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Pediatric Acute Respiratory Distress Syndrome

  • Author: Prashant Purohit, MD; Chief Editor: Timothy E Corden, MD  more...
 
Updated: Jan 21, 2016
 

Practice Essentials

Acute Respiratory Distress Syndrome (ARDS) continues to contribute significantly to the disease burden in today’s arena of pediatric critical care medicine. It is an acute, diffuse, inflammatory lung injury caused by diverse pulmonary and non-pulmonary etiologies. Pathophysiologically it is characterized by increased vascular permeability, increased lung weight and loss of aerated tissue within the 7 days of insult. Hypoxemia, bilateral opacities on the chest x-ray, decreased lung compliance and increased physiological dead space are telltale clinical signs. Diffuse alveolar damage characterized by edema, inflammation, hyaline membrane formation or pulmonary hemorrhage are the pathological hallmark.[1]

Here are the most recent practice essentials from critical care stand point. The Berlin definition eliminated the taxonomy of Acute Lung Injury (ALI) and classified ARDS in to mild, moderate and severe categories based on severity of oxygenation compromise. Minimum PEEP requirement was included for the assessment of oxygen requirement. It also eliminated necessity of pulmonary artery wedge pressure criteria for pulmonary edema. They instead suggested utilization of clinical criteria, in case of presence of risk factors of ARDS. They recommended echocardiogram and the other objective assessment, if the risk factors for ARDS are not present.[1]

A panel of 27 pediatric experts, the Pediatric Acute Lung Injury Consensus Conference (PALICC) Group, developed nomenclature pertinent to pediatric patients after that. They included oxygenation index (OI), oxygen saturation index (OSI) and S/F (SPO2/FiO2) ratio. The committee recommended utilization of low tidal volume (5-8 mL/kg of predicted body weight), positive end expiratory pressure (PEEP) in the range of 0-15 cm H2O, limiting plateau pressure to 28-32 cm H2O, permissive hypercapnia strategy and acceptance of low SPO2 in the range of 88-92% if PEEP is as high as 10 cm H2O. Routine use steroid, prone positioning, surfactant and liquid ventilation is not recommended. Utilization of High Frequency Oscillatory Ventilation (HFOV) can be considered in cases with plateau airway pressure higher than 28. Although PALICC had a weak agreement on this recommendation. Meticulous consideration of inhaled nitric oxide therapy in severe ARDS cases and in cases bridging to extra corporeal life support (ECLS).[2]    

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Background

The discussion of ARDS is incomplete without appreciating historic work by Ashbaugh and colleagues, who were first to describe the concept of ARDS in 1967. They presented eleven adults and one pediatric patient who suffered from acute onset of tachypnea and hypoxemia refractory to supplemental oxygen. The authors also discussed the benefits of positive end expiratory pressure (PEEP) for the management of atelectasis and a plausible role of corticosteroids in certain cases. The loss of lung compliance was noted clinically and pulmonary inflammation, edema and hyaline membrane formation were seen on autopsy. These observations were significant and remain indispensable even after 48 years.[3]

ARDS was referred as Adult Respiratory Distress Syndrome in some of the studies.[4]  But now it is consistently known as  acute respiratory distress syndrome (ARDS), because it is a well-known entity in pediatric population since the first description in 1967.[3]  In last 5 decades, our knowledge and experience has grown substantially and the definition continues to evolve. The American-European Consensus Conference (AECC) definition of ARDS was published in 1994[5, 6]  and had certain limitations which were addressed seventeen years later by Berlin definition in 2012.[1]  The Pediatric Acute Lung Injury Consensus Conference Group made recommendations relevant to the pediatric population afterwards.[2]

See the image below.

Chest radiograph in 3-year-old girl who developed 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.

See Acute Respiratory Distress Syndrome: A Complex Clinical Condition, a Critical Images slideshow, for more information on this life-threatening condition characterized by acute respiratory failure, hypoxemia, and pulmonary edema.

Definition

Berlin definition requires all of the following criteria to diagnose ARDS.[1]

  1. Onset: within one week of known insult or new/worsening respiratory symptoms
  2. Chest imaging (a radiograph or a computed tomogram) showing bilateral opacities consistent with pulmonary edema. This must not be fully explainable by effusion, collapse or nodules.
  3. Origin of edema: patient can be diagnosed with ARDS provided respiratory failure cannot be fully explained by cardiac failure or fluid overload as determined by treating physician based on available clinical information. If the risk factors for ARDS are not present, objective evidence (e.g. echocardiography) would be required to exclude cardiac failure or fluid overload.
  4. Oxygenation impairment: presence of hypoxemia is essential to the diagnosis of ARDS. The subgroup stratification of ARDS is determined by the degree of hypoxemia as below.

Mild: PaO2/FiO2 ratio > 200 to < 300 mm Hg with PEEP or CPAP > 5 cm H2O (could be derived from noninvasive ventilation in mild ARDS)

Moderate: PaO2/FiO2 ratio > 100 to < 200 mm Hg, PEEP > 5 cm H2O

Severe: PaO2/FiO2 ratio < 100 mm Hg, PEEP > 5 cm H2O

This PaO2/FiO2 ratio is applicable at the altitude < 1000 m. For altitudes > 1000 m, following correction factor should be applied: PaO2/FiO2 X (barometric pressure/760)

The Berlin definition eliminated the taxonomy of Acute Lung Injury (ALI) and created three 3 exclusive subgroups of ARDS as described above. A minimum PEEP level was also added across the subgroups along with the requirement of FiO2. They also removed the requirement of Pulmonary Artery Wedge Pressure (PAWP) to exclude cardiac origin of pulmonary edema. Instead, they suggest utilization of noninvasive tests like echocardiography to exclude hydrostatic edema, if the risk factors for ARDS are not present. 

Pediatric ARDS is distinct from adult ARDS in various aspects. Hence a panel of 27 experts met over the period of 2 years from March, 2012 to March 2014 to identify distinguishing features of pediatric ARDS, to define nomenclature and provide recommendation pertinent to the pediatric population with ARDS. The committee made 132 recommendations with strong agreement and 19 recommendations with weak agreement.48 The relevant recommendations are discussed throughout this article. Below are the two definitions (pediatric ARDS and at risk of pediatric ARDS) recommended by The Pediatric Acute Lung Injury Consensus Conference Group. (PALICC) [2]

Pediatric ARDS (PARDS) definition has incorporated Berlin definition criteria for onset of disease, chest imaging and origin of edema. The panel also included specific criteria for age, utilization of oxygen saturations (SPO2), OI (oxygenation index) and OSI (oxygen saturation index) as mentioned below. The purpose of utilizing SPO2 and OSI was to avoid invasive monitoring needed for obtaining PaO2.

Age: The panel recommended excluding patients with peri-natal lung diseases, otherwise no age specific criteria.

Oxygenation: Presence of hypoxemia is essential to the diagnosis of ARDS. Utilization of OI or SF ratio instead of P/F ratio was recommended.

Non-invasive mechanical ventilation, no stratification of severity

Full face mask bi-level ventilation or CPAP > 5 cm of H2O, PF ratio < 300 or SF ratio < 264

Invasive mechanical ventilation, with stratification of severity

Mild: OI 4-<8, OSI 5-<7.5; Moderate: OI 8-<16, OSI 7.5-<12.3, Severe: OI>16, OSI > 12.3

Special population (chronic lung disease, left ventricular dysfunction, cyanotic heart disease): Presence of standard criteria for age, onset, origin of edema, new infiltrates on chest imaging, and acute onset hypoxemia from baseline which meet the criteria of oxygenation as discussed above. All of these cannot be explained by underlying disease.

The panel also developed definition of “At risk of PARDS”. The definition had same criteria as PARDS for age, onset, chest imaging and origin of edema. The criteria for oxygenation were different as mentioned below. 

Oxygenation:

  • Non-invasive mechanical ventilation

Nasal mask CPAP or BiPAP, FiO2 > 40 to maintain oxygen saturations (SPO2) 88-97%

Oxygen via mask, nasal canula or high flow: SPO2 88-97 with age specific flow; 2L/min for age < 1 year, 4L/min for age 1-5 years, 6L/min for age 5-10 years and 8L/min for age > 10 years.

  • Invasive mechanical ventilation

          Oxygen supplementation to maintain SPO2 from > 88%, OI < 4 or OSI < 5

 

The equations can be derived as below.

  1. Oxygenation Index (OI) = (FiO2 X mean airway pressure X 100)/PaO2
  2. Oxygen Saturation Index (OSI) = FiO2 X mean airway pressure X 100 / SPO2
  3. The PaO2/FiO2 (P/F) ratio can be calculated using PaO2 in mm of Hg and FiO2 in decimal from 0.21 to 1.0.

For example, a patient receiving mechanical ventilation with a mean airway pressure of 20 cm H2O, FiO2 of 0.6 has SPO2 of 98% and PaO2 of 85 mm Hg.

OI = (0.6 X 20 x 100)/85 = 14.11

OSI = (0.6 X 20 x 100)/98 = 12.24

P/F ratio = 85/0.6 = 141.66

This patient has moderate ARDS. 

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

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Pathophysiology

ARDS follows cascade of events after direct pulmonary or systemic insult resulting into the disruption of alveolar-capillary unit. The pathophysiology of ARDS is complex and multifaceted involving 3 distinct components: (1) nature of the stimulus (2) host response to the stimulus, and (3) the role of iatrogenic factors. To understand this complex process, it is important to understand the physiology and functional anatomy.

Physiology and functional anatomy

Human lung development begins with 50 million alveoli in the neonatal lung and completes with 500 million alveoli and approximately 50 m2 of surface area in an adult lung. Substantial part of the alveolarization occurs during first 2 years of life. The normal alveolar epithelium is comprised of two distinct types of cells. Type I alveolar cells are flat, account for 90% of the alveolar surface area and are covered with a thin layer of alveolar lining fluid. They participate in the gas exchange and are exposed to very high oxygen concentration. So they are vulnerable to oxidative injury, but recent literature suggests that type I cells may have an active system against the oxidative stress. They are end cells because they are incapable of proliferation and differentiation. They actually arise from type II cells after the injury. Type II alveolar cells are cuboidal or rounded cells that account for the remaining 10% of alveolar surface area and are resistant to injury. They do not participate in the gas exchange but are involved in surfactant production, ion transport and other pulmonary defense mechanisms. [7, 8, 9, 10, 11, 12]

Alveolar epithelium and pulmonary microvascular endothelium create a two-layered alveolar-capillary barrier. This barrier serves the function of gas exchange, maintains the integrity of pulmonary morphology and protection from external injury. Disruption of this barrier results in increased permeability, influx of protein rich edema fluid into the alveolar sacs, dysfunction of surfactant production, and defective ion transport leading to impaired fluid clearance from alveolar cells. These changes are the hallmark of ARDS pathophysiology and are accompanied by dysregulated inflammation from dysfunctional leukocytes and influx of pro-inflammatory cytokines like interleukins and tumor-necrosis factor. The role of neutrophils in this mechanism is controversial. Animal models have favored both neutrophil dependent and neutrophil independent lung injury. It is also unclear if neutrophilic inflammation is the cause or the result of lung injury. Dysfunction of platelets and coagulation cascade results in microvascular thrombosis and capillary occlusion.[7, 8, 9, 10, 11, 12]

This course of ARDS pathophysiology was previously described into 3 histopathologic stages including exudative, proliferative and fibrotic phase. The timing of these stages is variable and in fact, recent evidence is suggestive of beginning of resolution and fibrotic phase early in the course of ARDS.[10]

At clinical level, respiratory distress occurs secondary to surfactant depletion, alveolar edema, 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 lung. In addition, the remaining viable lung may be conceptualized as being smaller rather than stiff. Although the total lung compliance is reduced, a small portion of the lung may be participating in the 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. Hypoxemia, hypercarbia, and small-vessel thrombosis together can elevate pulmonary arterial pressures. Persistent pulmonary hypertension can result in increased right ventricular work, right ventricular dilatation, and, ultimately, left ventricular outflow tract obstruction secondary to intraventricular septum shifting toward the left ventricle. These changes, in turn, may decrease cardiac output and further reduce oxygen delivery to vital organs.

Iatrogenic factors may further complicate the clinical picture. Oxygen toxicity, volutrauma, barotraumas, fluid overload can further aggravate the lung injury and worsening lung compliance and oxygenation.

Resolution of ARDS is again very complex and active process. Alveolar edema resolves by active transport mechanism, where water follows sodium and chloride ions. Termination of inflammation involves anti-inflammatory mediators like IL-10, tissue growth factor (TGF) β and pre resolution mediators like polyunsaturated fatty acids including lipoxins, resolvins, and protectins. Animal models have shown the role of platelets in repair of vascular endothelium, whereas epithelial repair is carried out by alveolar progenitor cells including type II alveolar cells, Clara cells and integrin α6β4 alveolar epithelial cells.[11]  If the injury is severe, disorganized and insufficient, epithelial repair may result into fibrosis and loss of lung function.

The description of ARDS pathophysiology comes from adults and mature animal studies. Future research has been encouraged in pediatric population and juvenile animals.[11]

 

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Etiology

ARDS occurs as consequences of diverse pulmonary and non-pulmonary etiologies. Most common conditions associated with ARDS are sepsis and infectious pneumonia (bacterial and viral).[8]  [13, 14, 15, 16, 17]  Sepsis related ARDS cases may carry poor prognosis, if they are associated with shock and thrombocytopenia. [15]  Other more common etiologies include bronchiolitis, aspiration pneumonia, aspiration of gastric contents, major trauma, pulmonary contusion, burns, inhalational injury, massive transfusions or transfusion-related acute lung injury (TRALI).[8, 13, 14, 15, 16, 17]  Transfusion of all type of blood products including packed red blood cells, fresh frozen plasma and platelets has been associated with development of ARDS.[18, 19]  Other causes include acute pancreatitis, fat embolism, envenomation, drowning or submersion injuries, drug reaction, malignancy and lung transplantation. [8, 13, 14, 15, 16, 17]  Ventilator induced lung injury (VILI) has also been documented as one of the etiologies for development of ARDS.[20]  Noninfectious lung injury can occur after stem cell transplantation. However, a separate entity of idiopathic pulmonary syndrome has been described as well in this context.[21, 22, 23]

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Epidemiology

The incidence of ARDS is certainly lower in pediatric population as compared to the adults. The adult studies have reported very wide range of incidence; from 17.9-86.2 per 100,000 person-years.[24, 25, 26, 27]  For the population 15 years and older, age adjusted incidence was 86.2 per 100,000 person-years, 38.5% hospital mortality; accounting for estimated 190,600 cases of acute lung injury, 74,500 deaths and 3.6 million hospital days each year in the United States.[27]

The incidence in the pediatric population is reported between 2.2 to 12.8 per 100,000 person-years. From the critical care perspective, ALI/ARDS accounts for 2.2% to 2.6% of PICU admissions, [13, 28]  8.3% of those receiving mechanical ventilation for more than 24 hours[29]  and the PICU and the hospital mortality ranging between 18% to 32.8%.[13, 30, 29, 31, 28]

The age related statistics of ARDS can be obtained by comparing the results of two different studies from King County, Washington, USA that were conducted around the same time between 1999 and 2000.[27, 31]  

Table. (Open Table in a new window)

Study Zimmerman JJ et al[31] Rubenfield GD et al[27]
Age in years 0.5 to 15 15 through 19 75 through 84
Incidence per 100,000 person-years 12.8 16 306
Mortality 18% 24% 60%

Incidence and severity of ARDS is somewhat similar at different geographical location. The study from Australia and New Zealand reported incidence of 2.95 per 100,000 person-years, 2.2% of PICU admissions and 30% of PICU mortality.[13]  A Dutch study reported incidence of 2.2 per 100,000 person-years and 20.4% mortality.[30]  Investigators in Spain found the incidence of 3.9 per 100,000 patients-years and the PICU mortality of 26%.[29]  German study showed incidence of 3.2 per 100,000 person-years.[32]  The incidence in the US based study was a little higher of 12.8 per 100,000 person-years, however the mortality was slightly lower 18%.[31]  Chinese literature revealed 2.6% of PICU admission for ARDS with a mortality of 32.8%.[28]

Of note, the above reported epidemiological data is from the studies prior to the Berlin definition, a study which eliminated the category of ALI and classified ARDS in to mild, moderate and severe. So the epidemiology of both ALI and ARDS has been included here. 

Environmental and Genetic Influence

ARDS develops after the insult from diverse etiologies discussed above. However the heterogeneity of susceptibility and the outcome is intriguing. This could partially be explained by environmental and genetic influences. However, the research is still growing in this area.

From the environmental stand point, literature from adult population has shown increased risk of ARDS with alcohol abuse[33, 34]  and smoking (active and passive) after blunt trauma.[35]  The association of passive smoking could be implied to the pediatric population.

From genetic stand point, a total of 34 genes have been reported to impact the ARDS susceptibility.[36] Majority of them are linked to the currently described pathophysiological pathways of ARDS. These include inflammation, epithelial cell function, endothelial cell function, coagulation, oxidative injuries, apoptosis and platelet cellular process.[36, 37, 38]  [39, 40] The other reported genetic mutations associated with ARDS were linked to surfactant dysfunction[36]  and  to the epidermal growth factor gene polymorphism in males.[41]

There is not enough literature suggesting ethnic differences for ARDS incidence and outcomes. Vast majority of initial genetic studies were in European population. The literature is scant for the other ethnic backgrounds. Thus far approximately nine genes in African population and three genes in Asian population have been reported to be linked with ARDS.[36]  Studies have reported poor outcomes in African American with ARDS as compared to the patients of the other ethnicity.[42, 43, 44] Although in one study higher mortality was associated with higher severity of illness on presentation in patients with black race. Higher mortality in Hispanic patients was not explainable by severity of illness on presentation in the same study.[43]

Some of the epidemiological studies have reported slightly higher incidence of ARDS among male children (54% to 63%)[13, 29, 31] , however the mortality (31% in male children) was not significantly different.[13]  Although one adult study reported higher mortality among males.[44]

There is also not enough literature in the area of genetics pertinent to the pediatric ARDS in the context of growing lung and developing immunity.[2]

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Contributor Information and Disclosures
Author

Prashant Purohit, MD Pediatric Intensivist, Kapi’olani Medical Center for Women and Children

Disclosure: Nothing to disclose.

Coauthor(s)

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

Disclosure: Nothing to disclose.

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/ Holtz Children's Hospital, Jackson Memorial Medical Center; Medical Director, Palliative Care Team, Holtz Children's Hospital; Medical Manager, FEMA, South Florida Urban Search and Rescue, Task Force 2

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, Wilderness Medical Society

Disclosure: Nothing to disclose.

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

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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, American College of Emergency Physicians

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, Wisconsin Medical Society

Disclosure: Nothing to disclose.

Additional Contributors

Garry Wilkes, MBBS, FACEM Director of Clinical Training (Simulation), Fiona Stanley Hospital; Clinical Associate Professor, University of Western Australia; Adjunct Associate Professor, Edith Cowan University, Western Australia

Disclosure: Nothing to disclose.

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.

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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.
Study Zimmerman JJ et al[31] Rubenfield GD et al[27]
Age in years 0.5 to 15 15 through 19 75 through 84
Incidence per 100,000 person-years 12.8 16 306
Mortality 18% 24% 60%
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