23/3/24, 16:41 Acute severe asthma exacerbations in children younger than 12 years: Endotracheal intubation and mechanical ventilation

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Acute severe asthma exacerbations in children younger

than 12 years: Endotracheal intubation and mechanical
ventilation
AUTHOR: Joy D Howell, MD
SECTION EDITORS: Gregory Redding, MD, Adrienne G Randolph, MD, MSc
DEPUTY EDITOR: Elizabeth TePas, MD, MS

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Feb 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:

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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

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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

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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
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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

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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

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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

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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.)

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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).
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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].
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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

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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
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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

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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),
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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.

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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.)

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

Use of UpToDate is subject to the Terms of Use.

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Topic 97585 Version 8.0

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GRAPHICS

Initial ventilator settings in children with status asthmaticus

Recommended initial Maximum recommended

Parameter
setting setting

Tidal volume 8 to 10 mL/kg 12 mL/kg

Respiratory rate 8 to 12 breaths/minute 16 breaths/minute

Inspiratory time 0.75 to 1 second 1.5 seconds

I:E ratio 1:3 to 1:5 >1:3

Inspiratory flow 4 to 10 L/kg/minute 4 to 10 L/kg/minute

Minute ventilation <115 mL/kg/minute <115 mL/kg/minute

I:E ratio: the ratio of inspiratory to expiratory time.

Graphic 77503 Version 5.0

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Obstructed medium and small airways with mechanical ventilation and

progressive dynamic hyperinflation

Obstructed medium and small airways with mechanical ventilation and progressive dynamic
hyperinflation from insufficient expiratory time. Note the failure of flow to return to 0 during exhalation
on the flow versus time graph (top). The pressure-time graph (middle) displays progressive air trapping
and generation of auto-PEEP. The volume-time graph (bottom) displays a progressive rise in lung
volumes as air is trapped with each breath.

PEEP: positive end-expiratory pressure.

Original figure modified for this publication. From: Khemani RG, Bart RD III, Newth CJL. Respiratory monitoring during mechanical
ventilation. Paeds Child Health 2007; 17:193. Illustration used with the permission of Elsevier Inc. All rights reserved.

Graphic 118005 Version 1.0

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Trigger threshold for auto-PEEP

Effect of auto-PEEP on elevation of the triggering threshold in a mechanically ventilated patient with
obstructive airways disease. This figure representation shows airway pressure over time. The solid blue
line demonstrates the circuit pressure as measured by the ventilator manometer, and the dashed red line
is the alveolar pressure. In the absence of auto-PEEP, the sensitivity setting of –1 cm H2O would be
achieved by the patient making inspiratory efforts at the end of expiration, when airway pressure is at its
minimum. In the presence of auto-PEEP, alveolar pressure remains positive. In this setting, the patient's
inspiratory effort needs to decrease airway pressure not only by the –1 cm H2O sensitivity set on the
machine, but also by the amount of positive alveolar pressure (auto-PEEP). In this figure, the patient's
inspiratory efforts are insufficient to trigger the ventilator, and the patient is "locked out," being unable
to get a breath because of an inability to overcome the elevated effective triggering threshold rendered
by auto-PEEP.

PEEP: positive end-expiratory pressure.

Adapted from Puritan-Bennett 1994, Form AA-1888.

Graphic 64640 Version 5.0

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Contributor Disclosures
Joy D Howell, MD No relevant financial relationship(s) with ineligible companies to disclose. Gregory
Redding, MD No relevant financial relationship(s) with ineligible companies to disclose. Adrienne G
Randolph, MD, MSc Grant/Research/Clinical Trial Support: Illumina Inc. [Multisystem Inflammatory
Syndrome]. Consultant/Advisory Boards: ThermoFisher [Sepsis]; Volition, Inc. [Sepsis]. All of the relevant
financial relationships listed have been mitigated. Elizabeth TePas, MD, MS No relevant financial
relationship(s) with ineligible companies to disclose.

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