Clinical review: severe asthma

Abstract

Severe asthma, although difficult to define, includes all cases of difficult/therapy-resistant disease of all age groups and bears the largest part of morbidity and mortality from asthma. Acute, severe asthma, status asthmaticus, is the more or less rapid but severe asthmatic exacerbation that may not respond to the usual medical treatment. The narrowing of airways causes ventilation perfusion imbalance, lung hyperinflation, and increased work of breathing that may lead to ventilatory muscle fatigue and life-threatening respiratory failure. Treatment for acute, severe asthma includes the administration of oxygen, beta2-agonists (by continuous or repetitive nebulisation), and systemic corticosteroids. Subcutaneous administration of epinephrine or terbutaline should be considered in patients not responding adequately to continuous nebulisation, in those unable to cooperate, and in intubated patients not responding to inhaled therapy. The exact time to intubate a patient in status asthmaticus is based mainly on clinical judgment, but intubation should not be delayed once it is deemed necessary. Mechanical ventilation in status asthmaticus supports gas-exchange and unloads ventilatory muscles until aggressive medical treatment improves the functional status of the patient. Patients intubated and mechanically ventilated should be appropriately sedated, but paralytic agents should be avoided. Permissive hypercapnia, increase in expiratory time, and promotion of patient-ventilator synchronism are the mainstay in mechanical ventilation of status asthmaticus. Close monitoring of the patient's condition is necessary to obviate complications and to identify the appropriate time for weaning. Finally, after successful treatment and prior to discharge, a careful strategy for prevention of subsequent asthma attacks is imperative.

Figure 1

Relationship of volume and pressure in the respiratory system. Dynamic hyperinflation adds an elastic load to inspiratory muscles: to initiate inspiratory flow the inspiratory muscles must first overcomeintrinsic positive end-expiratory pressure (PEEP_I). Dynamic hyperinflation shifts tidal breathing to a less compliant part of the respiratory system pressure-volume curve leading to an increased pressure-volume work of breathing. FRC, functional residual capacity.

Figure 2

Pneumomediastinum-bilateral pneumothorax in an intubated patient in status asthmaticus. Radiolucent stripes along the soft tissues of the mediastinum, and the continuous diaphragm sign indicate the presence of pneumomediastinum. Bilateral pneumothorax is also seen (deep costophrenic sulcuses and hyperlucent hemidiaphragms bilaterally). Subcutaneous emphysema is also seen on the left of the figure.

Figure 3

Tracheoesophageal fistula in an intubated patient in status asthmaticus (iatrogenic complication). (a) The chest x-ray shows an abnormal distension of the fundus of the stomach. (b) The overinflated balloon of the endotracheal tube is evident in the computerized tomography of the chest and upper abdomen. The lumen of the endotracheal tube is seen centrally. The nasogastric tube is slightly displaced on the left by the endotracheal balloon and indicates the position of the esophagus. (c) At lower level, the trachea has a normal configuration. The nasogastric tube is again seen, but the esophagus is dilated with air (tracheoesophageal fistula). (d) Extensive dilatation of the fundus of the stomach is seen. The nasogastric junction is indicated by the visualization of the nasogastric tube.

Figure 4

Measurement of the end-inspired volume (V_EI) above apneic functional residual capacity (FRC) in order to estimate lung hyperinflation. The total exhaled volume during a period of apnea (20–60 seconds) is measured. V_EI is the volume of gas at the end of inspiration above FRC and is the sum of the tidal volume and the volume at end exhalation above FRC (V_EE). Published with permission from American Review of Respiratory Disease [68].

Figure 5

Measurement of end-inspiratory plateau pressure, an estimate of average end-inspiratory alveolar pressures. The peak-to-plateau gradient is easily determined by stopping flow at end-inspiration and can be used as a measure of the severity of inspiratory airway resistance. The plateau pressure is a reflection of the respiratory system pressure change resulting from the delivery of the tidal volume, added to any level of intrinsic positive end-expiratory pressure. The plateau pressure is a useful marker of lung hyperinflation and should be maintained at less than 30 cmH₂O. The dotted line indicates a high peak-to-plateau gradient observed in status asthmaticus. Published with permission from Principles of Critical Care [69].

Figure 6

Measurement of intrinsic positive end-expiratory pressure. Intrinsic positive end-expiratory pressure is the lowest average alveolar pressure achieved during the respiratory cycle and is obtained by an end-expiratory hold manoeuvre. In the non-obstructed patient, alveolar pressure (P_ALV) equals pressure at the airway opening (P_AO) both at end inspiration and end expiration. In the severely obstructed patient, P_ALV may increase because of air trapping, and at end expiration P_ALV does not equal P_AO. If an expiratory hold manoeuvre is performed, P_AO will rise, reflecting the degree of lung hyperinflation. Published with permission from Principles of Critical Care [69].