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Causes of acute respiratory distress in children
Author:
Debra L Weiner, MD, PhD
Section Editor:
Gary R Fleisher, MD
Deputy Editor:
James F Wiley, II, MD, MPH
Contributor Disclosures
All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Oct 2016. | This topic last updated: Nov 24, 2014.
INTRODUCTION — Respiratory distress in children, particularly neonates and infants, must be
promptly recognized and aggressively treated because children may decompensate quickly.
Respiratory arrest is the most common cause of cardiac arrest in children. Factors that
exacerbate rapid respiratory compromise in children as compared to adults include smaller
airways, increased metabolic demands, decreased respiratory reserves, and inadequate
compensatory mechanisms. (See "Emergency airway management in children: Unique pediatric
considerations".)
This topic will review causes of acute respiratory distress in children. A detailed discussion of
the approach to children with acute respiratory distress and approach to children with severe
upper airway obstruction is found elsewhere. (See "Emergency evaluation and immediate
management of acute respiratory distress in children"and "Emergency evaluation of acute upper
airway obstruction in children".)
Other related topics including the initial assessment and stabilization of children with respiratory
and circulatory compromise and airway management techniques, including rapid sequence
intubation (RSI), and conditions causing respiratory distress in newborns are discussed
separately:
●(See "Initial assessment and stabilization of children with respiratory or circulatory
compromise".)
●(See "Basic airway management in children".)
●(See "Emergency endotracheal intubation in children".)
●(See "Rapid sequence intubation (RSI) in children".)
●(See "Overview of neonatal respiratory distress: Disorders of transition".)
●(See "Clinical features and diagnosis of meconium aspiration syndrome".)
●(See "Pathogenesis, clinical presentation, and diagnosis of apnea of prematurity".)
DEFINITION — Respiratory distress results when breathing does not match the body’s
metabolic demand for oxygenation and/or ventilation. Respiratory distress is typically
characterized by signs of increased work of breathing, such as tachypnea, use of accessory
muscles, and/or retractions [1]. A patient with inadequate respiratory effort may also have signs
of increased work of breathing, most commonly tachypnea but may have a respiratory rate that
is inappropriately slow for the clinical condition. They may also have an abnormal pattern of
respiration. (See "Emergency evaluation and immediate management of acute respiratory
distress in children", section on 'Evaluation'.)
Respiratory distress may develop in children due to multiple etiologies (table 1) that result in one
of the following final common pathways:
●Hypoxemia (see "Control of ventilation", section on 'Hypoxic challenge').
●Hypercarbia (see "Control of ventilation", section on 'Hypercapnic challenge').
●Difficulty with the mechanics of respiration, typically from airway obstruction, muscle
weakness, or discomfort (as may occur for patients who are splinting due to abdominal
pain).
●Disordered control of ventilation, in which respiration may be depressed (eg, opioid
overdose, severe head injury) or stimulated (eg, metabolic acidosis, hyperammonemia,
salicylate intoxication).
Respiratory distress in response to hypoxemia or hypercarbia can rapidly progress to lifethreatening respiratory failure. Neonates, infants, and young children are at particular risk given
their high oxygen consumption and decreased respiratory reserve. Children with inadequate
respiratory effort (as can occur with fatigue, muscle weakness or CNS depression) can quickly
develop significant physiologic compromise. (See"Emergency airway management in children:
Unique pediatric considerations".)
By contrast, children with respiratory distress secondary to altered stimulation of respiratory
centers or pain, who do not have significant cardiopulmonary disease, usually improve with
treatment of the primary condition and do not generally progress to respiratory failure.
CAUSES — Many conditions may cause acute respiratory distress in children (table 1). The
underlying etiology, while commonly within the respiratory system, may also be within other
systems, but the etiology may not be immediately obvious (eg, fever and rales may be due to
heart failure as the result of myocarditis rather than pneumonia which is more common).
Immediately life-threatening conditions — Any process that causes respiratory distress by
compromising ventilation and/or oxygenation can be life-threatening. Imminently life-threatening
conditions require early recognition and immediate, aggressive intervention.
Severe upper airway obstruction — Patients with complete upper airway obstruction have no
effective air movement, hence no audible speech, cry, or cough. Causes of complete upper
airway obstruction include foreign body aspiration, angioedema from anaphylaxis,
laryngospasm caused by hypocalcemia, and epiglottitis (table 2). Foreign body aspiration,
anaphylaxis, and epiglottitis, are discussed in detail separately. (See"Emergency evaluation of
acute upper airway obstruction in children", section on 'Causes' and "Epiglottitis (supraglottitis):
Clinical features and diagnosis" and "Anaphylaxis: Emergency treatment".)
Noisy inspiration (stridor) is a hallmark of severe partial upper airway obstruction although
absence of stridor does not preclude significant partial airway obstruction, especially in a patient
with depressed mental status. Common causes of severe partial upper airway obstruction
include foreign body aspiration, infection (most commonly croup), and injury (such as airway
thermal or chemical burns). Causes of acute upper airway obstruction that are commonly lifethreatening are discussed separately (table 2). (See "Emergency evaluation of acute upper
airway obstruction in children", section on 'Causes'.)
Tension pneumothorax — Tension pneumothorax is an acutely life-threatening emergency
that develops when increased intrathoracic volume from air that has leaked into the pleural
cavity causes a shift of mediastinal structures toward the opposite side, compressing the
contralateral lung and cardiac vessels. It is rapidly fatal without immediate decompression.
Hallmarks of tension pneumothorax are:
●Severe respiratory distress
●Shift of mediastinal structures, including the trachea, toward the side opposite of the
collapsed lung
●Ipsilateral hyperexpansion of the chest
●Decreased or absent breath sounds and hyper-resonance to percussion on the side of
the collapsed lung
In the rare patient with bilateral tension pneumothoraces, physical findings may be symmetric.
Tension pneumothorax is usually due to penetrating or blunt trauma, including mechanical
ventilation and cardiopulmonary resuscitation but it can also occur as the result of a
spontaneous pneumothorax. Although tension usually develops immediately, it may be delayed
for up to 24 hours, particularly if the pneumothorax is spontaneous and develops slowly.
Bedside ultrasound can rapidly confirm the diagnosis of pneumothorax. (See"Imaging of
pneumothorax", section on 'Ultrasound' and "Spontaneous pneumothorax in children", section
on 'Clinical features'.)
Needle decompression can be a life-saving, temporizing measure that any physician should be
able to perform. If immediately available, a thoracostomy tube can be placed in children with a
tension pneumothorax without first performing needle thoracostomy only if the tube can be
placed without delaying decompression; otherwise needle thoracostomy should be performed
immediately, followed by chest tube or pigtail catheter placement as soon as possible.
(See "Placement and management of thoracostomy tubes", section on 'Tube
thoracostomy'and "Placement and management of thoracostomy tubes", section on 'Needle
thoracostomy'.)
Pulmonary embolism — Pulmonary embolism (PE) is a life-threatening condition that can
cause respiratory distress. It is an uncommon condition in children and is often associated with
the use of central venous lines or access devices [2]. Other risk factors for PE include
immobility, a hypercoagulable state (such as factor V Leiden mutation, protein S or protein C
deficiency), congenital heart disease, trauma, surgery, nephrotic syndrome, systemic lupus
erythematosus, hormone birth control, malignancy and complications of some chemotherapeutic
regimens (such as L-asparaginase and steroids for acute lymphoblastic leukemia).
(See"Venous thrombosis and thromboembolism in infants and children: Risk factors and clinical
manifestations", section on 'Clinical manifestations'.)
Cardiac tamponade — Cardiac tamponade occurs when blood, serous fluid, or air under
tension fills the pericardial sack, resulting in life-threatening compromise of venous return and
decreased stroke volume. Cardiac tamponade can present acutely with hypotension. Children
may also have signs of respiratory distress or apnea [3,4]. The classic signs of pericardial
tamponade, referred to as Beck's triad (hypotension, jugular venous distention, and muffled
heart sounds), are present in less than one-third of patients [3]. Pulsus paradoxus (a drop in the
systolic blood pressure of >10 mmHg upon inspiration and, when severe, a weakening or
disappearance of the peripheral pulse upon inspiration) is an indication for pericardiocentesis in
children with pericardial effusion. Bedside ultrasound, can be used to rapidly identify fluid in the
pericardial sac in patients with cardiac tamponade, and guide pericardiocentesis. (See "Pulsus
paradoxus in pericardial disease" and"Pulsus paradoxus in pericardial disease", section on
'Measurement of pulsus paradoxus' and "Pulsus paradoxus in pericardial disease", section on
'Pulsus paradoxus in cardiac tamponade' and "Emergency pericardiocentesis".)
Acute cardiac tamponade is rare in children and is usually the result of trauma, particularly
penetrating cardiac injury. It is rapidly fatal. In children, accumulation of fluid in the pericardial
sac is usually insidious as a result of infection, inflammation (most commonly collagen vascular
disease), malignancy (eg, mediastinal lymphoma), or cardiac surgery (post-pericardiotomy
syndrome). Effusion may progresses to tamponade.
Other traumatic conditions — In addition to tension pneumothorax and cardiac tamponade,
several other traumatic conditions may cause respiratory distress including flail chest,
pulmonary contusion, pneumothorax, hemothorax, hemorrhagic shock, and central nervous
system trauma.
●Flail chest – Flail chest occurs when multiple rib fractures result in a loss of stability of
the chest wall. The flail segment retracts with inspiration and bulges with exhalation,
resulting in inefficient expansion of the thorax, inefficient ventilation, and a significant
increase in the energy expenditure for breathing (figure 1). The mechanism of injury usually
is direct impact. Flail chest is uncommon in children because the greater deformability of
immature bone makes rib fractures less likely than in adults, and when present, is often
associated with pulmonary contusion. Even without rib fractures, children may have
significant pulmonary injury. (See "Chest wall injuries in children", section on 'Flail chest'.)
●Pulmonary contusion – In children, pulmonary contusion occurs when traumatic force is
applied to the chest wall and results in parenchymal damage with hemorrhage and edema.
The initial presentation of children with pulmonary contusion is often dominated by clinical
features associated with extrathoracic injuries. Nevertheless, pulmonary contusion should
be suspected in any child with significant blunt force to the thorax, whether or not there are
signs of respiratory distress or chest wall injury. Decreased breath sounds, rales, or
rhonchi may be noted on physical examination. Chest radiography should be performed for
all children with respiratory distress and may reveal pulmonary contusion. Further imaging
with computed tomography (CT) may be useful when the plain films are negative if
identification of a pulmonary contusion would affect management (eg, in anesthetic
management for patients requiring emergent surgery). (See "Pulmonary contusion in
children", section on 'Clinical features' and "Pulmonary contusion in children", section on
'Primary evaluation and management'.)
●Pneumothorax– Pneumothorax occurs when air leaks from the lungs into the pleural
space, resulting in collapse of the lung. It may be caused by blunt or penetrating trauma
that creates air leak by directly damaging intrathoracic structures or indirectly due to
increased intrathoracic pressure that ruptures respiratory structures. Chest radiograph
reveals echogenicity in the region of the noninflated lung.
●Open pneumothorax occurs when ambient air enters the pleural space during inspiration
through a traumatic chest wall defect (ie, a "sucking wound"). As a result, the mediastinum
shifts toward the normal hemithorax and the lung within the injured hemithorax remains
collapsed. During expiration, air exits the pleural space through the chest wall defect and
the mediastinum swings back toward the injured hemithorax. Expiratory air from the normal
lung (ie, “pendulum air”) fills the collapsed lung. The “mediastinal flutter" may cause
respiratory failure. Chest radiograph, an open pneumothorax is characterized by a visible
chest wall defect and by massive expiratory mediastinal shift towards the injured side: this
mediastinal behavior is different from tension pneumothorax where the expiratory shift of
the mediastinum occurs towards the normal lung, resulting from air-trapping in the affected
pleural space. Ultrasound for pneumothorax. (See "Imaging of pneumothorax", section on
'Types of pneumothorax'.)
Treatment of open pneumothorax consists of placing sterile petroleum gauze over the open
wound and taping the dressing on three sides to act as a flutter valve that prevents air
entry through the wound upon inspiration but allows air to escape during exhalation. A
chest tube or pigtail catheter should also be placed. (See "Placement and management of
thoracostomy tubes", section on 'Tube thoracostomy'.)
●Hemothorax – In patients with massive hemothorax, respiratory distress results from the
inability of the lung to expand on the affected side and from hemorrhage shock.
Thoracostomy tube placement and fluid resuscitation are key interventions. (See "Trauma
management: Approach to the unstable child", section on 'Breathing'.)
●Smoke inhalation – Smoke inhalation may cause respiratory distress due to thermal
injury to the upper and lower airways, hypoxic gas inhalation, bronchopulmonary exposure
to toxins with direct lung injury,and/or systemic toxicity from carbon monoxide and cyanide.
Thermal injury to the upper airway is suggested by stridor, respiratory distress, facial burns,
oropharyngeal blisters or edema, and carbonaceous sputum and warrants early
endotracheal intubation. (See "Inhalation injury from heat, smoke, or chemical irritants",
section on 'Subsequent care' and "Inhalation injury from heat, smoke, or chemical
irritants" and "Inhalation injury from heat, smoke, or chemical irritants", section on 'Initial
care and disposition'.)
●Submersion injury – Children with nonfatal drowning have varying degrees of
hypoxemia due to fluid aspiration or reflex laryngospasm inducing noncardiogenic
pulmonary edema and acute respiratory distress syndrome. Pulmonary insufficiency can
develop insidiously or rapidly. Findings include tachypnea, dyspnea, rales, and wheezing.
Chest radiograph may be normal or show focal or diffuse pulmonary edema.
(See "Drowning (submersion injuries)".)
●Hemorrhagic shock – Massive hemorrhage can cause respiratory distress from hypoxia
and acidosis (as the result of decreased oxygen carrying capacity due to hypovolemic
shock). (See "Trauma management: Approach to the unstable child", section on
'Circulation'.)
●Central nervous system trauma – Central nervous system injury involving the brain or
spinal cord, may result in life-threatening apnea or respiratory depression. (See "Initial
approach to severe traumatic brain injury in children", section on
'Evaluation' and "Evaluation of cervical spine injuries in children and adolescents", section
on 'Vital signs'.)
Biological or chemical weapons — Several biologic and chemical agents that are potential
weapons of terrorism or warfare produce respiratory distress as their most predominant effect
[5,6]. Although exposure to these agents is fortunately rare, prompt recognition is essential in
order to contain the exposure and prepare for mass casualties. Children often manifest
symptoms prior to adults because of greater exposure per unit body mass, particularly since
many agents are heavier than air and are therefore at greatest concentration lower to the
ground, the level at which children breath, and because children have less compensatory
capacity. The respiratory symptoms are typically nonspecific. Biologic agents include
inhalational anthrax, pneumonic plague, pneumonic tularemia, melioidosis, and the toxins
staphylococcus enterotoxin B and ricin. Chemical agents such as chlorine, phosgene, sarin,
ricin and cyanide can also cause respiratory distress. (See"Identifying and managing casualties
of biological terrorism" and "Chemical terrorism: Rapid recognition and initial medical
management".)
Other conditions
Respiratory tract conditions — Respiratory distress can occur as the result of upper or lower
respiratory tract processes. The clinical manifestations of respiratory distress depend, in part, on
the location of the disease process. As an example, stridor develops in children with upper
airway obstruction, whereas rales are characteristic of alveolar disease. (See "Emergency
evaluation and immediate management of acute respiratory distress in children", section on
'Physical examination'.)
Infections — Respiratory distress as the result of an infectious process usually develops
gradually but can be acute in onset if structures of the upper airway are directly involved.
Patients are often febrile. (See"Emergency evaluation of acute upper airway obstruction in
children".)
Common infectious causes of respiratory distress include:
●Uvulitis – Children and adolescents with uvulitis may present with fever, sore throat,
difficulty swallowing, pain with swallowing, drooling, and/or respiratory distress. The clinical
features vary depending upon the etiology. Respiratory distress is uncommon in infectious
uvulitis unless there is associated epiglottitis. Uvulitis is a clinical diagnosis. The uvula is
red and swollen and may be covered by purulent exudates (picture 1). (See "Uvulitis:
Clinical features and treatment", section on 'Clinical features'.)
●Peritonsillar abscesses – Peritonsillar abscess typically causes local pain, sore throat,
trismus, difficulty swallowing, and muffled ("hot potato") voice. Patients with peritonsillar
abscesses exhibit tonsillar and peritonsillar swelling and erythema with deviation of the
uvula to the unaffected side. It is rare that the swelling is so severe that it obstructs the oral
airway enough to cause difficulty breathing. Peritonsillar abscess is most commonly
caused by Group A streptococcus but can be caused by other bacteria and sometimes
develops secondary to Epstein-Barr virus (ie, mononucleosis). Peritonsillar abscess is
more common in older children and adolescents. The onset of symptoms is typically
gradual. (See "Peritonsillar cellulitis and abscess", section on 'Evaluation and diagnosis'.)
●Retropharyngeal abscesses – Children with retropharyngeal abscesses may develop
stridor and typical signs of respiratory distress if the abscess impedes on the trachea.
Retropharyngeal abscess usually develops in infants and toddlers (image 1 and image 2).
Additional findings include drooling, dysphagia, torticollis, meningismus, and change in
voice. (See "Retropharyngeal infections in children", section on 'Presentation'.)
●Croup – Croup (laryngotracheobronchitis) is the most common infectious cause of upper
airway obstruction in children between 6 and 36 months of age but can be seen from early
infancy through school age (image 3 and image 4). The etiology may be viral (most
commonly due to infection with parainfluenza virus) or allergic (spasmodic croup). Most
patients with spasmodic croup are older than those with infectious croup. (See "Croup:
Clinical features, evaluation, and diagnosis", section on 'Epidemiology' and"Croup: Clinical
features, evaluation, and diagnosis", section on 'Etiology'.)
The onset of symptoms with croup due to infection is usually gradual, beginning with nasal
congestion, and coryza. Symptoms generally progress over 12 to 48 hours to include fever,
usually <39°C although may be higher especially if due to influenza, hoarseness, barking
cough, and stridor. Onset of spasmodic croup is abrupt and symptoms are limited to barky
cough. Barky cough, for infectious or spasmodic croup, most commonly begins during the
night or with napping. Respiratory distress increases as upper airway obstruction becomes
more severe. Rapid progression or signs of lower airway involvement suggests a more
serious illness. Symptoms typically persist for three to seven days with resolution of barky
cough by day four in most children. Deviations from this expected course should prompt
consideration of diagnoses other than laryngotracheitis. Some children with severe or
recurrent croup may have underlying airway abnormalities (eg, subglottic hemangioma).
(See "Croup: Clinical features, evaluation, and diagnosis", section on 'Clinical
presentation'.)
●Tracheitis – Tracheitis, is an invasive infection of the soft tissues of the trachea.
Classically, it is caused by bacteria, most commonly Streptococcus or Staphylococcus
aureus including MRSA (picture 2) as a secondary infection in a child with croup (image 5)
but may occur as a primary infection. Increasingly, cases due to viral infection or cases no
pathogen identified have been reported. In patients with respiratory failure due to upper
airway infection, tracheitis is more common than epiglottitis or croup. The predominant
clinical features of tracheitis are those of airway obstruction: stridor, cough, and respiratory
distress accompanied by fever, highest in patients with bacterial or influenza as the
etiology. Children younger than two to three years of age may be at increased risk for
severe disease because of their relatively narrow airway diameter. In children with signs of
total or near-total airway obstruction, airway control precedes diagnostic evaluation.
(See "Bacterial tracheitis in children: Clinical features and diagnosis", section on 'Clinical
features'.)
●Bronchiolitis – Bronchiolitis (caused most commonly by respiratory syncytial virus and
not uncommonly by influenza) typically affects children younger than two years of age. It is
characterized by several days of upper airway symptoms, most classically nasal
congestion and copious nasal secretions, followed by onset of lower airway symptoms that
include wheezing, rales, rhonchi, and cough. Neonates and very young infants may have
apnea, and it may be the presenting manifestation. Peak severity of illness is usually
between days 4 and 6 with resolution of symptoms between days 10 and 14. A detailed
review of bronchiolitis can be found separately. (See "Bronchiolitis in infants and children:
Clinical features and diagnosis".)
●Pneumonia – Pneumonia is a common cause of lower airway disease in infants and
children. The disease process is more likely to be localized in the setting of bacterial
pneumonia, whereas patients with viral and atypical pneumonias, such as Mycoplasma or
Chlamydia, tend to have diffuse peribronchial, interstitial processes. (See "Communityacquired pneumonia in children: Clinical features and diagnosis", section on 'Clinical
evaluation'.)
Asthma — Bronchospasm due to reactive airways can cause severe respiratory distress. It may
be triggered by infection, exercise, environmental irritants, stress, and/or gastroesophageal
reflux. Respiratory distress from bronchospasm may be exacerbated by alveolar disease (as a
result of infection) and/oratelectasis. Assessment of severity and acute management of children
with asthma exacerbations in the outpatient setting are discussed separately. (See "Acute
asthma exacerbations in children: Emergency department management", section on 'Overview
of treatment' and "Acute asthma exacerbations in children: Home/office management and
severity assessment", section on 'Assessment of exacerbation severity'.)
Anaphylaxis — Anaphylaxis and anaphylactoid reactions (most commonly caused by food or
medications) may be severe and life-threatening, particularly when edema involves the
retropharynx and/orlarynx. In the lower airways, anaphylaxis usually causes bronchospasm
(table 3). Onset is most often sudden, and there may be associated signs and symptoms, such
as facial swelling, urticaria, vomiting, dizziness, and/orsyncope. (See "Anaphylaxis: Acute
diagnosis", section on 'Symptoms and signs'.)
Foreign body — Foreign bodies that partially obstruct the upper airway or those lodged in the
lower airways or esophagus, are not usually acutely life-threatening but often cause respiratory
distress. Children with a foreign body in the upper airway, or with an esophageal foreign body
compressing the airway, are more likely to acutely develop severe symptoms, typically choking,
drooling, dysphagia, and/or stridor. In comparison, foreign body in the lower airway, most
commonly manifests as unilateral wheeze, but presentation may be delayed days to weeks and
manifest as fever, rales, or cough due to infection. Children with significant upper airway
obstruction may develop pulmonary edema following relief of the obstruction (see "Airway
foreign bodies in children", section on 'Presentation'). Rarely, a foreign body lodged in the
esophagus will cause esophageal erosion resulting in mediastinitis. (See "Foreign bodies of the
esophagus and gastrointestinal tract in children", section on 'Clinical manifestations'.)
Airway anomalies — Fixed and functional congenital abnormalities of the airway that include
vocal cord paralysis, mass, tracheal stenosis, ring, sling, tracheoesophageal fistula and
laryngomalacia may all cause respiratory distress most commonly in the neonate or infant.
Laryngospasm, hypocalcemic tetany, paradoxical vocal cord movement, and vocal cord
paralysis are acquired causes of upper airway obstruction that may be seen at any age.
Pulmonary edema — Noncardiogenic pulmonary edema may occur from upper airway
obstruction (such as from foreign body or croup), pulmonary irritants, submersion injury, severe
central nervous system insult and acute salicylate toxicity. (See "Neurogenic pulmonary
edema" and "Salicylate poisoning in children and adolescents".)
Chest wall and thoracic cavity abnormalities — Disease processes involving the chest wall
structure (such as asphyxiating thoracic dystrophy, muscular dystrophy, severe pectus
excavatum) may severely restrict lung expansion, limiting ventilatory efforts. (See "Diseases of
the chest wall".)
Mass lesions in the chest or mediastinum may be congenital or acquired and include
diaphragmatic hernia, esophageal anomalies, bronchopulmonary sequestration, benign and
malignant masses and vascular anomalies. They cause respiratory compromise usually by
compression of the airway. (See "Bronchopulmonary sequestration" and "Clinical assessment of
the child with suspected cancer", section on 'Mediastinal masses'and "Approach to the adult
patient with a mediastinal mass".)
Pleural effusion may be caused by infection, inflammation, ischemia, malignancy, organ failure,
drug hypersensitivity, venous or lymphatic obstruction and trauma. Infectious causes are most
common in children. The onset and progression of respiratory distress is usually gradual.
(See "Epidemiology; clinical presentation; and evaluation of parapneumonic effusion and
empyema in children", section on 'Clinical presentation'.)
Cardiovascular conditions — Cardiovascular causes of respiratory distress may be congenital
or acquired.
Congenital heart disease — Congenital cardiac anomalies with right-to-left shunting of
deoxygenated blood result in reduced oxygen saturation of blood entering the systemic
circulation, causing hypoxia with cyanosis (table 4). Signs of respiratory distress other than
cyanosis may not be present, however, unless the child is also in heart failure. (See "Cardiac
causes of cyanosis in the newborn".)
Acute decompensated heart failure — Heart failure may develop due to a congenital or
acquired cardiac condition. For congenital heart defects, the time of onset of congestive heart
failure (CHF) is dependent on the specific heart defect and its severity. As an example, a
newborn with an obstructive left-sided heart lesion, such as severe coarctation of the aorta, may
develop severe CHF when the ductus arteriosus closes. (See "Cardiac causes of cyanosis in
the newborn", section on 'Heart failure'.)
The most common acquired conditions that cause CHF in children are myocarditis and
supraventricular tachycardia that persists for more than 12 to 24 hours. Other conditions include
valvular heart disease, myocardial dysfunction, sepsis, metabolic disturbance, fluid overload,
severe anemia, ischemia, and myocardial infarction. (See "Clinical manifestations and diagnosis
of myocarditis in children" and "Supraventricular tachycardia in children: AV reentrant
tachycardia (including WPW) and AV nodal reentrant tachycardia", section on 'Heart
failure' and "Etiology and diagnosis of heart failure in infants and children".)
Respiratory manifestations of CHF include tachypnea, dyspnea, orthopnea, cough, wheeze, and
rales. Other manifestations include poor feeding, tiring with feeds, failure to thrive, pallor,
diaphoresis, tachycardia, murmur, gallop, rub, thready pulses, jugular venous distension,
cardiomegaly, hepatomegaly, and/or edema.
Pericarditis — Inflammation of the pericardium from pericarditis may cause chest pain that
results in splinting with respiration and if severe, could compromise cardiac output resulting in
inadequate oxygenation. (See "Clinical presentation and diagnostic evaluation of acute
pericarditis", section on 'Clinical features'.)
Cardiac arrhythmia — Both tachyarrhythmias and bradyarrhythmias can cause respiratory
distress if circulatory function is inadequate to meet tissue demands especially if circulatory
compromise results in metabolic acidosis. Supraventricular tachycardia is the most common
arrhythmia in children and can cause heart failure with tachypnea as a manifestation.
Ventricular tachycardia, atrial fibrillation, atrial flutter, and atrioventricular block are less common
and more likely to occur in children with underlying structural heart disease or in the case of AV
bock, in patients with Lyme Disease. (See "Supraventricular tachycardia in children: AV
reentrant tachycardia (including WPW) and AV nodal reentrant tachycardia" and "Management
and evaluation of wide QRS complex tachycardia in children".)
Myocardial infarction — Coronary vasospasm (variant angina) and myocardial infarction are
rare causes of respiratory distress and are associated with chest or supraumbilical abdominal
pain in children and adolescents. Coronary vasospasm is associated with transient ischemic
changes on ECG, normal coronary arteriography, reversible septal akinesia by
echocardiography, and cardiac enzyme elevation. (See"Vasospastic angina" and "Causes of
nontraumatic chest pain in children and adolescents", section on 'Cardiac disease'.)
Myocardial infarctions occur more frequently in adolescent males and are associated with
substance abuse and smoking.
Neurologic and muscle diseases — Central nervous system (CNS) disturbances typically
cause respiratory compromise as the result of depressed ventilation. Conditions may be
congenital (such as CNS malformation, neuromuscular disease, seizures) or acquired (eg,
intoxication, CNS infection, seizures, or brain or spinal cord trauma) and may involve the
central and/or the peripheral nervous system (table 5). Children with central causes may have
hypo or hyperventilation, decreased gag reflex, and/or decreased pharyngeal tone. Associated
neurologic findings include focal neurologic deficits, hypo or hypertonia, and/or altered level of
consciousness. Fever, headache, and/or stiff neck suggest CNS infection. (See "Evaluation of
stupor and coma in children", section on 'Evaluation'.)
Acute muscle weakness may result in dysfunction of respiratory muscles causing respiratory
compromise. Etiologies include conditions that affect the cerebral cortex, spinal cord, anterior
horn cell, peripheral nerve, neuromuscular junction, and muscle (table 6). (See "Etiology and
evaluation of the child with weakness".)
Gastrointestinal conditions — Gastroesophageal reflux can cause stridor due to irritation of
infraglottic structures, or pneumonia due to aspiration. (See "Clinical manifestations and
diagnosis of gastroesophageal reflux disease in children and adolescents", section on 'Clinical
manifestations'.)
Abdominal processes that cause pain (such as appendicitis or intraabdominal injury) or
distention (as with a small bowel obstruction) may cause respiratory distress as the result of
splinting or interference with excursion of the diaphragm. (See "Acute appendicitis in children:
Clinical manifestations and diagnosis", section on 'Clinical manifestations' and "Intestinal
malrotation in children", section on 'Clinical presentation'.)
Metabolic and endocrine diseases — Tachypnea, with or without hyperventilation, may occur
as a compensatory mechanism in children with metabolic acidosis from any cause (table 7).
(See "Approach to the child with metabolic acidosis", section on 'Clinical manifestations'.)
Less common metabolic and endocrine conditions that can cause tachypnea include disorders
that cause hyperammonemia (because ammonia stimulates central hyperventilation),
mitochondrial disorders (through interruption of oxygen metabolism) and hyperthyroidism (as a
result, in part, of increased metabolic rate). (See"Urea cycle disorders: Clinical features and
diagnosis", section on 'Clinical features'.)
Hematologic conditions — Respiratory distress may develop in patients with decreased
oxygen delivery to tissues due to acute onset of severe anemia (eg, hemolytic uremic
syndrome, autoimmune hemolytic anemia, aplastic crisis) or the presence of a significant
amount of abnormal hemoglobin with decreased or absent oxygen-carrying capacity (eg, sickle
cell disease, methemoglobinemia, carbon monoxide poisoning). See selected topic reviews.
Neonatal polycythemia may cause respiratory distress as a result of compromised oxygen
delivery due to sludging of blood and/or acute decompensated heart failure. (See "Neonatal
polycythemia", section on 'Cardiorespiratory effects'.)
Acute on chronic diseases — Children with chronic disease may develop acute respiratory
distress or worsening of a chronic respiratory condition. Examples include:
●Children who have chronic causes of upper airway obstruction (such as
laryngotracheomalacia, an anatomic abnormality of the airway, or tonsillar hypertrophy)
often have worsening obstruction when they develop an acute condition such as an upper
respiratory tract infection (table 8A-B). (See "Assessment of stridor in
children" and "Emergency evaluation of acute upper airway obstruction in children", section
on 'Causes'.)
●Children with chronic pulmonary diseases such as cystic fibrosis or bronchopulmonary
dysplasia are at increased risk for bronchopulmonary infections. Patients with asthma are
at increased risk for pneumothorax and pneumomediastinum, which is usually
asymptomatic. (See "Cystic fibrosis: Clinical manifestations of pulmonary
disease" and "Management of bronchopulmonary dysplasia", section on 'Acute
exacerbations'.)
●Acute chest syndrome is a cause of respiratory distress that occurs in children with sickle
cell disease. (See "The acute chest syndrome in children and adolescents with sickle cell
disease".)
●Patients with neuromuscular disease may develop upper airway obstruction from poor
pharyngeal muscle tone, pneumonia from aspiration, or atelectasis from impaired
respiratory effort. (See "Respiratory muscle weakness due to neuromuscular disease:
Clinical manifestations and evaluation".)
SUMMARY
●Respiratory distress may develop in children due to multiple etiologies that result in one of
the following final common pathways (table 1) (see 'Definition' above):
•Hypoxemia (see "Control of ventilation", section on 'Hypoxic challenge').
•Hypercarbia (see "Control of ventilation", section on 'Hypercapnic challenge').
•Difficulty with the mechanics of respiration, typically from airway obstruction, muscle
weakness, or discomfort (as may occur for patients who are splinting due to
abdominal pain).
•Disordered control of ventilation, in which respiration may be depressed (eg, opioid
overdose, severe head injury) or stimulated (eg, metabolic acidosis,
hyperammonemia, salicylate intoxication).
●Respiratory distress in response to hypoxemia or hypercarbia can rapidly progress to lifethreatening respiratory failure. Neonates, infants, and young children are at particular risk
given their high oxygen consumption and decreased respiratory reserve.
(See 'Definition' above and "Emergency airway management in children: Unique pediatric
considerations".)
●Many conditions may cause acute respiratory distress in children (table 1). The inciting
condition, while commonly within the respiratory system, may also be within other systems,
may not be immediately obvious (eg, fever and rales may be due to heart failure due to
myocarditis rather than pneumonia which is more common). (See 'Causes' above.)
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