Pediatric Acute Respiratory Distress Syndrome 

  • Author: Andrew K Feng, MD; Chief Editor: Timothy E Corden, MD   more...
 
Updated: Jul 19, 2011
 

Background

In 1967, Ashbaugh reported a clinical entity of dyspnea, cyanosis resistant to supplemental oxygen, and bilateral chest infiltrates on chest radiography.[1] Because of this entity’s apparent similarity to the recently described respiratory distress syndrome (RDS) observed in newborns, it was termed adult respiratory distress syndrome. Although originally described in adults, this syndrome occurs in children of all ages; hence, it is now known as acute respiratory distress syndrome (ARDS).

Since that time, an immense body of work has grown around the study of ARDS and the best treatment strategies. The most significant changes in mechanical ventilation management over the past several years have been the recommendations for the use of lower tidal volumes and limitation of pressure.[2, 3] Other studies on specific therapies have been less consistent in demonstrating decreased morbidity and mortality. Clearly, the etiologies for ARDS include a broad spectrum of disease, making it extremely difficult to identify a single therapeutic agent that will have a significant impact on outcome.

Definition

In 1994, a European–North American consensus conference agreed on standard definitions of ARDS and of a less severe injury, acute lung injury (ALI).[4] Criteria include (1) acute bilateral infiltrates on chest radiographic appearance, (2) the ratio of the partial pressure of oxygen in arterial blood to the fraction of inspired oxygen (PaO2/FiO2 or PF ratio) of less than 200 for ARDS and less than 300 for acute lung injury (ALI), and (3) noncardiogenic pulmonary edema based on an assessment of the left atrial filling pressure by means of a wedged pulmonary artery catheterization or clinical assessment. Typically in children, chest radiographs or echocardiograms are substituted for pulmonary artery catheterization to assess left atrial filling pressures, especially given the relatively low incidence of cardiogenic pulmonary edema in children. (See Pathophysiology.)

More recently, Khemani and colleagues proposed using a pulse oximetry saturation ratio (SF) in pediatric patients by substituting the pulse oximetry saturation (SpO2) for PaO2 as an alternative to the more invasive arterial blood sampling needed to calculate the PaO2/FiO2 ratio.[5] A later study by Thomas and colleagues performed a post hoc data analysis of 255 children to correlate SF and PF ratios as well as oxygenation indices (OIs) with lung injury severity and substituting SpO2 for PaO2 to calculate an oxygenation saturation index (OSI) for corresponding lung injuries.[6] The chart below summarizes the SF values, correlating PF values, and corresponding sensitivity and specificity.

Table. SF Values, Correlating PF Values, and Corresponding Sensitivity and Specificity (Open Table in a new window)

KhemaniThomasOIOSI
ALI (sensitivity/specificity)263 (93%/43%)253 (93%/43%)5.3 (92%/86%)6.5 (70%/86%)
ARDS (sensitivity/specificity)201 (84%/78%)212 (76%/83%)8.1 (79%/92%)7.8 (64%/82%)

Go to Acute Respiratory Distress Syndrome and Barotrauma and Mechanical Ventilation for complete information on these topics.

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Pathophysiology

Acute lung injury follows a direct pulmonary or systemic insult resulting in injury to the alveolar-capillary unit. Several diseases can cause ARDS, more commonly following pneumonia, aspiration, and sepsis.

The pathophysiology of ARDS is complex and multifaceted. It may be considered as 3 distinct components: (1) the nature of the stimulus that initiates or causes ARDS, (2) the host response to this stimulus, and (3) the role that iatrogenic damage plays in the progression and outcome of this condition. The course of ARDS can be divided into 3 histopathologic stages, as follows:

  • Exudative: Injury to lung endothelial cells and alveolar epithelial cells occurs during days 1-7 of the initial injury. Air spaces are then filled with exudate and fluid, and the development of microvascular thrombi leads to capillary occlusion.
  • Proliferative: This stage occurs between the first and third week after the initial insult. Type II pneumocytes, fibroblasts, and myofibroblasts proliferate, resulting in widening of the alveolar septa and conversion of intra-alveolar hemorrhagic exudate into cellular granulation tissue.
  • Fibrotic: After 3 weeks from the time of injury, the lungs exhibit remodeling and fibrosis.

During the exudative stage, the initiating stimulus leads to a cascade of effects, the most immediate of which is an increase in alveolar and pulmonary capillary permeability. Protein-rich fluid engulfs the alveolus, activated neutrophils and macrophages follow, and an inflammatory cascade is initiated. This cascade involves the release of interleukins (ILs), tumor necrosis factor (TNF), and other inflammatory mediators. Neutrophils release oxidants, leukotrienes, and various proteases.

The net effect at a cellular level is massive cell damage, alveolar denudation, and sloughing of cell debris into the lumen of the alveolus. Furthermore, surfactant is markedly inactivated.

Meanwhile, in the pulmonary capillary bed, endothelial cells swell, platelets aggregate, and a procoagulant cascade arises, leading to small-vessel thrombosis.

On the clinical level, work of breathing increases secondary to surfactant depletion, alveolar filling, cellular debris within the alveoli, and increased airway resistance. Surfactant loss leads to alveolar collapse because of increased surface tension, which is analogous to the situation observed in premature infants with infant RDS (IRDS). As alveoli collapse, closing lung volume capacity rises above the patient’s functional residual capacity (FRC), further increasing atelectasis and the work of breathing. This is reflected as reduced compliance; that is, additional pressure is required to generate a unit volume.

In addition, the remaining viable lung may be conceptualized as being smaller rather than stiff. Although the total lung compliance is reduced, as little as 25% of the lung may be participating in gas exchange. Those remaining intact lung regions have better compliance and are thus subject to overdistention and potential air leak complications (eg, pneumothorax) when exposed to excessive inflating pressures.

The net effect is impairment in oxygenation. A widened interstitial space between the alveolus and the vascular endothelium decreases oxygen-diffusing capacity. Hypoxia arises as a result of the change described above. Collapsed alveoli result in either low ventilation-perfusion (V/Q) units or a right-to-left pulmonary shunt. The end result is marked venous admixture, the process whereby deoxygenated blood passing through the lungs does not absorb sufficient oxygen and causes a relative desaturation of arterial blood when it mixes with blood that is already oxygenated.

Pulmonary hypertension may also ensue from ARDS. Hypoxia, hypercarbia, and small-vessel thrombosis combine to elevate pulmonary artery pressures. Persistent pulmonary hypertension can result in increased right ventricular work, right ventricular dilatation, and, ultimately, left ventricular outflow tract obstruction secondary to intraventricular septal shifting toward the left ventricle. These changes, in turn, may decrease cardiac output and further reduce oxygen delivery to vital organs.

Iatrogenic problems may further complicate the patient’s clinical picture. Oxygen toxicity can be seen with prolonged FiO2 of greater than 60%, leading to secondary lung injury from oxygen free radical damage. A high FiO2 (>95%) may also cause absorption atelectasis, further reducing the number of patent alveoli.

Finally, fluid resuscitation may lead to further alveolar and pulmonary interstitial flooding, with worsening compliance and oxygenation.

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Etiology

One of the most common diseases associated with ARDS is sepsis and septic shock. Other more common etiologies include infectious pneumonia, aspiration pneumonia, aspiration of gastric contents and other noxious substances (eg, hydrocarbons), burn injury, inhalational injury (eg, thermal injury, noxious gases), transfusion-related acute lung injury (TRALI), pancreatitis, fat embolism, and ventilator-induce lung injury (VILI). Failure of other organ systems not uncommonly results in ARDS.

Most near-drowning victims aspirate at least some water. Both freshwater and saltwater aspiration result in pulmonary edema. If near-drowning occurs in stagnant or contaminated water, the risk of bacterial pneumonia is high. However, neither corticosteroids nor prophylactic antibiotics are beneficial.

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Contributor Information and Disclosures
Author

Andrew K Feng, MD  Attending Physician, Division of Pediatric Critical Care, Kapiolani Medical Center for Women and Children

Andrew K Feng, MD is a member of the following medical societies: Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

G Patricia Cantwell, MD, FCCM  Professor of Clinical Pediatrics, Chief, Division of Pediatric Critical Care Medicine, University of Miami, Leonard M Miller School of Medicine; Medical Director, Palliative Care Team, Director, Pediatric Critical Care Transport, Holtz Children's Hospital, Jackson Memorial Medical Center; Medical Manager, FEMA, Urban Search and Rescue, South Florida, Task Force 2; Pediatric Medical Director, Tilli Kids – Pediatric Initiative, Division of Hospice Care Southeast Florida, Inc

G Patricia Cantwell, MD, FCCM is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Lennox H Huang, MD  Chair, Department of Pediatrics, McMaster University School of Medicine; Chief of Pediatrics, McMaster Children's Hospital

Lennox H Huang, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Physician Executives, Canadian Medical Association, Ontario Medical Association, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Dale W Steele, MD  Associate Professor of Emergency Medicine and Pediatrics, Warren Alpert Medical School of Brown University; Attending Physician, Department of Pediatric Emergency Medicine, Rhode Island Hospital

Dale W Steele, MD is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Garry Wilkes  MBBS, FACEM, Director of Emergency Medicine, Calvary Hospital, Canberra, ACT; Adjunct Associate Professor, Edith Cowan University; Clinical Associate Professor, Rural Clinical School, University of Western Australia

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Grace M Young, MD  Associate Professor, Department of Pediatrics, University of Maryland Medical Center

Grace M Young, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Emergency Physicians

Disclosure: Nothing to disclose.

Barry J Evans, MD  Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center

Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Chief Editor

Timothy E Corden, MD  Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, and Wisconsin Medical Society

Disclosure: Nothing to disclose.

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Eight-year-old girl with diagnosis of pneumonia. Chest radiograph on day of admission.
Fourteen-month-old boy with diagnosis of exacerbation of bronchopulmonary dysplasia. Chest radiograph on day of admission.
Eight-year-old girl with pneumonia and impending respiratory failure. Chest radiograph on day 2.
Fourteen-month-old boy with exacerbation of bronchopulmonary dysplasia and impending respiratory failure. Chest radiograph on morning of day 2.
Fourteen-month-old boy with exacerbation of bronchopulmonary dysplasia and respiratory failure. Chest radiograph on afternoon of day 2.
Fourteen-month-old boy with exacerbation of bronchopulmonary dysplasia, respiratory failure, and severe hypoxemia. Chest radiograph on evening of day 2.
Chest radiograph in 3-year-old girl who developed acute respiratory distress syndrome due to overwhelming gram-negative sepsis. Salient features include endotracheal tube; diffuse, bilateral infiltrates; air bronchograms on left side; and central venous catheter. Ratio of arterial oxygen tension to fraction of inspired oxygen at time of chest radiography was 100.
Chest radiograph demonstrates complication of acute respiratory distress syndrome. Patient presented with respiratory failure after near-drowning episode. Peak inspiratory pressures were 40 cm water. Patient had sudden desaturation and decreased bilateral air entry, as well as cool peripheries and decreased blood pressure. Needle evacuation of both pleural spaces confirmed pleural air. Chest tubes were placed, with immediate improvement in clinical status. Pulmonary status continued to deteriorate; high-frequency oscillatory ventilation was given. Patient subsequently required second chest tube on left side.
Chest CT in 6-month-old male infant with newly diagnosed cystic fibrosis. Patient was intubated for respiratory failure and subsequently developed acute respiratory distress syndrome. Image demonstrates numerous cystic and bronchiectatic areas. Note dorsal distribution of atelectasis, particularly on right side.
Typical pressure-volume curve may provide information regarding lung compliance, lung hysteresis, and critical opening and closing pressures. Evidence of pulmonary overdistention may also be observed.
Subcutaneous emphysema and pneumothorax.
Table. SF Values, Correlating PF Values, and Corresponding Sensitivity and Specificity
KhemaniThomasOIOSI
ALI (sensitivity/specificity)263 (93%/43%)253 (93%/43%)5.3 (92%/86%)6.5 (70%/86%)
ARDS (sensitivity/specificity)201 (84%/78%)212 (76%/83%)8.1 (79%/92%)7.8 (64%/82%)
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