Contemporary treatment of children with critical and near-fatal asthma

Abstract

Asthma is the most common chronic illness in childhood. Although the vast majority of children with acute asthma exacerbations do not require critical care, some fail to respond to standard treatment and require escalation of support. Children with critical or near-fatal asthma require close monitoring for deterioration and may require aggressive treatment strategies. This review examines the available evidence supporting therapies for critical and near-fatal asthma and summarizes the contemporary clinical care of these children. Typical treatment includes parenteral corticosteroids and inhaled or intravenous beta-agonist drugs. For children with an inadequate response to standard therapy, inhaled ipratropium bromide, intravenous magnesium sulfate, methylxanthines, helium-oxygen mixtures, and non-invasive mechanical support can be used. Patients with progressive respiratory failure benefit from mechanical ventilation with a strategy that employs large tidal volumes and low ventilator rates to minimize dynamic hyperinflation, barotrauma, and hypotension. Sedatives, analgesics and a neuromuscular blocker are often necessary in the early phase of treatment to facilitate a state of controlled hypoventilation and permissive hypercapnia. Patients who fail to improve with mechanical ventilation may be considered for less common approaches, such as inhaled anesthetics, bronchoscopy, and extracorporeal life support. This contemporary approach has resulted in extremely low mortality rates, even in children requiring mechanical support.

Conflict of interest statement

Conflicts of interest: None.

Figures

Figure 1

Schematic representation of the airway gas flow tracing over time during volume control ventilation. A) Normal tracing with no evidence of increased airway resistance. B) Expiratory flow does not return to zero prior to the initiation of the following breath, resulting in gas trapping and auto-PEEP. C) After ventilator setting optimization (lower respiratory rate and longer expiratory time), expiratory flow returns to baseline prior to initiation of the following breath.

Figure 2

Schematic representation of the airway pressure waveform over time during volume control ventilation. The peak-to-plateau pressure difference (double-headed arrow) is obtained after an inspiratory hold by comparing the peak pressure and the measured plateau pressure.

Figure 3

Upper panel: schematic representation of the measurement of end-inspiratory lung volume above functional residual capacity both with (A) and without (B) positive end-expiratory pressure by a period of apnea during steady-state ventilation. Lower panel: the effect of positive end-expiratory pressure (0, 5, 10 and 15cmH2O) on lung volumes at each level of minute ventilation (respiratory rate 10, 16 and 20 breaths/min). Note that the application of positive end-expiratory pressure leads to a progressive increase in lung volume due to increased functional residual capacity and volume of trapped gas above functional residual capacity, particularly at faster respiratory rates. FRC - functional residual capacity; FRCPEEP - functional residual capacity resulting from PEEP; PEEP - positive end-expiratory pressure; VEI - end-inspiratory lung volume above FRC; VT - tidal volume; VTrap - volume of trapped gas above FRC; RR - respiratory rate. Source: Tuxen DV. Detrimental effects of positive end-expiratory pressure during controlled mechanical ventilation of patients with severe airflow obstruction. Am Rev Respir Dis. 1989;140(1):5-9.(82)

Figure 4

Schematic representation of capnogram tracings under various clinical conditions. The interrupted lines mark the reference value for arterial partial pressure of carbon dioxide. Under normal conditions (a), the end-tidal carbon dioxide tracing plateaus during exhalation and approximates the partial pressure of carbon dioxide. In near-fatal asthma (b) severe airflow obstruction is manifested by the up-sloping of the expiratory phase tracing and absence of a plateau, suggesting incomplete exhalation prior to the following inspiration. Note the wider gap between the end-tidal carbon dioxide and partial pressure of carbon dioxide. Attempting to address the higher partial pressure of carbon dioxide by increasing the respiratory rate (c) leads to an even higher partial pressure of carbon dioxide and a wider gap between the partial pressure of carbon dioxide and end-tidal carbon dioxide, along with hyperinflation and its attendant side effects. Decreasing the respiratory rate (d) leads to a longer expiratory time and more complete exhalation, with an end-tidal carbon dioxide measurement that more closely reflects the partial pressure of carbon dioxide. ETCO2 - end-tidal carbon dioxide; PaCO2 - partial pressure of carbon dioxide.