Early tracheotomy for acute severe asthma

BACKGROUND： Few studies have reported the effects of early tracheotomy in acute severe asthmatic patients. We report two patients with acute severe asthma who were successfully treated with early tracheotomy.

METHODS： The two patients with acute severe asthma were retrospectively reviewed. They had been treated at the Department of Emergency and Critical Care， Renji Hospital， Shanghai Jiaotong University School of Medicine.

RESULTS： They developed progressively hypercapnia and severe acidosis， and were not improved after conventional therapies. Early tracheotomy after mechanical ventilation decreased airway resistance and work of breathing， and corrected hypercapnia and acidosis. Adequate gas exchange was maintained after tracheotomy. The two patients were subsequently weaned from mechanical ventilation and discharged.

CONCLUSION： Early tracheotomy could be a valuable approach in certain patients with severe asthma.

KEY WORDS： Early tracheotomy； Acute severe asthma； Extubation； Mechanical ventilation； Work of breathing

World J Emerg Med 2011；2（2）：154-156

INTRODUCTION

Acute severe asthma （status asthmaticus） is a life-threatening emergency because of refractory respiratory failure. Patients are severely dyspneic， cyanosed， and often moribund. Although there appears to be a trend toward increased survival after mechanical ventilation for patients with acute asthma， ventilation of critically ill asthmatic patients continues to be a potentially perilous venture associated with significant morbidity and mortality.[1] Tracheotomy is often performed when patients fail to wean from ventilation. As reported by Lee et al，[2] patients with early tracheotomy compared with those with delayed tracheotomy showed significantly lower hospital mortality （31.7% vs. 61.7%， P

Case reports

Case 1. A 50-year-old man with asthma was admitted to the emergency department of our hospital because of sudden onset of dyspnea， cough and chest tightness. On arrival he complained of severe shortness of breath and was only able to speak with short sentences. Examination revealed widespread wheeze and accessory muscle breathing. Chest radiograph showed bilateral infiltration. The results of labortory examination including biochemistry analysis of blood were nothing abnormal. Initial arterial blood gas （ABG） was pH 7.11， PaO2/FIO2 151.6 mmHg， and PaCO2 101.0 mmHg. The patient was transferred to ICU and administered with repeated nebulized bronchodilators， high-dose of corticosteroids， antibiotics， and noninvasive ventilation， but he was not improved. At 7 hours after admission， arterial blood gas analysis revealed worsening of respiratory acidosis and hypercapnia （pH 7.1， PaCO2 109 mmHg， PaO2 58 mmHg）， indicating the need of tracheal intubation. Combined with sedation and analgesia， neuromuscular blocking agents， mechanical ventilation was performed with a low respiratory rate， prolonged expiratory time， and low extrinsic positive end-expiratory pressure. However， adequate oxygenation and ventilation were not achieved with poor compliance and high resistance. After 48 hours of ventilation， the airway pressure of the patient remained high （Plateau airway pressure>40 cmH2O） and tidal volumes

Case 2. A 24-year-old man with asthma was admitted to ICU for sudden onset of dyspnea and tightness. Physical examination revealed widespread wheeze and subcutaneous emphysema on the face， neck， shoulders and upper part of the chest. Chest radiograph showed extensive subcutaneous emphysema and pneumomediastinum. Arterial blood gas analysis revealed acute hypercapnic respiratory failure （pH 7.329， PCO2 57.1 mmHg， PO2 55.2 mmHg ）. He was initially treated with conventional medication， but failed. At 20 hours after admission， repeated chest radiograph revealed pneumomediastinum with left pneumatothorax. A second arterial blood gas analysis revealed increased hypercapnia （pH 7.183， PaCO2 98.2 mmHg， PaO2 51.2 mmHg）. He was intubated， and closed drainage was performed on the left pneumatothorax. Despite multiple ventilatory mode changes， maximal bronchodilator therapy， and antibiotic treatment， PaO2 was still lower than 60 mmHg. At 72 hours after intubation， PaCO2 rose to 73.7 mmHg， airway pressure remained high， and tidal volumes were unacceptably low. Then tracheotomy was performed. At 48 hours after tracheotomy， the plateau airway pressure decreased （23 cmH2O）， tidal volume increased （440 mL）， and PaCO2 value decreased accordingly （PaCO2 62.3 mmHg， pH 7.358）. He was extubated on the 10th day and discharged from the hospital 18 days later.

DISCUSSION

The causes of death from severe asthma include arrhythmia， hypoxemia secondary to ventilation/perfusion （V/Q） mismatch， and alveolar hypoventilation. The major physiologic changes associated with severe asthma are airflow limitation， bronchial hyperresponsiveness， airway closure， loss of elastic recoil， and hyperinflation （or air trapping）. Optimal treatment includes nebulized or intravenous beta-2 agonists， nebulized anticholinergics， intravenous corticosteroids， and sometimes intravenous aminophyl-line and magnesium sulphate. Mechanical ventilation is an effective measure to correct hypoxemia and hypercapnea. Once the patient was intubated， primary focus must be on avoiding excessive airway pressure and minimizing lung hyperinflation. To achieve this goal it is often necessary to hypoventilate the patient and thus to tolerate hypercapnia， which is termed "controlled hypoventilation" or "permissive hypercapnia". Despite progress in mechanical ventilation and newer drug therapies， there remains a significant mortality and morbidity in severe cases.[4]

Among those refractory patients， additional methods have been attempted such as buffer therapy with bicarbonate or amino alcohol tromethamine， inhaled anesthesia， airway clearance with bronchoscopy and mucolytics， helium-oxygen mixture （heliox）， and extracorporeal membrane oxygenation. However， the efficacy of the aforementioned modalities has not been confirmed.

In our study， the two patients were irresponsive to all conventional therapies until they gained significant improvement at 48 hours after tracheostomy. It seems that tracheostomy can minimize airway hypersensitivity due to endotracheal tubes， and improve secretion drainage that prevents sputum plug. Several studies[2-4] have focused on the benefit of early tracheostomy in intubated patients. Jaeger et al[5] suggested the larger the diameter and the shorter the tube， the lower the resistance. On the other hand， irregular tube walls （with secretions） and the sharper any curve in the tube will present greater resistance. After measuring the internal volume （dead space） of standard endotracheal tubes and tracheostomy tubes， Davis et al[6] found there were a difference of

We consider that if Pplat under 30 cmH2O or pH above 7.2 can not be maintained （despite the use of deep sedation/paralysis）， the ventilated asthmatic patient must be examined for causes of decreased respiratory system compliance. If there are no such causes， tracheotomy must be performed within 72 hours.

Early tracheotomy is rarely described as a therapy for patients with life-threatening asthma. Our data suggest that early tracheotomy may be beneficial for asthmatic patients resistant to conventional therapy including mechanical ventilation. But additional evidence especially randomized controlled trial is needed in order to guide decision-making in clinical practice.

Funding： None.

Ethical approval： Not needed.

Conflicts of interest： None.

Contributors： Huang H proposed the study and wrote the first draft. All authors contributed the design and interpretation of the study and to further drafts.

REFERENCES

1 McFadden ER Jr. Acute severe asthma. Am J Respir Crit Care Med 2003； 168： 740-759.

2 Lee JC， Fink MP. Early percutaneous dilatational tracheostomy leads to improved outcomes in critically ill medical patients as compared to delayed tracheostomy. Crit Care 2005； 9： E12.

3 Afessa B， Morales I， Cury J D. Clinical course and outcome of patients admitted to an ICU for status asthmaticus. Chest 2001； 120： 1616-1621.

4 Krishnan V， Diette GB， Rand CS， Bilderback AL， Merriman B， Hansel NN， et al. Mortality in patients hospitalised for asthma exacerbations in the United States. Am J Respir Crit Care Med 2006； 174： 633-638.

5 Jaeger JM， Littlewood KA， Durbin CG Jr. The role of tracheostomy in weaning from mechanical ventilation. Respir Care 2002； 47： 469-480.

6 Davis K Jr， Campbell RS， Johannigman JA， Valente JF， Branson RD. Changes in respiratory mechanics after tracheostomy. Arch Surg 1999； 134： 59-62.

7 Diehl JL， El Atrous S， Touchard D， Lemaire F， Brochard L. Changes in the work of breathing induced by tracheotomy in ventilator-dependent patients. Am J Respir Crit Care Med 1999； 159： 383-388.

8 Rumbak MJ， Newton M， Truncale T， Schwartz SW， Adams JW， Hazard PB. A prospective， randomized， study comparing early percutaneous dilational tracheotomy to prolonged translaryngeal intubation （delayed tracheotomy） in critically ill medical patients. Crit Care Med 2004； 32： 1689-1694.

Received December 1， 2010

Accepted after revision May 5， 2011