eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Critical Care

Acute Respiratory Distress Syndrome

Author: Lennox H Huang, MD, Associate Chair (Clinical), Assistant Professor, Department of Pediatrics, McMaster University School of Medicine; Interim Chief of Pediatrics, McMaster Children's Hospital
Contributor Information and Disclosures

Updated: Dec 1, 2009

Introduction

Background

In 1967, Ashbaugh first described adult respiratory distress syndrome, now known as acute respiratory distress syndrome (ARDS).1 He reported a clinical entity of dyspnea, cyanosis resistant to supplemental oxygen, and bilateral chest infiltrates on chest radiography. Because of its apparent similarity to the recently described respiratory distress syndrome (RDS) observed in newborns, it was termed adult RDS. An immense body of work has grown around the study of this condition. However, until recently, a lack of diagnostic standardization confused efforts to accurately define the incidence and predisposing factors for this condition. In addition, an inability to agree on a consistent definition of this syndrome hindered attempts at therapeutic trials.

In 1994, a European–North American consensus conference agreed on standard definitions of ARDS and an illness less severe than ARDS, namely, acute lung injury (ALI).2 The definition is based on (1) chest radiographic appearance, (2) the ratio of the partial pressure of oxygen in arterial blood to the percentage inhaled oxygen concentration (PaO2/FiO2 ratio), and (3) assessment of the left atrial filling pressure by means of a wedged pulmonary artery catheterization or clinical assessment.

ARDS is considered to be present in the setting of bilateral infiltrates on chest radiography, a PaO2/FiO2 ratio of less than 200, and a left atrial filling pressure of less than 18 mm Hg or no clinical or radiologic evidence of elevated left atrial pressure. ALI is similarly defined, with the difference being that the PaO2/FiO2 ratio is less than 300. Unlike earlier definitions of ARDS, the PaO2/FiO2 ratio is defined regardless of the level of positive end-expiratory pressure (PEEP).

Pathophysiology

The pathophysiology of ARDS is complex and multifaceted. It may be considered as 3 distinct components, which are the nature of the stimulus that initiates or causes ARDS, the host response to this stimulus, and, finally, the role that iatrogenic damage plays in the progression and outcome of this condition. There are 3 pathohistologic stages of ARDS which are further discussed under histology.

An 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, 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, endothelial cells swell, platelets aggregate, and a procoagulant cascade may arise, leading to small-vessel thrombosis. At a physiologic level, the consequences of the reactions outlined above are myriad.

Surfactant depletion, alveolar flooding, cellular debris within the alveoli, and increased airway resistance all lead to increased work of breathing. 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 decreases below the patient's functional residual capacity (FRC), further increasing the work of breathing. This is reflected as reduced compliance; that is, additional pressure is required to generate a unit volume.

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 oxygenated adequately. Hence, relatively deoxygenated arterial blood attempts to supply respiratory muscles that are working harder than usual. These muscles become fatigued; the body is unable to maintain such sustained work of breathing, and respiratory failure ensues.

In addition, hypoxia, hypercarbia, and small-vessel thrombosis combine to elevate pulmonary artery pressures, leading to increased right ventricular work, increased right ventricular filling, and, ultimately, a septal shift toward the left ventricle. These changes, in turn, may decrease cardiac output, further reducing oxygen delivery to the tissues.

Iatrogenic problems may further complicate the patient's clinical picture. High-inspired oxygen concentration (FiO2 >95%) may cause absorption atelectasis, further reducing the number of patent alveoli. Oxygen toxicity can be seen with FiO2 more than 60% over time, leading to additional inflammation secondary to free radical damage.

High mean airway pressures during attempts to maintain adequate oxygenation and ventilation may decrease cardiac output. In addition, high peak airway pressures may cause air leaks (eg, pneumothoraces), which may acutely compromise cardiac and respiratory function. Ventilator-induced lung injury (VILI), discussed in detail below, may further complicate and accelerate disease progression.

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

Frequency

United States

Incidence of ARDS widely varies, partly because of differing and changing definitions of the disease. Moreover, to determine an accurate estimate, all cases in a given population must be ascertained. This may be problematic; however, recent data are available from numerous facilities, both in the United States and internationally. These data may clarify the true incidence of this condition.

An initial study in 1972 revealed that the annual incidence in adults is 75 cases per 100,000 population. A study from Utah showed an estimated incidence of 4.8-8.3 cases per 100,000 population. A study is currently underway in Seattle; the investigators are using the consensus definition to determine the incidence of ALI and ARDS in the United States.

With regard to the pediatric age group, little data are available concerning incidence in children on a population basis. However, in the early 1990s, Fackler et al examined all pediatric intensive care unit (PICU) admissions at 40 institutions. Data from 8000 admissions were analyzed, and 679 patients were identified as having ARDS.

International

Using the consensus conference definition (see Background), researchers from Denmark, Sweden, and Iceland reported annual rates of 17.9 cases per 100,000 population for ALI and 13.9 cases per 100,000 population for ARDS.

A more recent population-based study in Germany showed a low prevalence of 5.5 X 10-5 cases per year and an incidence of 3. 2 X 10-5 cases per year in pediatric patients aged 1 month to 18 years.

Mortality/Morbidity

A true estimate of morbidity and mortality highly depends on accurate definitions of ALI and ARDS. Nevertheless, published estimated mortality rates from ARDS vary in both adult and pediatric populations. Studies from the early 1980s revealed mortality rates of 29-94% for children; however, the definition of ARDS was not standardized at that point.

In 1995, Timmons and colleagues reported that acute hypoxic respiratory failure (defined as mechanical ventilation with a PEEP >6 cm and H2 O and FiO2 >0.5 for >12 h) was associated with a mortality rate of 43%, as shown in a survey of 41 PICUs.3 The patient subset classified as having ARDS had a mortality rate of 51%.

Mortality rates tended to decline, as shown in studies from the 1990s, which yielded mortality rates of 30-50%. Pediatric studies over the past 5 years have demonstrated morality rates of 8-26%.4,5,6,7 Many explanations have been posited for this change, including the emergence of skilled highly specialized PICUs; improvement in the transportation of critically ill children; changes in the definition of the illness itself; and, finally and most importantly, changes in the management, specifically ventilator management, of this illness.

Ventilator management has been given credence in a landmark study of ARDS in adults in which a strategy of low-tidal-volume, permissive hypercapnia was effective in reducing mortality. Patients with ARDS treated with an initial tidal volume of 12 mL/kg and a plateau pressure of less than 50 cm H2 O were compared with patients treated with initial tidal volume of 6 mL/kg and a plateau pressure of 30 cm H2 O or less. The trial was prematurely ended because of a significant difference (P = 0.007) in mortality between the groups. Mortality rates were 31% versus 39.8% with low versus conventional tidal volumes. A secondary outcome measure, days without ventilator assistance, was also significantly different between the groups. This study has not been replicated in pediatric patients, but principles of gentle ventilation have been extrapolated and almost universally applied in PICUs.

Morbidity resulting from ARDS may be divided into pulmonary and extrapulmonary morbidity. This distinction is somewhat artificial because increasing evidence suggests that pulmonary injury, specifically VILI, and extrapulmonary injury are inextricably linked. Traditionally recognized pulmonary complications resulting from ARDS and its treatment include air-leak syndromes, specifically pneumothoraces, pneumomediastinum, pneumopericardium, and subcutaneous emphysema. Conventional thinking has been that air-leak syndromes were associated with high ventilatory pressures and that their presence was associated with an excess mortality rate.

In 1998, Weg et al concluded that high ventilator pressures were not correlated with the development of air-leak syndrome.8 In addition, air-leak syndromes were not associated with mortality. The incidence of pneumothorax in the study was 6.9%. An air leak of some description developed in 10% of patients.

Clinical

History

The history in patients with acute respiratory distress syndrome (ARDS) is generally remarkable for evidence of the precipitating event. The presence of comorbid pathologies, iatrogenic complications, and multiorgan-system failure may complicate the clinical pictures.

  • Cough may be present, reflecting a primary lung injury, such as pneumonia or aspiration. Absence of a cough or gag reflex in a patient with symptoms and signs consistent with ARDS who had a witnessed episode of vomiting suggest that aspiration may have been the primary risk factor for ARDS.
  • Dyspnea usually develops shortly after the initiating stimulus, and it becomes progressively severe, reflecting the increasing alveolar flooding and decreasing pulmonary compliance.

Physical

The evident physical signs primarily reflect lung pathology and other organ injury associated with ARDS.

  • Tachypnea is an early sign as pulmonary edema develops, as pulmonary compliance decreases, as tidal volume decreases toward the functional residual capacity (FRC), and, therefore, as the work of breathing increases.
  • Cyanosis may become apparent with increasing hypoxemia. Remembering that clinically evident cyanosis requires a certain minimum hemoglobin concentration is important, particularly in the patient with trauma.
  • Fever may reflect the underlying process causing ARDS (eg, pneumonia, sepsis) or may reflect massive cytokine release.
  • Crackles may be audible throughout the lung fields, signifying pulmonary edema.
  • Physical signs of air leak syndromes may manifest in the late stages of ARDS. These include pneumothoraces, pneumomediastinum, pneumopericardium, and subcutaneous emphysema.
    • Features of a pneumothorax include decreased air entry on the side of the air leak, an increased percussion note on the same side, and tracheal deviation toward the side of collapse in a simple pneumothorax or toward the contralateral side in a tension pneumothorax.
    • Heart sounds may be muffled, and signs of decreased cardiac output may be observed with a tension pneumothorax.

Causes

Multiple risk factors exist for ARDS. Approximately 20% of patients with ARDS have no identified risk factor. Given the number of adult studies, major risk factors associated with the development of ARDS include the following:

  • Bacteremia
  • Sepsis
  • Trauma, with or without pulmonary contusion
  • Fractures, particularly multiple fractures and long bone fractures
  • Burns
  • Massive transfusion
  • Pneumonia
  • Aspiration
  • Drug overdose
  • Near drowning
  • Postperfusion injury after cardiopulmonary bypass
  • Pancreatitis
  • Fat embolism

More on Acute Respiratory Distress Syndrome

Overview: Acute Respiratory Distress Syndrome
Differential Diagnoses & Workup: Acute Respiratory Distress Syndrome
Treatment & Medication: Acute Respiratory Distress Syndrome
Follow-up: Acute Respiratory Distress Syndrome
Multimedia: Acute Respiratory Distress Syndrome
References
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Further Reading

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Keywords

acute respiratory distress syndrome, adult respiratory distress syndrome, ARDS, respiratory distress syndrome, RDS, shock lung, Da Nang lung, respirator lung, acute lung injury, ALI, ventilator-induced lung injury, VILI, infant respiratory distress syndrome, IRDS, severe acute respiratory syndrome, SARS, pneumothoraces, pneumomediastinum, pneumopericardium, subcutaneous emphysema, pneumonia, aspiration, cough, multiorgan-system failure, cyanosis, hypoxemia, pulmonary edema, bacteremia, near drowning, pancreatitis

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Contributor Information and Disclosures

Author

Lennox H Huang, MD, Associate Chair (Clinical), Assistant Professor, Department of Pediatrics, McMaster University School of Medicine; Interim 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.

Medical Editor

G Patricia Cantwell, MD, Associate Clinical Professor, Department of Pediatrics, University of Miami; Director of Pediatric Critical Care Medicine, Miller School of Medicine, Jackson Children's Hospital
G Patricia Cantwell, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Emergency Physicians, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

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.

CME Editor

Mary E Cataletto, MD, Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Professor of Clinical Pediatrics, State University of New York at Stony Brook; Director of Children's Sleep Services, Winthrop University Hospital
Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Chest Physicians
Disclosure: Shering Plough Pharmaceuticals Honoraria Consulting

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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