective.(3,4) Effective mechanical ventilation in these patients may be difficult due to significant air-trapping and complications such as pneumothoraces.(5)
The aims of mechanical ventilation in exacerbations of asthma are to reduce dynamic hyperinflation, reduce gas trapping and limit barotrauma whilst maintaining adequate oxygenation and, to a lesser extent, limiting hypercarbia. (6,7) Acute severe asthma may be associated with significant pulmonary hyperinflation with increases in functional residual capacity of up to twice normal values.(8) This hyperinflation results from critical limitation of expiratory flow, due mainly to reduced pulmonary elastic recoil of unclear mechanism with an abnormally high outward recoil of the chest wall via activation of the inspiratory muscles during expiration and severely reduced airway caliber. (8) Expiration is markedly prolonged such that inspiration begins before static equilibrium is reached and end-expiratory alveolar pressure remains positive (intrinsic PEEP).(7,8)
There is no evidence to favour any particular benefit in volume, pressure or time-cycled ventilatory modes, the optimal inspiratory flow waveform or optimum PEEP in asthma.(6-8) Long expiratory times with inspiratory: expiratory ratios in excess of 1:2, low tidal-volume (5-6ml/kg) and slower respiratory rates (8-10 breaths per minute) are required to limit further dynamic hyperinflation.(6) Positive end-expiratory pressure was traditionally avoided due to fears of barotrauma but there is evidence that judicious use of lower values (5-10 cmH20) may help overcome lower airway obstruction and allow alveolar emptying.(8)
A strategy of permissive hypercapnia should be adopted (i.e. pH > 7.2) as there is little evidence that high levels of carbon dioxide are harmful outside the settings of raised intracranial pressure of severe myocardial depression.(7) Inhaled bronchodilator therapy may be continued during invasive ventilation via metered dose inhalers administered into a spacer device inserted into the inspiratory limb of the ventilator circuit or continuous ultrasonic nebulisation. Circuit humidification should be stopped during the administration of metered dose medication as this can considerably effect the dose of drug delivered.
Mechanical ventilation traditionally involves endotracheal intubation; in the patient who is in extremis, induction of anaesthesia may be associated with significant cardiovascular instability. (9) In recent years, non-invasive ventilation has emerged as a potential therapy; it has been suggested that this treatment is both safe and improves pulmonary function and in severe asthma with moderate hypercapnic acidosis.(10) A number of observational studies have suggested a reduced need for endotracheal intubation and relatively low rate of complications.(10-12) To date studies examining this treatment have been relatively small and often retrospective. However, rates of intubation in asthma remain relatively low, even in the setting of hypercapnia. A recent Cochrane review concluded that whilst this treatment shows promise, no conclusive benefit is yet demonstrated.(13) It may be prudent to consider a trial of this therapy in a critical care setting for 1-2 hours.(6)
No particular consensus regarding the optimum ventilatory strategy in patients such as this exists; it is possible that deterioration to essentially respiratory arrest could have been avoided with rapid application of non-invasive ventilation in the Emergency Department. Limiting barotrauma is essential and perhaps this may have been achieved with earlier institution of continuous neuromuscular blockade.
- Anderson HR, Gupta R, Strachan DP, Limb ES. 50 years of asthma: UK trends from 1955 to 2004. Thorax. 2007 Jan;62(1):85–90.
- Parulekar AD, Alobaidy A, Hanania NA. Asthma outcomes revisited. Curr Opin Pulm Med. 2013 Jan;19(1):6–12.
- Turner S, Paton J, Higgins B, Douglas G, British Guidelines on the Management of Asthma. British guidelines on the management of asthma: what’s new for 2011? Thorax. 2011 Dec;66(12):1104–5.
- British Thoracic Society Scottish Intercollegiate Guidelines Network. British Guideline on the Management of Asthma. Thorax. 2008. pages iv1–121.
- de Latorre FJ. Management of acute severe asthma. Resuscitation. 2000 Nov;47(3):335–8.
- Phipps P, Garrard CS. The pulmonary physician in critical care . 12: Acute severe asthma in the intensive care unit. Thorax. 2003 Jan;58(1):81–8.
- Stather DR, Stewart TE. Clinical review: Mechanical ventilation in severe asthma. Crit Care. 2005;9(6):581–7.
- Oddo M, Feihl F, Schaller M-D, Perret C. Management of mechanical ventilation in acute severe asthma: practical aspects. Intensive Care Med. 2006 Apr;32(4):501–10.
- Brenner B, Corbridge T, Kazzi A. Intubation and mechanical ventilation of the asthmatic patient in respiratory failure. J. Allergy Clin. Immunol. 2009 Aug;124(2 Suppl):S19–28.
- Fernández MM, Villagrá A, Blanch L, Fernández R. Non-invasive mechanical ventilation in status asthmaticus. Intensive Care Med. 2001 Mar;27(3):486–92.
- Murase K, Tomii K, Chin K, Tsuboi T, Sakurai A, Tachikawa R, et al. The use of non-invasive ventilation for life-threatening asthma attacks: Changes in the need for intubation. Respirology. 2010 May;15(4):714–20.
- Boldrini R, Fasano L, Nava S. Noninvasive mechanical ventilation. Curr Opin Crit Care. 2012 Feb;18(1):48–53.
- Ram FSF, Wellington S, Rowe BH, Wedzicha JA. Non-invasive positive pressure ventilation for treatment of respiratory failure due to severe acute exacerbations of asthma. Cochrane Database Syst Rev. 2005;(1):CD004360.