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SPECIAL ISSUE ARTICLE
Acute Respiratory Failure in Children
Matthew L. Friedman, MD; and Mara E. Nitu, MD
ABSTRACT
This article reviews the definition, pathophysiology, etiology, assessment, and management of acute respiratory failure in children. Acute respiratory failure is the inability of the
respiratory system to maintain oxygenation or eliminate carbon dioxide. Acute respiratory
failure is a common cause for admission to a pediatric intensive care unit. Most causes of
acute respiratory failure can be grouped into one of three categories: lung parenchymal
disease, airway obstruction, or neuromuscular dysfunction. Many patients with acute respiratory failure are managed successfully with noninvasive respiratory support; however,
in severe cases, patients may require intubation and mechanical ventilation. [Pediatr Ann.
2018;47(7):e268-e273.]
A
cute respiratory failure in children is the inability of the respiratory system to support
oxygenation, ventilation, or both. Hypoxic respiratory failure is defined by
an arterial partial pressure of oxygen
(PaO2) below 60 mm Hg, which typically produces an arterial oxygen saturation
of 90%. Ventilation is the elimination
of CO2 and is measured by the arterial
partial pressure of CO2 (PaCO2). Acute
hypercarbic respiratory failure is defined
by an acute increase in PaCO2 greater
than 50 mm Hg. It is typically associated
with a respiratory acidosis pH of <7.35.
Venous blood may be sampled in lieu
of arterial blood to obtain the venous
partial pressure of CO2 (PvCO2); how-
ever, it can only be accurately stated that
the PaCO2 is no higher than the PvCO2.
Therefore, when PvCO2 is <50 mm Hg,
acute hypercarbic respiratory failure can
be ruled out but a PvCO2 of 55 mm Hg
does not guarantee a diagnosis of hypercarbic respiratory failure. PvCO2 is
a test that has high sensitivity but poor
specificity for diagnosing hypercarbic
respiratory failure. PvCO2 should be interpreted carefully based on location of
sampling, manner of sampling, and cardiac output.
EPIDEMIOLOGY
Acute respiratory failure is a common reason for admission to the pediatric intensive care unit (PICU). The
Matthew L. Friedman, MD, is the Medical Director of Community Hospital North; and an Assistant
Professor of Clinical Pediatrics. Mara E. Nitu, MD, is the Division Chief of Pediatric Critical Care, the Vice
Chair of Clinical Affairs for Pediatrics, and a Professor of Clinical Pediatrics. Both authors are affiliated
with the Section of Pediatric Critical Care, Riley Hospital for Children, Indiana University School of
Medicine.
Address correspondence to Matthew L. Friedman, MD, 705 Riley Hospital Drive, Phase 2, Room 4927,
Riley Hospital for Children, Indianapolis, IN 46202; email: friedmml@iu.edu.
Disclosure: The authors have no relevant financial relationships to disclose.
doi:10.3928/19382359-20180625-01
e268
epidemiology is not well described
due to inconsistent and heterogeneous
diagnostic criteria. In patients with
respiratory failure who have underlying pediatric acute respiratory distress
syndrome (ARDS), epidemiologic
data reveal an annual incidence of
2.3% of PICU admissions, and a mortality rate of 24% to 34%.1,2
PHYSIOLOGY AND
PATHOPHYSIOLOGY
Normal control of breathing is a
complex interaction between the vasculature, brain, lungs, and respiratory
apparatus. Peripheral chemoreceptors,
located in the aortic and carotid bodies, are sensitive to PaO2, PaCO2, and
pH. A decrease in PaO2, a decrease
in pH or an increase in CO2 results
in signaling to increase ventilation.
Central chemoreceptors in the brain
are sensitive to cerebral spinal fluid
(CSF) pH. The blood-brain barrier allows CO2, but not hydrogen ions, to
pass freely so the CSF pH is determined by PaCO2. Therefore, the central chemoreceptors can detect small
changes in CO2. Input from peripheral
and central chemoreceptors is integrated in the brainstem. The pons and
medulla generate periodic impulses to
trigger breathing. Injury to the brainstem leads to characteristic, abnormal
respiratory patterns based on the level
of injury.3 The cortex can override this
automatic mechanism with voluntary
respiratory effort.
The main muscle of inspiration is
the diaphragm, which is innervated
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SPECIAL ISSUE ARTICLE
by the phrenic nerve that originates
from spinal nerve roots C3 to C5.
Thus, patients with spinal cord injuries at or above this level are at risk
for diaphragmatic paralysis and respiratory failure. Phrenic nerve stimulation causes contraction and flattening
of the dome-shaped diaphragm. This
leads to an increase in intrathoracic
volume and consequently a decrease
in intrathoracic pressure. A negative
pressure gradient is generated between the alveoli and the external environment, resulting in net movement
of air to the alveoli. This negative
pressure breathing is contrasted to the
positive pressure breathing of invasive
mechanical ventilation.
Thoracic spinal nerve roots innervate the external intercostal muscles to
aid in inspiration by pulling the chest
upward and anteriorly. Exhalation is a
passive process during quiet breathing
due to the elastic recoil of the lungs
and chest wall. When exercising or in
respiratory distress, exhalation can be
an active process assisted by internal
intercostal muscles pulling the rib
cage inwards and down, and abdominal wall musculature contracting and
forcing abdominal contents upward
into the thoracic cavity and increasing
intrathoracic pressure.
Compared to adults, children, particularly infants, are at higher risk of
acute respiratory failure. The small diameter of children’s airway results in
a high resistance to flow. Resistance
is proportional to the inverse of the
radius of the airway to the 4th power;
thus, even small changes in the airway
radius can result in large increases in
airway resistance, leading to severely
decreased airflow. The pediatric airway is small and can be further narrowed by secretions, edema, or bronchoconstriction. Young children also
have underdeveloped collateral venti-
PEDIATRIC ANNALS • Vol. 47, No. 7, 2018
lation and an acute angle of the right
upper lobe bronchus, predisposing
them to atelectasis.4 The chest wall
of a child is more compliant, which
from a mechanical standpoint, is disadvantageous for normal breathing.
The diaphragm of children fatigues
quicker than adults due to fewer type1 muscle fibers. Lastly, in young infants, the central control of breathing
is immature and prone to apnea and
bradypnea.5
Impairments in oxygenation or ventilation leading to respiratory failure
are most often due to ventilation/perfusion (V/Q) mismatch. Although the
ideal 1:1 ratio of ventilation to perfusion is rare, in acute lung disease the
mismatch becomes more severe. Lung
segments perfused but not ventilated
are considered dead space (V/Q approaches infinity). Examples of dead
space ventilation include anatomical
dead space (large airways), pulmonary embolism, and severe pulmonary
hypertension. Clearance of CO2 is impaired when dead space is increased,
resulting in hypercarbia. Areas of the
lung that have perfusion but no ventilation result in shunt physiology
(V/Q = 0). In shunt physiology, blood
passes from pulmonary artery to pulmonary vein without being exposed to
an aerated alveolar membrane, resulting in hypoxemia. Examples of shunt
are lung collapse and pulmonary arterial-venous connections. In most
lung diseases, there is heterogeneity
in V/Q mismatch from 0 to infinity
(Figure 1).
Respiratory failure may also be the
result of impaired diffusion of oxygen
across the alveolar-capillary membrane. Diffusion limitation may coexist with V/Q mismatch. An example
of diffusion impairment is pulmonary
fibrosis. Hypercarbia due to diffusion impairment is rare because CO2
diffuses across the alveolar-capillary
membrane more rapidly than oxygen.
ETIOLOGY
Acute respiratory failure has three
major etiological categories: intrinsic
and acquired lung disease, airway disorders, and neuromuscular dysfunction (Table 1). Diseases that lead to
respiratory failure from pulmonary
pathology are caused by V/Q mismatching, gas diffusion impairment,
or both. Airway disorders more commonly lead to respiratory failure in
more children than adults due to the
smaller radius of the airway. Neuromuscular causes of respiratory failure
can occur anywhere from the central
nervous system to the innervated muscles of respiration.
EVALUATION
The initial assessment of children
with concern for impending acute respiratory failure aims to determine
the degree of respiratory impairment.
Experienced clinicians can make this
determination quickly at the bedside
by astute observation. Assessment of
patient vital signs, general appearance, lung examination, and mental
health status allow for a rapid determination of the severity of illness
and often suggest which interventions
may be required to appropriately intervene to reverse the course of illness
or to avoid respiratory arrest. Tachypnea and hypoxemia are common
manifestations of acute respiratory
failure, although tachycardia is often
an underappreciated sign of impending respiratory failure. Increased work
of breathing manifests as retractions,
grunting, head bobbing, nasal flaring,
or belly breathing. Children with respiratory failure due to neuromuscular
weakness or central nervous system
dysfunction may not exhibit typical
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SPECIAL ISSUE ARTICLE
Figure 1. Three alveolar capillary units depicting
normal (V/Q = 1), dead space (V/Q approaching
infinity), and shunt (V/Q = 0) physiologies. V/Q,
ventilation/perfusion.
TABLE 1.
Causes of Acute
Respiratory Failure
Lung parenchyma
• Pneumonia
• Bronchiolitis
• Asthma
• Acute respiratory distress syndrome
due to sepsis or trauma
• Aspiration
Pulmonary edema
• Airway
• Croup
• Foreign body
• Subglottic stenosis
• Vascular ring
• Airway malacia
Neuromuscular dysfunction
• Myopathy
• Neuropathy (ie, Guillain-Barré
syndrome)
• Neuromuscular junction disorders (ie,
myasthenia gravis)
• Central nervous system dysfunction
(travel, infection, seizure)
should be obtained to aid the specific
diagnosis.
Auscultation of the lung fields is
helpful for both diagnosis and management. Prolonged exhalation or audible wheeze is suggestive of lower
airway bronchoconstriction. Localized findings suggest a focal pneumonia or foreign body aspiration.
Absence of breath sounds can be
due to pneumothorax, pleural effusion, or dense consolidation of lung.
Rales in all lung fields is commonly
due to pulmonary edema or diffuse
interstitial edema. Stridor is generated by turbulent airflow secondary
to narrowing in the upper airway and
may occur in croup, external airway
compression, and high foreign body
aspiration.
Altered mental status may be a
cause or consequence of respiratory
failure. Patients who are hypercarbic
present with somnolence, whereas
hypoxic patients are often agitated
due to the lack of oxygen delivery
to the end organs including the central nervous system. Children with
traumatic brain injury and a Glascow Coma Score of 8 or less should
be promptly intubated for airway
protection. The use of the Glascow
Coma Score for nontraumatic causes
of altered mental health status is less
well established but provides a common language for communicating
an objective measure to trend over
time. A neurological examination,
particularly mental health status and
strength, is important to help identify
neuromuscular causes of respiratory
failure.
• Diaphragmatic paralysis
signs of increased respiratory effort, thus a higher index of suspicion
is warranted; an arterial blood gas
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DIAGNOSIS
The initial evaluation of a child
in respiratory distress includes a targeted but thorough history and physical examination. A thorough history
directed at identifying inciting signs
and symptoms may aid clinicians in
the underlying etiology of the acute
respiratory failure. Initial laboratory data include blood gas sampling
to assess acid/base status as well as
oxygenation and ventilation. Arterial blood gas is preferred to venous
blood gas due to the ability to assess
oxygenation.
Chest radiography will frequently
identify the inciting cause of respiratory failure including inflammatory
or infectious conditions, radiopaque
foreign bodies, atelectasis, or effusions. Chest radiograph also assesses
for pathology that needs emergent
intervention such as pneumothorax.
Neither the chest radiograph nor
the results of the blood gas analysis
should delay the emergent management of an acutely deteriorating patient who requires intubation and mechanical ventilation.
Respiratory secretions can be sent
for microbiologic, cytology, and histologic testing. A variety of methods
can be used to sample secretions.
The gold standard bronchoscopy
with bronchoalveolar lavage (BAL)
is the most invasive method but has
the advantages of obtaining the deepest lung sample and visualizing the
airways. If an infectious source of
respiratory failure is suspected, the
secretions are sent for the following laboratory tests: gram stain, acid
fast bacillus stain, cell count, bacterial culture (possibly also fungal and
mycobacterial culture), and/or viral
polymerase chain reaction. BAL can
also diagnose pulmonary hemorrhage, pulmonary hemosiderosis, and
aspiration pneumonitis.
MANAGEMENT
Supportive respiratory care is the
mainstay of management. Classical-
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SPECIAL ISSUE ARTICLE
ly, this consists of endotracheal intubation and mechanical ventilation.
Although invasive mechanical ventilation is still commonly employed,
there has been a dramatic increase
in the use of noninvasive respiratory
support options. 6 Noninvasive ventilation modalities include high flow
nasal cannula oxygen (HFNCO2),
continuous positive airway pressure
(CPAP), and bi-level positive airway
pressure (BiPAP).
HFNCO2 is a popular mode of respiratory support for infants and small children. At high flow rates the air delivered
by nasal cannula is heated and humidified to avoid complications and for patient comfort. The physiological definition of “high flow” is a flow rate greater
than minute ventilation. Minute ventilation is equal to respiratory rate times
tidal volume. HFNCO2 improves acute
respiratory failure by providing high
FiO2 to treat hypoxia and by providing
positive pressure in the alveoli and small
airways to help reduce work of breathing.7 In larger patients, HFNCO2 may be
used to improve oxygenation but flow
rates must be high (30-60 L/min) to improve the work of breathing.8 Although
continuous positive pressure is supplied,
HFNCO2 should not be used as a substitute for CPAP where an actual endexpiratory pressure can be targeted.
Mask CPAP and BiPAP are classic modalities for noninvasive ventilation. CPAP provides a single pressure
throughout the respiratory cycle to
maintain lung expansion. Patients can
breathe spontaneously around the CPAP
pressure. BiPAP is a synchronized mode
of ventilation that provides an inspiratory pressure to assist with ventilation
in addition to the lower continuous positive end-expiratory pressure. CPAP and
BiPAP are usually delivered through a
tight-fitting mask that covers the nose or
nose and mouth. The masks needed for
PEDIATRIC ANNALS • Vol. 47, No. 7, 2018
CPAP and BiPAP can lead to facial skin
breakdown and aspiration of secretions
or emesis.
Certain patient populations clearly
benefit from noninvasive ventilation to
try to stave off intubation and mechanical ventilation.9 Patients with asthma are
notoriously difficult to ventilate after
intubation due to air trapping from persistent bronchospasm. Conversely, they
often respond well to BiPAP with decreased work of breathing.9-11 BiPAP is
also helpful in patients with neuromuscular weakness, as it aids both inspiration
and maintenance of lung recruitment.
The use of noninvasive ventilation modalities has shown promise in reducing
the incidence of intubation.11 However,
lack of improvement of oxygenation and
ventilation early after noninvasive ventilation measures are started is associated
with need for intubation, thus patients
must be assessed frequently to evaluate
their response to these interventions.12
Invasive positive pressure ventilation
with endotracheal intubation is often required in pediatric acute respiratory failure. Indications for intubation are failure
of oxygenation or ventilation despite
noninvasive respiratory support or patients’ inability to protect their own airway. Intubation should be performed by
or in the presence of a clinician with expertise in pediatric airway management.
Intubation is generally safe but there is a
6% risk of severe complication, including a 1.7% chance of cardiac arrest.12
Possible difficult airways should be
identified early, including craniofacial
abnormalities, difficulty opening mouth,
contraindication to extending neck or
prior history of difficult intubation. The
basic set of equipment needed for endotracheal intubation is shown in Table 2.
Recently, there has been an increase in
the use of video laryngoscopy.13
Most children with acute respiratory
failure are managed with conventional
TABLE 2.
Intubation Equipment
Checklist
Intravenous access
Sedation and analgesia
• Opioid
• Benzodiazepine
• Ketamine
• Etomidate
Paralytic
• Rocuronium
• Succinylcholine
Lidocaine
Atropine
Bag attached to O2 source
Appropriately sized mask
Suction catheter attached to suction
Endotracheal tubes
• Size = (age + 4)/4
• Cuffed tube one-half size smaller
Exhaled CO2
• ETCO2 (preferred)
• Color change thing
Stethoscope
Device or tape to secure tube
Abbreviation: ETCO2, end-tidal carbon dioxide.
mechanical ventilation after intubation.
Strategies for mechanical ventilation
drastically changed after data revealed
a 25% relative reduction in mortality in
adults with ARDS when ventilated with
a low-tidal volume strategy (6 mL/kg
vs 12 mL/kg).14 Some pediatric studies have replicated similar benefits.15,16
Patients with hypoxia requiring greater
than 0.4 FiO2 are treated with higher
peak end expiratory pressure to maintain
appropriate oxygenation while limiting
toxic O2 exposure to the lungs.17
Children who fail conventional mechanical ventilation due to hypoxia can
be transitioned to high-frequency oscillatory ventilation (HFOV). This ventilator uses a high mean airway pressure
to maintain lung recruitment while use271
SPECIAL ISSUE ARTICLE
ing very small tidal volumes. HFOV
is theorized to prevent ventilator-induced lung injury by avoiding high
dynamic pressures in noncompliant
lungs. In a study conducted before the
era of low tidal volume ventilation,
HFOV was shown to improve clinical outcomes in children. 18 Two large
adult trials have shown no mortality
benefit of HFOV and possibly more
adverse events.19,20
Inhaled nitric oxide selectively
dilates the pulmonary arterioles and
is a well-established treatment for
pulmonary hypertension. It also has
been used in patients with ARDS to
improve V/Q matching in the absence
of pulmonary hypertension. Inhaled
nitric oxide will distribute to the
well-ventilated areas of the lung and
preferentially dilate the arterioles in
those areas. Local blood flow increases, resulting in better V/Q matching.
Inhaled nitric oxide has shown to improve oxygenation and extracorporeal
membrane oxygenation (ECMO)-free
survival but not mortality in adult patients with ARDS. 21 Prone positioning
has been used based on physiological
arguments to improve V/Q matching.
The adult data are mixed and the one
large pediatric study did not show any
clinical benefit.22,23
In patients who cannot be oxygenated or ventilated by conventional
or advanced mechanical ventilation
techniques, ECMO may be required.
For refractory hypoxia or hypercarbia, the preferred modality is venovenous extracorporeal membrane
oxygenation (VV-ECMO). Venous
blood is removed from the body with
subsequent clearance of CO 2 and
oxygenation via an external artificial
membrane, and returned to the right
side of the heart. Currently, 64% of
children placed on VV-ECMO will
survive.24
e272
Weaning from mechanical ventilation requires improvement in underlying pathophysiology. Patients must be
on acceptably low ventilator settings
before extubation. The patient must
also be neurologically able to spontaneously breathe and protect their
airway. Secretions must not be excessive, especially in smaller children.
Children may need to transition to
noninvasive support after extubation
until their respiratory insufficiency
has resolved.
CONCLUSIONS
Acute respiratory failure in children is a common cause of admission
to the PICU with favorable outcomes
for most patients. Prognosis is mainly
dependent on the underlying etiology of the respiratory impairment. A
minority of patients will be unable to
wean from the ventilator and progress
to chronic respiratory failure requiring tracheostomy and long-term mechanical ventilation.
7.
8.
9.
10.
11.
12.
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