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Acute severe asthma exacerbations in children younger than 12 years: Endotracheal intubation and mechanical ventilation

Acute severe asthma exacerbations in children younger than 12 years: Endotracheal intubation and mechanical ventilation
Literature review current through: Jan 2024.
This topic last updated: Jul 18, 2018.

INTRODUCTION — Asthma is the most frequent cause of hospitalization among children in the United States and, as of 1999, was the source of nearly 500,000 admissions per year to pediatric intensive care units (PICUs) [1]. Asthma prevalence continues to rise. However, mortality rates in children and adults have begun to fall since 1999 [2].

Endotracheal intubation and mechanical ventilation of children with acute severe asthma exacerbation (ie, status asthmaticus) are discussed here. General intensive care unit (ICU) management, primarily pharmacotherapy, and non-ICU inpatient management are discussed in greater detail separately. Mechanical ventilation for adults with severe asthma is also reviewed separately. (See "Acute severe asthma exacerbations in children younger than 12 years: Intensive care unit management" and "Acute asthma exacerbations in children younger than 12 years: Inpatient management" and "Invasive mechanical ventilation in adults with acute exacerbations of asthma".)

Pharmacologic management of acute asthma exacerbations and management of chronic childhood asthma also are discussed separately. (See "Acute asthma exacerbations in children younger than 12 years: Emergency department management" and "Asthma in children younger than 12 years: Initial evaluation and diagnosis" and "Asthma in children younger than 12 years: Management of persistent asthma with controller therapies" and "Asthma in children younger than 12 years: Quick-relief (rescue) treatment for acute symptoms".)

GENERAL PRINCIPLES — Children with acute severe asthma who fail to improve with initial treatment in the emergency department should be admitted to the pediatric intensive care unit (PICU). Intensive care unit (ICU)-level management of these children entails the administration of glucocorticoids, aggressive bronchodilator therapy, and close monitoring [3]. Use of noninvasive positive pressure ventilation (NPPV) may help avoid the need for intubation in many patients who progress toward respiratory muscle fatigue by reducing the work of breathing until maximal therapeutic effects of pharmacotherapy take place. Earlier use in the emergency department, rather than waiting until admission to the PICU, is increasing as familiarly with this modality grows [4]. (See "Acute severe asthma exacerbations in children younger than 12 years: Intensive care unit management", section on 'Pharmacotherapy' and "Acute severe asthma exacerbations in children younger than 12 years: Intensive care unit management", section on 'Noninvasive positive pressure ventilation'.)

Mechanical ventilation is reserved for patients with continued progression toward respiratory failure despite maximal medical therapy. The use of mechanical ventilation during an asthma exacerbation has associated morbidities, but mortality due to complications that occurred after ICU admission is uncommon [5-9]. Within PICUs, mechanical ventilation rates for children with asthma vary from center to center, with published rates ranging from <1 percent to 10 to 20 percent [5,6,8]. (See 'Endotracheal intubation and mechanical ventilation' below and 'Outcomes' below and "Acute severe asthma exacerbations in children younger than 12 years: Intensive care unit management", section on 'Prognosis'.)

The need for mechanical respiratory support and potential invasive ventilation should be considered early in the course of illness. The best way to avoid intubation is to rapidly escalate the preintubation therapies in patients with a worsening trajectory indicated by increased work of breathing or carbon dioxide (CO2) retention. Several reports have shown that children intubated prior to ICU care are on mechanical ventilation for a shorter duration, most likely because the patients were intubated prior to intensive delivery of bronchodilators and glucocorticoids [6,8,10]. (See "Acute severe asthma exacerbations in children younger than 12 years: Intensive care unit management", section on 'Preintubation therapies'.)

Mechanical ventilation in a child with an asthma exacerbation is always challenging due to airway obstruction, impaired exhalation, and risk of barotrauma. The decision to intubate a patient to prevent severe hypoxia should be made with great care since tracheal stimulation can worsen the asthma exacerbation and frequently worsens airway obstruction and hypercarbia. (See 'Complications' below.)

Adjunctive therapies may be necessary for children who do not improve despite aggressive pharmacologic therapy and mechanical ventilation. (See 'Adjunctive therapies' below.)

SUPPORTIVE CARE — Children admitted to the intensive care unit (ICU) with severe asthma require close cardiopulmonary monitoring, particularly those on mechanical ventilation. Supportive measures for children with asthma who require mechanical ventilation include analgesia, sedation, and potentially also muscle relaxation if a spontaneous breathing mode is not used [6,11-13]. These supportive measures help to prevent breath stacking and ventilator dyssynchrony, which can aggravate hypercapnia. Most patients are also given intravenous fluids to treat dehydration and prevent hypotension. Sedation and paralysis are reviewed below. Other supportive measures are discussed in detail separately. (See "Acute severe asthma exacerbations in children younger than 12 years: Intensive care unit management", section on 'Supportive care'.)

Sedation and paralysis — A variety of agents can be used for sedation for the patient with asthma who requires intubation and mechanical ventilation. The sedative agents that can be used for intubation include fentanyl, midazolam, ketamine, propofol, and etomidate. Morphine may generate histamine release and therefore is generally avoided. Additionally, neuromuscular blocking agents may be used to optimize intubating conditions. Once patients are intubated, sedation is also used to promote patient/ventilator synchrony and blunt tachypnea in order to reduce the risk of air trapping and barotrauma.

Of the sedative agents that are available to facilitate intubation, ketamine is most commonly used. Ketamine, a synthetic derivative of phencyclidine, is often recommended as the induction agent of choice for the asthma patient requiring intubation because it has bronchodilatory as well as sedative effects. Ketamine also has been administered as a continuous infusion in patients receiving invasive or noninvasive positive pressure ventilation (NPPV) for asthma [14]. When used in this fashion, a loading dose of 2 mg/kg is followed by an infusion of 20 to 60 micrograms/kg/min [3]. The evidence in support of use of ketamine in children is limited. In one study, improvements were seen in the partial pressure of oxygen in arterial blood to the fraction of inspired oxygen (PaO2/FiO2) ratio in all patients studied, and dynamic compliance, partial pressure of carbon dioxide (pCO2), and peak inspiratory pressures (PIP) improved in those mechanically ventilated [3]. (See "Rapid sequence intubation (RSI) in children for emergency medicine: Medications for sedation and paralysis", section on 'Sedation (induction) agents'.)

Propofol is another agent that is used to facilitate intubation in children. It is a potent hypnotic/anesthetic agent that accomplishes global central nervous system depression via activation of gamma-aminobutyric acid (GABA) receptors. Propofol decreases the cerebral metabolic rate for oxygen consumption and reduces intracranial pressure. In addition, it is reported to have anti-inflammatory properties and to dilate central airways. For this reason, it is commonly used to facilitate intubation in patients with status asthmaticus [15]. There are documented reports of propofol-induced bronchoconstriction in some patients with atopy and drug-induced asthma but bronchodilation in others [16].

Unlike ketamine, for which there is no prohibition against prolonged use in the pediatric intensive care unit (PICU), prolonged use of propofol (>48 hours) is associated with propofol infusion syndrome that includes cardiac and renal failure, rhabdomyolysis, hepatomegaly, hyperkalemia, hypertriglyceridemia, and metabolic acidosis [16-18]. It occurs more commonly in children and in critically ill patients treated with glucocorticoids and catecholamines and is not recommended for continuous sedation in the PICU by the US Food and Drug Administration (FDA) [19-21]. Nonetheless, there are numerous studies that have demonstrated the safe use of propofol for sedation in over 500 PICU patients, suggesting that propofol can be at doses <4 mg/kg/hour for under 48 hours in this population [22-24].

A broad range of medications are also available for maintenance of sedation in intubated pediatric patients with asthma. Fentanyl and midazolam in combination are commonly used in the PICU setting to accomplish sedation [25]. Dexmedetomidine, a selective alpha-2-receptor agonist, is approved for use for up to 24 hours in the adult population. There are multiple reports of its safety and efficacy in the pediatric population [26]. Dosing is largely extrapolated from the adult literature. Patients are typically loaded with 0.5 to 1 mcg/kg over 10 to 20 minutes, but some pediatric centers reduce or eliminate the loading dose in an effort to avoid hypotension and bradycardia, the two most commonly encountered adverse effects in the pediatric population. The available literature espouses an infusion dose range from 0.2 to 0.7 mcg/kg/hour. The pediatric literature suggests that infusions can be safely given beyond the recommended limit of 24 hours and at doses as high as 2 mcg/kg/hour. In addition to sedation for the ventilated patient, dexmedetomidine is also used to facilitate tolerance of NPPV [27].

Neuromuscular blockade may be employed as an adjunct to intubation and to blunt tachypnea and ventilator dyssynchrony in sedated patients receiving assisted ventilation [11]. However, efforts should be made to discontinue the use of neuromuscular blocking agents as soon as is feasible since their use in combination with glucocorticoids is associated with an increased risk of myopathy of critical illness [5,28-34]. In addition, pressure support cannot be used in a paralyzed patient. Spontaneous breathing modes of mechanical ventilation are generally more comfortable and use substantially lower peak airway pressures. (See 'Pressure support' below and "Rapid sequence intubation (RSI) in children for emergency medicine: Medications for sedation and paralysis", section on 'Paralytic agents'.)

ENDOTRACHEAL INTUBATION AND MECHANICAL VENTILATION — Intubation should be approached cautiously in patients with status asthmaticus because manipulation of the airway can cause increased airflow obstruction due to exaggerated bronchial responsiveness. Adequate venous access, frequent noninvasive blood pressure monitoring, and sedation should be optimized before intubation. The clinician most experienced with airway management should perform the intubation. (See "Technique of emergency endotracheal intubation in children" and "Rapid sequence intubation (RSI) in children for emergency medicine: Approach".)

Clinicians must be prepared to manage acute deterioration due to tube malposition, tube obstruction, pneumothorax, equipment failure, and/or hypotension [35]. (See 'Complications' below.)

Indications — The decision to intubate a patient with status asthmaticus is made based upon clinical findings (eg, inability to speak, confusion or somnolence, hypoxia despite supplemental oxygen) and physiologic changes (eg, moderate-to-severe hypercapnia). Care must be taken to control the airway before the patient suffers a respiratory arrest or a hypoxic insult. (See "Technique of emergency endotracheal intubation in children".)

Indications for intubation in patients with acute severe asthma include:

Hypoxemia despite provision of high concentrations of oxygen or noninvasive positive pressure ventilation (NPPV; partial pressure of oxygen [pO2] <60 on 100 percent oxygen or NPPV)

Severe and unremitting increased work of breathing (eg, inability to speak)

Altered mental status

Respiratory or cardiac arrest

Hypercarbia alone is not an indication for intubation [5,36,37]. However, intubation is warranted if a patient demonstrates a progressively rising arterial partial pressure of carbon dioxide (PaCO2) despite maximal medical therapy and/or NPPV and if hypercarbia is causing significant respiratory acidosis or altered mental status.

Goals — The goals of endotracheal intubation and mechanical ventilation for children with status asthmaticus and respiratory failure are [38]:

To relieve work of breathing from the exhausted patient and allow respiratory muscle rest

To ensure adequate oxygenation (see 'Oxygenation' below)

To ensure sufficient (not necessarily normal) gas exchange (initial hypercarbia is tolerated) until airway obstruction can be reversed (see 'Ventilation strategy' below)

These goals should be accomplished with the fewest adverse effects. The patient should be given breaths with a bag and in-line manometer prior to initiating mechanical ventilation. Careful noting of the number of seconds needed for expiration to finish is important to avoid breath stacking, auto-positive end-expiratory pressure (PEEP), and the resultant increased end-expiratory and inspiratory lung volumes that increase alveolar pressure, the risk of barotrauma, and may compromise cardiac function by increasing pulmonary vascular resistance. The respiratory rate (RR) on the ventilator should be sufficiently low to permit a normal inspiratory time and a generous expiratory time. (See 'Complications' below.)

Oxygenation — Adequate oxygenation is usually achieved without difficulty in most patients with asthma since the airways, not the alveoli, are the primary targets of inflammation and bronchospasm. However, mucus plugging, atelectasis, hyperinflation, and ventilation/perfusion (V/Q) mismatch may contribute to hypoxemia. In mechanically ventilated patients, oxygenation is affected primarily by the fraction of inspired oxygen (FiO2) and mean airway pressure. (See 'Ventilator settings' below.)

Atelectasis that results from mucus plugging can usually be treated with judicious application of PEEP, as well as regular removal of secretions from the endotracheal tube [39]. In addition, positioning of the patient so that collapsed lung segments are nondependent helps to improve atelectasis.

If these measures prove insufficient, extrinsic PEEP above initial PEEP (3 to 5 cm H2O is suggested) may be carefully applied. The careful titration of PEEP may help recruit atelectatic lung units. Hyperinflation, however, by generating more zone I physiology (where alveolar pressure exceeds pulmonary arterial pressure), may produce V/Q mismatch and therefore worsen hypoxemia. (See 'Ventilator settings' below.)

Ventilation strategy — Successful mechanical ventilation in patients with asthma depends upon limiting the risk of hyperinflation and barotrauma. The risk of hyperinflation is reduced by decreasing the minute volume and permitting adequate time for complete exhalation before the next inhalation begins. Dropping the RR while maintaining a normal (constant) inspiratory time increases the expiratory time, thereby decreasing the ratio of inspiratory to expiratory time (I:E ratio) [11]. The risk of barotrauma is decreased by minimizing hyperinflation and peak inspiratory pressures (PIP). For these reasons, many consider pressure support ventilation (PSV) the ideal mode of ventilation for the intubated patient with asthma. However, pressure control and volume control may also be used. There is no evidence to support one mode of ventilation over another. (See 'Ventilator settings' below and 'Dynamic hyperinflation' below and 'Barotrauma' below.)

Diminishing the risk of hyperinflation and barotrauma requires acceptance of an initial PaCO2 that is higher than normal with an accompanying respiratory acidosis, a strategy that is called "permissive hypercapnia" or "controlled hypoventilation" [40,41]. A slow increase in PaC02 (approximately 10 mmHg/hour) permits intracellular buffering mechanisms to accommodate the decreasing serum pH [12]. This strategy is widely used in patients with asthma [40,42-44]. Permissive hypercarbia is well tolerated by children with normal cardiac function. However, those with concurrent chronic conditions, such as cyanotic heart disease, cardiomyopathy, or pulmonary hypertension, will probably not tolerate this strategy. Other potential contraindications to permissive hypercapnic ventilation include increased intracranial pressure, poor myocardial function, and coexistent metabolic acidosis (eg, patients with renal disease).

Ventilatory modes — A variety of ventilatory modes have been successfully employed in the management of patients with asthma who require intubation [11,45]. These include pressure control ventilation (PCV), pressure support ventilation (PSV), volume control ventilation (eg, pressure-regulated volume control [PRVC]), and synchronized intermittent mandatory ventilation (SIMV), which is delivered with pressure control (SIMV/PC) or volume control (SIMV/VC).

Volume control ventilation (eg, PRVC or SIMV/VC) allows for consistent minute ventilation (RR x tidal volume [TV]) in the face of changing airway resistance and lung compliance. PRVC assures that the patient receives the desired/set TV at the lowest peak pressure possible [12].

Volume control — In volume control ventilation (PRVC or SIMV/VC), inspiration is terminated after delivery of a preset TV. An advantage to volume control ventilation is that it permits comparison of PIP and plateau pressure (Pplat) measurements (peak-to-plateau measurements), which provides an indication of airway resistance and response to therapy [11]. A disadvantage is that peak pressures may be elevated, depending upon airway resistance, mucus plugging, and the degree of atelectasis. Volume control is an acceptable mode of mechanical ventilation and is preferred by some. However, the patient may need to be transitioned to PRVC and/or paralyzed if the PIP or Pplat rise above 35 cm or 30 H2O, respectively, with the caveat that use of neuromuscular blockade should be kept to a minimum in an effort to avoid myopathy of critical illness.

Pressure-regulated volume control — PRVC is a mode specific to the Servo 300 and Servo I ventilators (the latter has SIMV/PRVC) that assures the patient receives the desired/set TV but at the lowest peak pressure possible. PRVC offers advantages of both volume and PCV. These include optimal decelerating inspiratory flow, assured TV, and minimized airway pressures [11].

Pressure control — In pressure control ventilation (SIMV/PC), inspiration ceases when a preset maximum pressure is reached. The delivered volume varies depending upon lung mechanics (eg, airway resistance, lung compliance, hyperinflation), and minute ventilation is not assured.

Pressure support — PSV is flow cycled in that, once triggered by a demand valve, the preset pressure is sustained until the inspiratory flow tapers, usually to 25 percent of its maximal value [46]. The clinician determines the final airway pressure with PSV. TV and RR (ie, minute volume) are a consequence of patient-related variables plus ventilator settings. Increasing levels of PSV can be used to decrease patient effort early in the course of mechanical ventilation [13]. PSV decreases patient-ventilatory dyssynchrony and is useful when weaning from ventilatory support [5]. Functionally, PSV (invasive) is equivalent to bilevel positive airway pressure (BiPAP; noninvasive). As with PCV, minute ventilation is not assured. (See 'Weaning from mechanical ventilation' below.)

Synchronized intermittent mandatory ventilation — In SIMV, the ventilator delivers breaths based upon a preset TV or peak pressure and RR that are synchronized with the patient's inspiratory effort. However, if the patient fails to initiate a breath, a full TV breath will be delivered at the appropriate interval (ie, one breath every five seconds if the RR is set at 12 breaths per minute). SIMV can be delivered with volume control (SIMV/VC) or pressure control (SIMV/PC). Volume control is preferred at the author's institution. SIMV/VC along with PSV is useful when weaning from ventilatory support. (See 'Weaning from mechanical ventilation' below.)

Ventilator settings — The choice of mechanical ventilator settings must take into account the physiologic derangements of acute severe asthma, including airflow obstruction and atelectasis [11], as well as the objectives of minimizing hyperinflation and barotrauma.

Initial ventilator settings are adjusted as necessary to maintain adequate ventilation, as assessed by chest auscultation and measurement of arterial blood gases (table 1), and to prevent complications. The placement of an indwelling arterial catheter facilitates obtaining frequent arterial blood samples and continuous arterial pressure monitoring; however, many children who are intubated prior to intensive care unit (ICU) admission are intubated for a day or less and frequently may not require invasive vascular pressure monitors [6,8,10,47]. This is likely because the patients were intubated prior to intensive delivery of bronchodilators and glucocorticoids. (See 'Ventilation strategy' above and 'Complications' below and "Acute severe asthma exacerbations in children younger than 12 years: Intensive care unit management", section on 'Monitoring' and "Arterial puncture and cannulation in children".)

Fraction of inspired oxygen (FiO2) — The fraction of inspired oxygen (FiO2) should be set at 1.0 upon intubation. FiO2 is then decreased as tolerated to concentrations of 0.5 or lower to maintain oxygen saturation >92 percent [12]. Use of an FiO2 of 1.0 for prolonged periods in patients with asthma predisposes them to resorption atelectasis and should therefore be avoided.

Respiratory rate — The RR should be set near or below physiologic rates (8 to 12 breaths per minute) [40], keeping the minute ventilation under 115 mL/kg per minute. (See "Invasive mechanical ventilation in adults with acute exacerbations of asthma".)

Tidal volume — The delivered TV should initially be 6 to 8 mL/kg [12]. The peak and Pplat attained with these volumes should be noted and kept under 40 cm H2O and 30 to 35 cm H2O, respectively. Maintaining these limits helps to minimize dynamic hyperinflation and barotrauma [12]. The TV may need to be reduced if the peak pressure limit exceeds 40 cm H2O [11]. Reducing the TV will result in increased PaCO2. (See 'Dynamic hyperinflation' below and 'Barotrauma' below and 'Ventilation strategy' above.)

Inspiratory and expiratory times and inspiratory flow — Inspiratory times should be normal to slightly low for patient age (0.75 to 1.2 seconds) and the RR sufficiently low so that the expiratory time prevents breath stacking. Thus, the cycle time is six seconds if the RR is 10, and the I:E ratio is 1:5 if the inspiratory time is one second.

Expiratory time should be maximized to allow complete exhalation, avoid hypercarbia, and prevent dynamic hyperinflation and intrinsic PEEP (elevation of alveolar pressure above atmospheric pressure or set PEEP at the end of exhalation, also called auto-PEEP).

To this end, inspiratory flow should be set at the highest rate the patient can tolerate without generating excessively high peak pressures. Flow rates of 4 to 10 L/kg per minute, with a maximum of 80 to 100 L/minute, are typically employed in children during PCV [48].

Positive end-expiratory pressure (PEEP) — Some degree of extrinsic PEEP is necessary to compensate for the external resistance added to the respiratory tract by the endotracheal tube (eg, PEEP of 3 to 5 cm H2O). The use of extrinsic PEEP beyond this amount in the ventilated patient with asthma is considered controversial by some [11,12,49,50]. However, other experts feel that PEEP is a helpful intervention with proper precautions, particularly in patients with atelectasis, since PEEP can effectively stent open collapsed airways, improve ventilation, and potentially reduce air trapping [49]. Application of low levels of PEEP also may relieve dyspnea by facilitation of ventilator triggering and synchronization for intubated patients capable of taking spontaneous breaths [11,49,50]. Higher levels of PEEP (5 to 8 cm H2O) may be beneficial for children demonstrating persistent and severe hypercarbia despite appropriate TV (6 to 10 mL/kg) and expiratory times that permit complete exhalation.

We suggest setting PEEP at a minimum of 3 to 5 cm H2O initially. PEEP may be increased in increments of 1 cm H2O to determine whether additional PEEP improves ventilation. Most patients with asthma can be successfully managed with PEEP in the range of 3 to 8 cm H2O. Care must be taken to ensure that extrinsic PEEP does not exceed intrinsic or auto-PEEP. At the author's institution, PEEP is carefully titrated by senior clinicians present at the bedside assessing plateau pressures, auto-PEEP, work of breathing, and ventilator graphics (flow-time loops in particular). PEEP should be adjusted or diminished if adverse effects occur (eg, dynamic hyperinflation). (See 'Inspiratory and expiratory times and inspiratory flow' above and 'Dynamic hyperinflation' below.)

Monitoring — Mechanically ventilated patients may require arterial and central venous access for hemodynamic monitoring, in addition to standard cardiorespiratory monitoring. Of the graphics available on most modern ventilators, the flow time curve is one parameter that allows for relatively easy assessment of air trapping. If the patient has sufficient time to exhale, the expiratory flow should to return to zero before the next breath begins (figure 1). (See "Acute severe asthma exacerbations in children younger than 12 years: Intensive care unit management", section on 'Monitoring'.)

Delivery of inhaled medications — There are a variety of ventilator-compatible nebulization systems that allow for the continuous delivery of inhaled bronchodilators through the ventilator circuit. However, intravenous administration of bronchodilator therapy is probably a more reliable delivery route than inhalation in patients who present in extremis or who come to require noninvasive or invasive mechanical ventilation [51].

ADJUNCTIVE THERAPIES — In extreme cases, airflow obstruction is so severe that sufficient ventilation cannot be achieved despite intensive bronchodilator therapy, intravenous glucocorticoids, ventilatory support, sedation, and paralysis. In such cases, adjunctive therapies, such as inhalational anesthetics or extracorporeal membrane oxygenation (ECMO), may be successful as rescue measures. However, the routine use of these therapies cannot be recommended on the basis of existing clinical studies. They remain heroic rescue maneuvers for the extremely refractory patient.

Inhalational anesthetics — The inhalational anesthetics, halothane, isoflurane, and sevoflurane, are potent bronchodilators. The positive effects of isoflurane for status asthmaticus have been described in a few case series [52-54]. The ventilator used to deliver these agents must have a scavenger system to prevent staff exposure to the anesthetic agents. Their mechanisms of action are unknown but are purported to include direct smooth muscle relaxation, reduction of vagal tone, and synergy with catecholamines. Inhalation anesthetics can generate hypotension. Delivery in some pediatric intensive care units (PICUs) may be difficult given lack of familiarity with anesthesia machines by pediatric intensivists [52-55]. In addition, use of these agents is associated with substantially increased hospital costs. A majority of PICUs never use volatile agents [56].

Practical limitations to the use of inhalational anesthetics include the abrupt return of bronchoconstriction after discontinuation and the need for delivery via an anesthesia machine with proper scavenging of anesthetic gas (to avoid the second-hand inhalation of aerosolized anesthetic by health care personnel or other patients). This usually requires the bedside presence of an anesthesiologist, who can provide guidance regarding the dose, duration, and discontinuation of inhalational anesthetic.

The use of inhalational anesthetics may be tried as a rescue maneuver in children with acute severe asthma exacerbations who have continued ventilatory failure despite appropriate mechanical ventilation and aggressive medical therapy.

Extracorporeal membrane oxygenation — In case reports, ECMO has been used to successfully treat acute severe asthma [56-59]. However, the use of ECMO in such patients is a heroic measure that requires the availability of an ECMO center. The use of ECMO is precluded in all but the most desperate situations.

COMPLICATIONS — Complications can result from the asthma exacerbation itself or the treatments. Patients with an acute severe asthma exacerbation are at risk for progressive air trapping and alveolar hyperinflation, which may lead to alveolar rupture and hemodynamic compromise. Endotracheal intubation with mechanical ventilation in the child with asthma can be associated with significant morbidity including hypotension, barotrauma (including pneumothorax), and myopathy. These complications occur in 10 to 26 percent of children who are ventilated for asthma [6,9,40,60], and more than one-half of complications occur during or immediately after intubation [61]. Common causes of acute deterioration in intubated patients include tube displacement or malposition, tube obstruction, pneumothorax, and equipment failure [62].

Dynamic hyperinflation — Airflow obstruction during expiration slows lung emptying and may lead to increased lung volume. Expansion of lung volume may increase airway caliber and can reduce the resistive work of breathing. However, this physiologic response becomes maladaptive in patients with severe asthma because it increases mechanical load and elastic work of breathing [28]. Obstruction to expiratory airflow may lead to initiation of inspiration before the preceding exhalation is complete (ie, before the lung has reached the static equilibrium volume leaving lung volume above functional residual capacity [FRC]). This phenomenon is called dynamic hyperinflation (figure 1) [63].

Dynamic hyperinflation increases the magnitude of the drop in airway pressure that the patient must generate to trigger a breath, thereby increasing the patient's workload (figure 2). It can also cause alveolar overdistention resulting in hypoxemia, hypotension, or alveolar rupture. Dynamic hyperinflation can occur in patients with asthma in the absence of positive pressure, but it is more common, and potentially more difficult to manage, in ventilated patients due to the use of positive pressure.

There are several ways to assess for the presence of dynamic hyperinflation. These include measurement of the end inspiratory plateau pressure (Pplat), end-inspired volume (VEI) above apneic functional residual capacity, or intrinsic or auto-positive end-expiratory pressure (PEEP) [28]. The Pplat measure is obtained by pausing ventilation briefly (0.4 seconds) at end inspiration and measuring the airway pressure. Keeping Pplat below 30 cm H2O can decrease complications. Whether this measure is valid in children is unknown. The latter two measurements have limitations and are less commonly used. (See "Invasive mechanical ventilation in adults with acute exacerbations of asthma".)

Interventions to correct air trapping include decreasing the respiratory rate (RR; functionally increasing expiratory time), increasing inspiratory flow rates (functionally decreasing the inspiratory time), and lowering the tidal volume (TV). In adults, limiting minute ventilation is the key to avoiding dynamic hyperinflation. Keeping the minute ventilation under 115/mL/kg is a recommended goal in children (table 1). (See 'Ventilator settings' above and "Invasive mechanical ventilation in adults with acute exacerbations of asthma".)

Barotrauma — Pulmonary barotrauma in the mechanically ventilated patient is the result of alveolar rupture and is characterized by the development of extra-alveolar air. Barotrauma occurs when the transalveolar pressure increases to a degree that disrupts the structural integrity of the alveolus. This leads to alveolar rupture and interstitial emphysema. A pneumothorax results if the interstitial emphysema dissects along perivascular sheaths into the mediastinum and then the mediastinal parietal pleura ruptures. (See "Diagnosis, management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in adults".)

Dissection of air elsewhere along fascial planes can result in pneumomediastinum, pneumoperitoneum, or subcutaneous emphysema [64]. Other clinical manifestations of pulmonary barotrauma include bronchopleural fistula, tension pneumothorax, tension lung cysts, hyperinflation of the left lower lobe, systemic gas embolism, and subpleural air cysts [65].

Pneumothorax should be suspected if the patient becomes hypoxemic and hypotensive following intubation and the hypoxemia and hypotension do not respond to fluid administration and alteration in ventilatory pattern [5]. A chest radiograph should be performed promptly so that treatment can be provided expeditiously. Needled decompression may be required prior to radiographic confirmation if the patient has or is about to suffer cardiovascular collapse. The most experienced clinician should perform needle decompression or insertion of a chest tube for pneumothorax [62]. (See "Causes of acute respiratory distress in children", section on 'Tension pneumothorax'.)

Hypotension — Hypotension is a risk in any patient who is transitioned from negative- to positive-pressure ventilation. This risk is increased in patients with asthma who are mechanically ventilated. The hyperinflation that is intrinsic to asthma and the increased intrathoracic pressure associated with positive-pressure ventilation impede venous return to the heart. This effect may be compounded by the administration of sedatives and paralytics, which act as vasodilators and myocardial depressants. (See 'Sedation and paralysis' above.)

Several steps can be taken to minimize the risk of hypotension in patients with asthma who require mechanical ventilation. These include measures to limit peak pressure and avoid hyperinflation, as described above. Patients also may benefit from the administration of intravenous fluids to improve and optimize intravascular volume. Optimization of intravascular volume may help to blunt the tachycardia that results from vasodilation associated with systemic absorption of bronchodilators. (See 'Dynamic hyperinflation' above and "Acute severe asthma exacerbations in children younger than 12 years: Intensive care unit management", section on 'Fluid support'.)

Clinicians caring for children with acute severe asthma exacerbation who require mechanical ventilation may opt to give empiric fluid administration before intubating or make fluid boluses immediately available prior to sedation in anticipation of the hypotension that may be generated by sedative administration or the conversion to positive pressure ventilation. An extreme measure that can be taken if blood pressure fails to respond to volume resuscitation is to transiently disconnect the patient from the ventilator or manual resuscitator (bag valve mask or Ambu bag). This permits complete evacuation of the lung and, in turn, appropriate venous return to the heart. (See "Hypovolemic shock in children in resource-abundant settings: Initial evaluation and management", section on 'Fluid resuscitation'.)

Other complications — Other complications seen in children with severe asthma exacerbations managed in the intensive care unit (ICU), particularly those who require mechanical ventilation, include:

Nosocomial infection (eg, ventilator-associated pneumonia [VAP], pneumonitis, sinusitis, tracheobronchitis, central line-associated blood stream infection [CLABSI])

Gastrointestinal bleeding (see "Stress ulcers in the intensive care unit: Diagnosis, management, and prevention")

Myopathy and prolonged weakness; the risk increases with neuromuscular blockade and glucocorticoid use [29-34] (see 'Sedation and paralysis' above)

Subglottic stenosis

Aspiration at the time of intubation

Outcomes — Mechanical ventilation is associated with increased morbidity and resource utilization in children with acute severe asthma exacerbations.

In a population-based study using the largest all-payer hospital discharge database in the United States (Nationwide Inpatient Sample, 2009 to 2010), mechanical ventilation was infrequently required by children admitted to hospitals for status asthmaticus (0.55 percent incidence) but was associated with higher mortality rate and increased resource utilization [9]. Over the study period, an overall in-hospital mortality rate of 0.03 percent was seen among over 250,000 children and adolescents admitted for status asthmaticus, but a mortality rate of 4 percent was found among children receiving mechanical ventilation. In a separate study that reviewed asthma management in 1528 children who were treated in 11 pediatric ICUs (PICUs), the mortality rate for ventilated asthmatic children was 2 to 3 percent [5]. In a subsequent study published in 2012, reported mortality varied from 0.1 to 3 percent across pediatric centers for children admitted to the ICU [10].

WEANING FROM MECHANICAL VENTILATION — The primary goals for mechanical ventilation are to ease the patient's work of breathing and allow time for the bronchospasm and airway obstruction to improve. The majority of patients intubated prior to intensive care unit (ICU) care are extubated within a day [6], while children who have a trial of noninvasive positive pressure ventilation (NPPV) prior to intubation in the ICU are usually ventilated for two to three days [10,66]. Longer ventilation times are often required if the exacerbation is accompanied by pneumonia or other systemic illness. (See 'General principles' above.)

Positive response to therapy is indicated by [12]:

Improvement in and normalization of arterial blood gas measurements

Decrease in the amount of peak inspiratory pressure (PIP) necessary to deliver the desired tidal volume (TV)

Decreased wheezing in the expiratory phase of respiration

Decreased need for supplemental oxygen (indicating improvement in ventilation/perfusion [V/Q] mismatch)

As the clinical status improves, the patient can be permitted to breathe spontaneously [12]. Spontaneous modes such as pressure support allow the patient to determine the inspiratory and expiratory times. (See 'Ventilatory modes' above.)

A trial of extubation can be performed when the patient is comfortably achieving adequate oxygenation and effective ventilation. This is indicated by maintenance of a normal or near-normal partial pressure of carbon dioxide in arterial blood (PaCO2) or normal pH with minimal settings (positive end-expiratory pressure [PEEP] and pressure support of 5 cm H2O each) and a peripheral capillary oxygen saturation (SpO2) >95 percent with a fraction of inspired oxygen (FiO2) of ≤0.4 or less. Once the patient demonstrates readiness for extubation, sedation should be held until the patient demonstrates appropriate strength and wakefulness. Patients should be observed in the ICU for at least 24 hours following extubation to monitor for respiratory embarrassment including tachypnea, dyspnea, increased work of breathing, hypoxia, and atelectasis.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Asthma in children".)

SUMMARY

The decision to intubate a patient with status asthmaticus is made clinically based upon clinical findings and physiologic changes. Care must be taken to control the airway before the patient suffers a respiratory arrest or a hypoxic insult. The clinician most experienced with airway management should perform the intubation. (See 'Indications' above and "Technique of emergency endotracheal intubation in children" and "Rapid sequence intubation (RSI) in children for emergency medicine: Approach".)

Successful mechanical ventilation in patients with asthma depends upon limiting the risk of hyperinflation and barotrauma. This requires acceptance of an initial partial pressure of carbon dioxide in arterial blood (PaCO2) that is higher than normal with an accompanying respiratory acidosis, a strategy called "permissive hypercapnia" or "controlled hypoventilation." (See 'Ventilation strategy' above.)

Ventilator settings should be adjusted as necessary to maintain adequate exhalation, as assessed by chest auscultation and measurement of arterial blood gases, and to prevent complications (table 1). (See 'Ventilator settings' above.)

Supportive measures that help to prevent tachypnea, breath stacking, and ventilator dyssynchrony include analgesia, sedation, and paralysis. To minimize the risk of myopathy, neuromuscular blocking agents should be discontinued as soon as is feasible. (See 'Sedation and paralysis' above.)

Adjunctive therapies, such as general anesthesia or extracorporeal membrane oxygenation (ECMO), are rarely needed for patients who do not respond to aggressive pharmacologic therapy and mechanical ventilation. (See 'Adjunctive therapies' above.)

Complications can result from the asthma exacerbation itself or the treatments. Complications of mechanical ventilation in patients with asthma include hyperinflation, barotrauma, pneumothorax, myopathy, nosocomial infection, gastrointestinal bleeding, and subglottic stenosis. (See 'Complications' above.)

The mortality rate for ventilated children with acute severe asthma exacerbations is approximately 1 to 5 percent. (See 'Outcomes' above.)

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