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Re: NIV in acute asthma: why not ?

Dear Editor,

We read with interest the case report recently published by Agarwal R and colleagues(1). The authors concluded, "a trial of NIV in acute asthma may be justified in carefully selected and monitored patients who do not respond to initial medical therapy. However, as it role is not clear and as the condition of an asthmatic patient may deteriorate abruptly, extreme caution is advisable to recognize failure of NIV... Facilities for immediate endotracheal intubation and next level of treatment should be readily available.” We approved these conclusions and we proposed several comments on this case and on this management approach in accordance with our local experience and with current state of knowledge (2-4). In the case presented, patient was initially more hypoxemic (PaO2 8.4 kPa) as hypercapnic (PaCO2 4.9 kPa) with a grade I of severity in first arterial blood gas measurement. An initial chest X-ray was not described in this case. We can postulated that NIV failed because patient was also in acute respiratory failure secondary to a added complication (atelectasia, pneumonia).

In our experience, NIV for patients with severe status asthmaticus not improving under conventional medical therapy and on the edge of intubation is the only possibility of decreasing morbidity and mortality of this acute illness. We will try in this letter to explain our opinion. The severity of an acute asthmatic exacerbation may be assessed using a variety of signs like major dyspnea, tachypnea, the use of accessory respiratory muscles, the presence of a pulsus paradoxus, a quiet chest on auscultation and the decrease of the PEFR below 120 L/min. The appearance of these signs and the increase of the dead space lead to an acute respiratory failure with respiratory acidosis. This clinical condition is not a priory an absolute indication for intubation and mechanical ventilation. Indeed, only 8% of this population of patients needs in fine endotracheal intubation (5). The absence of response to the optimal medical treatment and especially the alteration of conscience are the absolute indications of intubation. Patients with status asthmaticus have a significant increase in both inspiratory and expiratory indexes of airways obstruction. They have also a considerable dynamic hyperinflation.

Inspiratory muscle fatigue and increased physiologic dead space lead to ventilatory failure and respiratory acidosis. In fact, hypercapnia does not occur, however, unless the FEV1 is less than 25 % of predicted. The pathophysiology of status asthmaticus includes airflow obstruction of both large and small airways, inhomogeneous lung inflation, dynamic hyperinflation, ventilation/perfusion mismatch and respiratory muscle fatigue. Airway wall inflammation, smooth muscle-mediated bronchoconstriction and intraluminal mucus explain airway obstruction. Lung hyperinflation is primarily related to the fact that the highly increased airway expiratory resistance, the high ventilatory needs, the relative short expiratory time and the increased post-inspiratory activity of inspiratory muscles do not permit the respiratory system to reach static equilibrium volume at the end of expiration. Therefore, inspiration begins at a volume in which the respiratory system exhibits a positive recoil pressure. This pressure is called intrinsic positive-end expiratory pressure (PEEPI) or auto-PEEP. At each respiratory cycle, this inflation can increase and compromise the respiratory function. This phenomenon is called dynamic hyperinflation and is directly proportional to minute ventilation and to the degree of airflow obstruction. This phenomenon causes substantial shortening of the diaphragm and the inspiratory intercostal and accessory muscles, thereby reducing their mechanical efficiency and endurance and increasing the risk for fatigue. As airway obstruction becomes more serious and the work of breathing becomes excessive, carbon dioxide production is greater than what can be eliminated by alveolar ventilation. Therefore, PaCO2 increases and a respiratory acidosis appears. Moreover, in asthma, large negative swings in intrapleural pressure can significantly impair right ventricular function.

The pathophysiologic condition of acute respiratory failure in asthma is in many ways similar to that of acute respiratory failure in patients with COPD. Although a large body of literature has clearly proved the efficacy and advantages of NPPV in patients with COPD with ARF, only a few reports had described this modality in patients with status asthmaticus. In our experience, we found NIV simple to implement and well tolerated by our patients with severe clinical conditions. Since many years, we known that application of CPAP causes bronchodilatation and decreases airway resistances, reexpands atelectasis and promotes elimination of secretions, rests the diaphragm and inspiratory muscles and may offset PEEPI, and also decreases the adverse hemodynamic effects of large peak and mean inspiratory pleural pressures. CPAP is also available for reexpanding atelectasis by increasing collateral flow (through collateral channels " Kohn channels") to obstructed lung region. But in patients with acute respiratory failure secondary to COPD, similar to patients with asthma, short-term application of CPAP does not improve gas exchange. However, when IPPV is added to CPAP, minute ventilation and gas exchange improve in proportion to the amount of pressure applied. In our clinical experience, when NPPV was used, the respiratory muscles appeared to be rapidly unloaded, dyspnea was resolved and respiratory rate was reduced. The effect on gases exchange was also rapidly observed. In our experience, the mechanical effect of an early application of NPPV seems faster than the pharmacological action. Currently, many experts find that there is insufficient evidence to recommend NIV in acute asthma. For these reasons, in our opinion, NIV for patients with severe status asthmaticus not improving under conventional medical therapy and on the edge of intubation is the only possibility of decreasing morbidity and mortality of this acute situation. However, it is mandatory to comply with the rules of maximal security in term of staff, rapid access to endotracheal intubation and monitoring.

References

1. Agarwal R, Malhotra P, Gupta D. Failure of NIV in acute asthma : case report and a word of caution. Emerg. Med. J. 2006;23: 9-10.

2.Thys F, Roeseler J, Marion E, El Gariani A, Meert P, Danse E et al. Non invasive ventilation in severe status asthmaticus, a new therapeutic approach ? Two case reports. Réan Urg 1998; 7: 423-6.

3. Thys F, Roeseler J, Reynaert M.S, Liistro G, Rodenstein D.O. Non invasive ventilation for acute respiratory failure: a prospective randomized placebo-controlled trial. Eur Respir J 2002; 20: 545-555.

4. 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; 1: CD004360.