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Pediatric Acute Respiratory Distress Syndrome Treatment & Management

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

Approach Considerations

The cornerstone of management is impeccable intensive care.  Careful utilization of mechanical ventilation while minimizing the risk of ventilator-induced lung injury (VILI) and multiple organ dysfunction syndrome (MODS) is essential. Critical aspects are maintaining nutrition, meticulous management of fluid and hemodynamics, appropriate levels of sedation and judicious consideration of neuromuscular blocking agents. Early anticipatory management may avoid late complications including sepsis and poor outcome. Treat the primary cause (eg, sepsis, pneumonia), whenever possible.

Many of the therapies and strategies proposed for ARDS are founded on rational physiologic and pathologic principles, but they have not been shown to have unequivocal benefits. Reasons include an incomplete understanding of the pathophysiology of ARDS, the lack of a standardized diagnostic test, and the heterogeneity of the illness and the patient population. Research is evolving in this area. 

Although they have shown promise in animal and small-scale human studies, many pharmaceutical agents have not demonstrated an unequivocal benefit in large trials. These agents include systemic pulmonary vasodilators, pentoxifylline, various antioxidants, ketoconazole, anticytokines, and antiproteases. Their use is not discussed further.

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


Initial Considerations

It is important that patients get appropriate level of care from the beginning while the ARDS is still under evolution, especially those who qualify for at risk of PARDS. When patients present in the ED with increased work of breathing secondary to worsening lung compliance, increasing mean airway pressure and instituting other alveoli-recruiting maneuvers may offer the most benefit in addition to administering supplemental oxygen. This can be achieved either invasively (ie, with tracheal intubation and mechanical ventilation) or noninvasively.

If the patient continues to have good respiratory effort and adequate oxygenation, noninvasive positive airway pressure support may be all that is required in the ED setting.

If intrahospital transfer from the ED to the pediatric intensive care unit (PICU) is indicated, the patient must be accompanied by providers who are competent to secure and manage the airway. This team often includes a physician, a nurse, and a respiratory therapist.

Interhospital transfer may be indicated. Transfer to a center skilled in pediatric intensive care should be mandatory for any patient at risk of developing ARDS or any patient with full-blown ARDS. Ideally, a dedicated team with expertise in the transport of critically ill children should perform the transfer via ground, rotor, or fixed wing transport. In critically ill children, transporting them to a facility that offers pediatric extracorporeal membrane oxygenation (ECMO) capabilities is preferable.



Ventilation is the cornerstone of treating the patient with ARDS. Striking a balance between the levels of ventilator support while minimizing VILI is essential.

Noninvasive ventilation

Noninvasive ventilation has been used early in ALI and ARDS in adult population.[50, 51]  Continuous positive airway pressure (CPAP) and bilevel positive airway pressure (BiPAP) therapies via nasal mask or face mask have been successful in maintaining adequate oxygenation and ventilation in some patients who present with impending acute respiratory failure and who otherwise would require tracheal intubation. Lack of improvement of P/F ratio in first few hours or on first day can be a good indicator for failure of NPPV.[52, 53]  The benefits of NPPV include improvement of oxygenation and work of breathing without the expense of invasive mechanical ventilation, none or minimal sedation, and patients are able to regulate their own minute ventilation. Pediatric experience in use of NPPV for ARDS or acute hypoxemic respiratory failure is growing as well. Immunocompromised individuals would be at more advantage from the avoidance of invasive mechanical ventilation. Panel of experts had a week agreement on recommendations for use of NPPV in early PARDS cases (88% agreement) and for immunocompromised children with PARDS (80% agreement). [2, 54, 55, 56, 57, 58]

More recently use of high-flow nasal cannula system including Vapotherm (Vapotherm; Stevensville, MD) is becoming popular mode.[59]   The literature is minimal for its use in ARDS.

Conventional Mechanical Ventilation

In the event that a patient requires intubation for ARDS, it may be prudent to use a cuffed endotracheal tube regardless of the age of the patient. Historically, children younger than 8 years used to be intubated with uncuffed tubes. However, because of worsen lung compliance in ARDS; cuffed tubes are often required to effectively inflate the lungs. Otherwise, excessive air may leak around the endotracheal tube resulting in inadequate oxygenation and ventilation.[2]

It is difficult to attain gas exchange in the collapsed and fluid-filled alveoli. A nearly linear increase in functional residual capacity (FRC) develops as positive end-expiratory pressure (PEEP) is increased over a range from 0-15 mm Hg with recruitment of terminal airways and alveoli and improved oxygenation. Meticulous use of alveolar recruitment maneuver with incremental and decremental PEEP to achieve adequate oxygenation has been recommended as well. PEEP more than 15 might be required in severe ARDS cases. Close monitoring of plateau pressure and hemodynamics are imperative while using high PEEP. Lower levels of oxygen saturations in the range of 88-92% are acceptable after PEEP is as high as 10.[2]  Mercat et al reported that a strategy of using PEEP to maximize alveolar recruitment in the adult population reduced the duration of organ failure and mechanical ventilation.[60]

To minimize the barotrauma and volutrauma, it is recommended to limit the inspiratory plateau pressure to 28 cm H2O in most of the cases and in the range of 29-32 in patients with reduced chest wall compliance from obesity or other reasons.[2]

Traditionally, a low tidal volume strategy has been emphasized. Ranieri et al provided additional information to suggest that low tidal volume may be beneficial, reporting reported lowered levels of cytokines in bronchoalveolar lavage (BAL) fluid and plasma in patients treated with low tidal volume. The authors postulated that decreased levels of cytokines reflect reduced inflammation in organs other than the lungs, leading to a possible survival benefit.[61]  The study by Amato et al[62] showed improved 28 days survival and decreased incidence of barotrauma. The results were confirmed by a large multicenter study conducted by ARDS Network trial.[63] In this NIH study, the control group was ventilated with a tidal volume of 12 mL/kg adjusted to maintain a plateau pressure of 45-50 cm water. In the study group, tidal volume was reduced to 6 mL/kg and then as low as 4 mL/kg to maintain a plateau pressure less than 30 cm water. The trial was prematurely terminated when an interim analysis showed a markedly reduced mortality rate in the group receiving low tidal volume (31% vs 39.8%, p=0.007). Since then low tidal volume has become a routine practice for ARDS patients and no further trials are required at this stage.[64]

The twin goals of permissive hypercapnia and open lung maintenance are achieved by optimizing PEEP and minimizing delivered tidal volumes. PEEP is optimized by keeping it above the lower inflection point on a pressure-volume curve (ie, Pflex) and below the upper inflection point where overdistention occurs (see the image below). This general approach has been assessed in a number of studies.

Typical pressure-volume curve may provide informat 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.


Hickling et al gave one of the original descriptions of permissive hypercapnia, reporting a significant reduction in mortality rates, associated with ventilator strategy that will allow permissive hypercapnia.[65]  Amato et al reported that their strategy of ventilating at a low tidal volume with an elevated carbon dioxide level and preventing alveolar closure by optimizing PEEP was associated with lower mortality rate (38% versus 71%).[62] Most recent recommendations were to maintain pH between 7.15 – 7.30 to maintain lung protective strategy with permissive hypercapnia. It will not be recommended in cases with intracranial hypertension, pulmonary hypertension, hemodynamic instability and significant ventricular dysfunction. Although there was a weak agreement (92%) for the recommendation regarding permissive hypercapnia. [2]

Numerous ventilator modes are available; however, there are few if any data to indicate that any of these modes is superior to any other.

Another technique that has been studied is high-frequency ventilation (HFV). Two modes of HFV are high-frequency oscillatory ventilation (HFOV) and high-frequency jet ventilation (HFJV). HFJV is rarely used in pediatric practice and therefore will not be discussed further.

High Frequency Oscillatory Ventilation (HFOV)

HFOV may be thought of as the ultimate in high-PEEP low-tidal-volume strategy. Because of the extremely small tidal volumes used, HFOV minimizes repetitive opening and closing and possibly reduces VILI, if the lung is sufficiently recruited. Because of the extremely high respiratory rates, carbon dioxide can be maintained at satisfactory levels. Recruiting (or opening) the atelectatic areas of the lung is critical to maintaining lung volume at the FRC. Optimal lung volume is gauged with clinical assessment, monitoring of arterial oxygen saturation, ABG measurements, and lung inflation on chest radiography.

Historically use of HFOV has been reported to have association with some form of adversity. The first ever HFOV trial was in animals by Lunkenheimer in Germany.[66]  It was designed to for the purpose of ventilation during thoracic surgery and bronchoscopy avoiding lung excursions. However, it was not pursued further because it was associated with decreased cardiac output from high mean airway pressures. Later on, HFOV became popular among neonatologists and a large multicenter trial was conducted in USA. The “HIFI study” showed that HFOV did not offer any advantages over CMV and was associated with increased incidences of air leak and grade 3 and 4 intraventricular hemorrhages.[67]  A recent large multicenter trial was conducted in five countries among the adult population by the OSCILLATE Trial Investigators showed that the early application of HFOV as compared with low tidal volume high PEEP strategy did not reduce, but might increase mortality. In fact, the study was stopped after 548 of planned 1200 patients based on the recommendations of data monitoring committee.[68]  Another multicenter trial by the OSCAR study group showed no difference in 30 days mortality.[69]  There was one pediatric multicenter, prospective, randomized control trial which showed improved oxygenation (A-a gradient and OI) but did not show any reduction in 30 days mortality or days on mechanical ventilation. Of note this study was cross over study and was not powered to evaluate mortality.[70]  In a recent study, application of both the HFOV and early HFOV had poor outcomes as compared to the CMV group.[71]

However, it still remains a question if HFOV helps in “rescue” situations where patients are severely ill and have failed conventional ventilation treatment. Other therapeutic modalities for the rescue of ARDS patients, such as ECMO, have their own potential harms. Benefits of inhaled nitric oxide in ARDS is limited to improved oxygenation only and has not shown improvement in mortality.[72]  While the other modalities of mechanical ventilation like APRV (airway pressure release ventilation) or VDR (volumetric diffusive respiration) have not undergone enough trials to prove their benefits or harms, current options are limited. 

After above mentioned rigorous discussion, it is apparent that the potential harms associated with HFOV may not be trivial. Choosing HFOV as a ventilator strategy should be individualized and carefully evaluated for every patient until further larger studies are available to provide definite evidence in favor or against the use of HFOV. Current recommendations are to consider it for moderate to severe ARDS cases with plateau pressure higher than 28. Although there was a weak agreement (92%). [2]

Airway pressure–release ventilation (APRV) is a relatively new mode of ventilation that allows spontaneous ventilation with mean airway pressures similar to that achieved with HFOV. Case studies report the successful use of APRV in ARDS; however, data are insufficient to compare it with conventional ventilation or HFOV.

Prone positioning

As an adjunct to ventilator management, prone positioning has been advanced as a means of improving oxygenation in adults and children with severe ARDS. It is thought that turning patients prone helps optimize ventilation/perfusion (V/Q) matching by reducing atelectasis in dependent areas of the lung.

Many trials have shown improved oxygenation with prone positioning; however, a multicenter trial of 102 patients demonstrated no significant difference in clinical outcomes, including ventilator-free days.[73]  The study population had a mortality rate of only 8%, suggesting that prone positioning may still have a role in extremely ill patients with ARDS. Prone positioning is not recommended as routine therapy for ARDS until further pediatric studies in this context. Although there was weak agreement on this recommendation (92%).[2]  It can still be attempted in a patient with profound hypoxemia. But the decision should be determined by the treating physician based on patient’s condition and risk versus benefit ratio.

Use of neuromuscular blocking agents

Use of the neuromuscular blocking agent cisatracurium over the initial 48 hours of treatment for adults with severe ARDS—that is, arterial oxygen tension (PaO2)/FiO2 ratio < 150—appears to increase ventilator-free days, reduce barotrauma, and possibly improve survival without increasing the occurrence of muscle weakness in this patient population.[74] Care should be used in extrapolating those results to the pediatric population, given the differences in ARDS mortality rates and the varying causes of ARDS mortality. Current recommendations are in favor of neuromuscular blockade (NMB), if sedation alone is inadequate to achieve effective mechanical ventilation. There was a strong agreement for this recommendation by the panel of experts.[2]


Go to Barotrauma and Mechanical Ventilation for complete information on this topic.


Surfactant Therapy

One of the key events in the progression of ARDS is a reduction in both volume and function of surfactant. In addition, surfactant inhibitors may be present in the alveolus. Based on positive results of many clinical trials of infant respiratory distress syndrome (IRDS), numerous studies have been conducted to examine the role of exogenous surfactant in the treatment of ARDS.

Administration of exogenous surfactant has many theoretical benefits, as demonstrated in vitro. These include the prevention of alveolar collapse, maintenance of pulmonary compliance, optimization of oxygenation, enhancement of ciliary function, enhancement of bacterial killing, and downregulation of the inflammatory response.

Studies of various surfactants and different modes of delivery in adults have not yielded a consensus regarding the efficacy of surfactant in ARDS. In vitro data and extrapolated data from neonatal in vivo studies suggest that animal-derived surfactant may be superior to synthetic surfactant. In addition, inhalation may be inefficient as a means of delivery.

A growing body of literature supports the use of surfactant for severe pediatric ARDS.[75]  A retrospective chart review of 19 patients showed improvement in oxygenation index and hypoxemia score but no change in other outcome measures. Prospective studies from the late 1990s to early 2000 involving porcine or bovine surfactant showed variable outcomes, ranging from improvement in only oxygenation to shortened ventilation and PICU stay.[76, 77, 78, 79]


A randomized, controlled multicenter study by Willson et al using a natural exogenous surfactant (calfactant) demonstrated a significant reduction in mortality, with an absolute risk reduction of 17%.[80]  This reduction was most pronounced in patients younger than 12 months, who had a corresponding absolute risk reduction of 33%.

Significant improvement was also demonstrated in the oxygenation index, in ventilator-free days, and in rates of failure with conventional mechanical ventilation. One confounding factor was that the placebo group had more immunocompromised patients than the treatment group.

Data from a cost-effectiveness study suggested that the use of exogenous surfactant may be cost-effective in an American healthcare setting. The expense of the surfactant was offset by early PICU discharge. Mortality benefits and ventilator-free days were not factored into the model.[81]

According to most recent recommendations from Pediatric Acute Lung Injury group, use of exogenous surfactant is not recommended in PARDS until further studies.[2]


Nitric Oxide Therapy

Nitric oxide (NO) is a potent vasodilator, first described in 1989. Its use in neonatal persistent pulmonary hypertension was described over 2 decades ago. The action of vasodilatation is mediated via cyclic GMP pathway.[82]  Inhaled nitric oxide (iNO) is a selective pulmonary vasodilator, as it rapidly binds to hemoglobin and is inactivated before reaching the systemic circulation. It may have numerous attractive properties in patients with ARDS. Mainly, it reduces hypoxic pulmonary vasoconstriction (HPV). Inhaled NO diffuses to only relatively well-aerated parts of the lung lessen any local HPV. This helps in improvement of ventilation-perfusion mismatch and so oxygenation. By reducing hypoxic pulmonary vasoconstriction (HPV), iNO may reduce right-sided pulmonary pressures. This, in turn, lessens the degree of leftward septal shift, which improves cardiac output. Other benefits may include decreased pulmonary edema while pulmonary pressures are reduced.

Initial studies showed improvement in OI and improvement in outcome with use of iNO in pediatric patient with acute hypoxemic respiratory failure (AHRF). This was a small study.[83]

A systematic review and meta-analysis of 12 different trials showed that although NO temporarily improves oxygenation, it does not improve survival and actually it may cause harm in both children and adults.[72]  A recent study that looked to test the hypothesis that inhaled nitric oxide (iNO) would lead to improved oxygenation and a decrease in duration of mechanical ventilation in pediatric patients with acute respiratory distress syndrome reported that the use of iNO was associated with a significantly reduced duration of mechanical ventilation and significantly greater rate of extracorporeal membrane oxygenation-free survival.[84]

A multicenter study of the use of iNO (10-ppm dose) in children with acute hypoxic respiratory failure was reported. Although oxygenation acutely improved at 4 hrs and 12 hrs in the group treated with iNO, there was no difference at 72 hrs and there was no survival benefit.[85]  Data from a post-hoc analysis suggested that patients with severe respiratory failure (oxygenation index >25) or immunocompromise may have benefited from the use of iNO.[86]

Although many studies demonstrated improvement in surrogate measures (eg, oxygenation, degree of ventilator support), no differences are noted in primary outcome measures (eg, mortality, ventilator-free days, time to extubation). Reasons for this lack of clinical benefit are unclear. One possible explanation is that ARDS tends to be a heterogeneous lung disease, in contrast to persistent pulmonary hypertension of the newborn. Alternatively, the fact that most patients with ARDS die from sepsis, MODS, or their primary illness may imply that no survival benefit is observed with improved oxygenation and decreased ventilator support.

According to most recent recommendation from Pediatric Acute Lung Injury Consensus Conference Group, the routine use of inhaled nitric oxide is not recommended. It may be considered in patients with pulmonary hypertension or right ventricular dysfunction. It may also be considered in severe form and in cases for bridge to extra corporeal life support.[2]


Liquid Ventilation

Perfluorocarbons (PFCs) have numerous attractive properties that facilitate their use in liquid ventilation. Because PFCs are chemically and biologically inert, with a high vapor pressure that ensures rapid evaporation when exposed to the atmosphere, both oxygen and carbon dioxide dissolve easily in PFC liquid.

Perceived advantages of PFCs in the treatment of ARDS include the ability to maintain an open lung and to minimize repetitive opening and closing of the alveoli. This ability has given rise to the terms “liquid PEEP” and “PEEP in a bottle.” In addition, a lavage effect may clear the alveoli and small airways of debris and inflammatory mediators, reducing ongoing inflammation. PFCs are also thought to have intrinsic anti-inflammatory actions.

By flowing preferentially to dependent areas of the lung where alveolar collapse is maximal, intra-alveolar pressure is increased; hence, perfusion to these areas is decreased, which may improve V/Q matching.

Two types of liquid ventilation have been described: partial liquid ventilation (PLV), in which a volume of liquid equal to the FRC is instilled, and total liquid ventilation (TLV). In contrast to PLV, TLV requires that the lung be filled completely with PFC and that the patient be ventilated with a specially designed liquid ventilator. For logistical reasons and because no data suggest that TLV is superior to PLV, PLV has been used more widely than TLV.

Little convincing data are available to assess the use of PFC liquid ventilation in ARDS. Investigators from 2 uncontrolled trials (1 in adults and 1 in pediatric patients) described its use in conjunction with extracorporeal life support (ECLS).[87, 88]  However, according to review by Cochrane database, there were no benefits from PLV and there were increased risk of adversity from PLV.[89]  According to most recent recommendation from Pediatric Acute Lung Injury Consensus Conference Group, the routine use of liquid ventilation (partial or total) is not recommended.[2]


Extracorporeal Life Support

ECLS has been used since the 1970s to improve oxygenation, ventilation, or both in critically ill patients with severe ARDS. A number of modalities have been reported, including ECMO, which may consist of an arterial and venous cannula (AV-ECMO) or 2 venous cannulae (VV-ECMO), and extracorporeal carbon dioxide removal (ECCO2 R), which has been used most commonly in Europe.

Extracorporeal membrane oxygenation

A large randomized study of the efficacy of ECMO in adults with severe ARDS was published in 1979. The study demonstrated improvement in gas exchange but no improvement in mortality.[90]

A report from single university center had a total of 2000 patients from 1973 to 2010. This included neonate, children and adults with various indications for ECMO. In children with respiratory failure, they reported discharge in 76% of patients. They suggested that ECMO may be of benefit in children with severe acute respiratory failure unresponsive to maximal conventional therapy.[91]

In a multicenter retrospective cohort trial of 331 children across 32 hospitals reported data that ECMO was associated with improved survival.[92]  This study had a number of limitations. It was not a controlled trial. Secondly, it was not sufficiently powered.

Numerous studies from the United Kingdom showed that the use of ECMO in neonates with respiratory failure was associated with improved outcomes.[93, 94, 95]

With pediatric ECMO, the survival rate is approximately 50%. This is markedly less than the reported survival rate of 80% in neonates treated with ECMO. The reasons for this disparity may include the heterogeneity of illness leading to respiratory failure in the pediatric population, the relatively limited experience with pediatric versus neonatal ECMO, or a reluctance to commence ECMO that leads to delays that further exacerbate lung damage.

At present, the question of who should receive ECMO has no certain answer. Candidates should have severe lung disease that progresses despite maximal conventional medical therapy. The disease process leading to respiratory failure should have a reasonable potential for reversibility and recovery. Objective indicators include alveolar-arterial (A-a) gradients of more than 450 mm Hg and ventilator peak pressures of more than 40 cm water.

Exclusion criteria include cerebral hemorrhage, preexisting chronic lung disease, congenital or acquired immunodeficiency, congenital anomalies, or other organ failure associated with poor outcomes. Ventilation for more than 10 days before ECMO may require a meticulous evaluation for patient's candidacy for ECMO. However, there are no strict criteria at this time for patient selection.[2]

Why ECMO may confer a survival benefit is unclear. Possibilities include the ability to rest the lung by reducing excess stretch (ie, high pressures) and reducing repetitive opening and closing (ie, high ventilator rates). Oxygen toxicity may be minimized. Fluid balance can be optimized with aggressive diuresis or with renal replacement therapy.

According to PALICC, ECMO should be considered in children with severe PARDS where rest of the other strategies discuss above failed. It is difficult to determine who would benefit from ECMO and who will not.[2]  

Extracorporeal carbon dioxide removal

The rationale of ECCO2 R is similar to that for ECMO—namely, to allow the lung to rest while carbon dioxide is removed and excessive hypercarbia is prevented.[96]  Limited data are available concerning this modality in the pediatric population.


Steroid Therapy

The use of steroids is reported as a therapy for ARDS. Numerous reported trials demonstrated no benefit with large doses of steroids administered as a short course in the early phases of ARDS. However, many investigators contend that ongoing or late-stage ARDS is partly an inflammatory condition. Hence, by virtue of their anti-inflammatory properties, steroids may be beneficial when used in the fibroproliferative phase.

In a randomized double-blind placebo-controlled trial in adults with ARDS who were not improving, Meduri et al suggested late use of steroids to attenuate ARDS and improve survival.[97]  Another study of randomly assigned 180 patients, who were in to at least seventh day of ARDS, showed no improvement in survival at 60 days. Additionally, the patients who received steroid on or after 14th day of illness demonstrated increased risk of death. Moreover, the incidence of neuromuscular weakness was higher in the steroid group.[98]  In a meta-analysis of five cohort studies and four randomized controlled trial, use of low dose steroid was associated with improved survival and morbidity. No adverse effects were seen with use of steroid.[99]  Children meeting criteria for ARDS (both Berlin 2012 and AECC 1994 acute lung injury) and pediatric ARDS (PARDS, as defined by PALICC 2015) were enrolled for an observational, single-center prospective trial. This study showed increased duration of ventilator with steroid use.[100]

Studies conducted thus far have shown variable results. The use of steroid in pediatric ARDS is not recommended per PALICC.[2]

To the authors’ knowledge, no study has been performed to examine the potential role of inhaled steroids in ARDS.


Diet and Activity

The thinking regarding the role of nutrition in patients with ARDS has undergone a paradigm shift. As attention was being given to the role of adequate nutrition in the critically ill patient, bacterial overgrowth in the gastrointestinal (GI) tract resulting from antibiotic use and the late introduction of feeding was postulated to contribute to bacterial translocation across the bowel wall. Hence, the standard practice of introducing early enteral feeding when possible has expanded.

In situations of feeding intolerance, efforts to optimize enteral nutrition include the placing of a transpyloric tube (duodenal or jejunal), administering continuous drip feeds, and administering promotility agents (metoclopramide or erythromycin).

In some patients with limited pulmonary reserve, high-energy loads may lead to respiratory failure because of marked carbon dioxide production.

Intravenous fat emulsions have been associated with worsening pulmonary mechanics in some patients with ARDS. At present, the published evidence is inconclusive, being limited to animal data and findings in small case series. Caution should be exercised if parenteral nutrition is required during the early stages of ARDS.

Activity restriction

In general, the patient’s activity depends on the severity of the precipitating illness (eg, trauma, sepsis) and ARDS limits. If the patient recovers, no limitation on activity is usually necessary, except in the few patients with evidence of extensive pulmonary scarring or fibrosis.



Few cases of ARDS can be anticipated before presentation; however, all children with chronic lung disease should receive influenza and pneumococcal vaccines. Administer respiratory syncytial virus (RSV)–specific vaccines as indicated.

ARDS secondary to aspiration may be prevented by the use of appropriate intubation techniques (eg, rapid-sequence intubation). Although no evidence is definitive, early intervention with noninvasive ventilation in patients with respiratory failure may reduce the risk of progression of ARDS.


Consultations and Long-Term Monitoring

Consult a pediatric intensivist. Consider also consulting a critical care specialist, an infectious diseases specialist, an otolaryngologist, or a pulmonologist as necessary.

Periodic outpatient follow-up may be necessary for those with severe residual lung damage to assess the need for oxygen supplementation and to monitor for the development of restrictive lung disease. The most common complaint after intensive-care hospitalization for ARDS is muscular weakness, which may persist for weeks after discharge.

Contributor Information and Disclosures

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

Disclosure: Nothing to disclose.


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.

  1. ARDS Definition Task Force, Ranieri VM, Rubenfeld GD, Thompson BT, Ferguson ND, Caldwell E, et al. Acute respiratory distress syndrome: the Berlin Definition. JAMA. 2012 Jun 20. 307(23):2526-33. [Medline].

  2. Pediatric Acute Lung Injury Consensus Conference Group. Pediatric acute respiratory distress syndrome: consensus recommendations from the Pediatric Acute Lung Injury Consensus Conference. Pediatr Crit Care Med. 2015 Jun. 16 (5):428-39. [Medline].

  3. Ashbaugh DG, Bigelow DB, Petty TL, Levine BE. Acute respiratory distress in adults. Lancet. 1967 Aug 12. 2 (7511):319-23. [Medline].

  4. Petty TL, Ashbaugh DG. The adult respiratory distress syndrome. Clinical features, factors influencing prognosis and principles of management. Chest. 1971 Sep. 60 (3):233-9. [Medline].

  5. Bernard GR, Artigas A, Brigham KL, et al. Report of the American-European consensus conference on ARDS: definitions, mechanisms, relevant outcomes and clinical trial coordination. The Consensus Committee. Intensive Care Med. 1994. 20(3):225-32. [Medline].

  6. Bernard GR, Artigas A, Brigham KL, Carlet J, Falke K, Hudson L, et al. The American-European Consensus Conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med. 1994 Mar. 149 (3 Pt 1):818-24. [Medline].

  7. Andrew B Lumb MB BS FRCA. Functional anatomy of the respiratory tract. Nunn’s Applied Respiratory Physiology. Seventh Edition. Churchill Livingstone Elsevier Ltd.; 2010. 13-26.

  8. Ware LB, Matthay MA. The acute respiratory distress syndrome. N Engl J Med. 2000 May 4. 342 (18):1334-49. [Medline].

  9. Berthiaume Y, Voisin G, Dagenais A. The alveolar type I cells: the new knight of the alveolus?. J Physiol. 2006 May 1. 572 (Pt 3):609-10. [Medline].

  10. Dos Santos CC. Advances in mechanisms of repair and remodelling in acute lung injury. Intensive Care Med. 2008 Apr. 34 (4):619-30. [Medline].

  11. Sapru A, Flori H, Quasney MW, Dahmer MK, Pediatric Acute Lung Injury Consensus Conference Group. Pathobiology of acute respiratory distress syndrome. Pediatr Crit Care Med. 2015 Jun. 16 (5 Suppl 1):S6-22. [Medline].

  12. Chen J, Chen Z, Chintagari NR, Bhaskaran M, Jin N, Narasaraju T, et al. Alveolar type I cells protect rat lung epithelium from oxidative injury. J Physiol. 2006 May 1. 572 (Pt 3):625-38. [Medline].

  13. Erickson S, Schibler A, Numa A, Nuthall G, Yung M, Pascoe E, et al. Acute lung injury in pediatric intensive care in Australia and New Zealand: a prospective, multicenter, observational study. Pediatr Crit Care Med. 2007 Jul. 8 (4):317-23. [Medline].

  14. Pepe PE, Potkin RT, Reus DH, Hudson LD, Carrico CJ. Clinical predictors of the adult respiratory distress syndrome. Am J Surg. 1982 Jul. 144 (1):124-30. [Medline].

  15. Fein AM, Lippmann M, Holtzman H, Eliraz A, Goldberg SK. The risk factors, incidence, and prognosis of ARDS following septicemia. Chest. 1983 Jan. 83 (1):40-2. [Medline].

  16. Paret G, Ziv T, Augarten A, Barzilai A, Ben-Abraham R, Vardi A, et al. Acute respiratory distress syndrome in children: a 10 year experience. Isr Med Assoc J. 1999 Nov. 1 (3):149-53. [Medline].

  17. Cullen ML. Pulmonary and respiratory complications of pediatric trauma. Respir Care Clin N Am. 2001 Mar. 7 (1):59-77. [Medline].

  18. Gong MN, Thompson BT, Williams P, Pothier L, Boyce PD, Christiani DC. Clinical predictors of and mortality in acute respiratory distress syndrome: potential role of red cell transfusion. Crit Care Med. 2005 Jun. 33 (6):1191-8. [Medline].

  19. Khan H, Belsher J, Yilmaz M, Afessa B, Winters JL, Moore SB, et al. Fresh-frozen plasma and platelet transfusions are associated with development of acute lung injury in critically ill medical patients. Chest. 2007 May. 131 (5):1308-14. [Medline].

  20. Neto AS, Simonis FD, Barbas CS, Biehl M, Determann RM, Elmer J, et al. Lung-Protective Ventilation With Low Tidal Volumes and the Occurrence of Pulmonary Complications in Patients Without Acute Respiratory Distress Syndrome: A Systematic Review and Individual Patient Data Analysis. Crit Care Med. 2015 Oct. 43 (10):2155-63. [Medline].

  21. Haddad IY. Stem cell transplantation and lung dysfunction. Curr Opin Pediatr. 2013 Jun. 25 (3):350-6. [Medline].

  22. Cooke KR. Acute lung injury after allogeneic stem cell transplantation: from the clinic, to the bench and back again. Pediatr Transplant. 2005 Dec. 9 Suppl 7:25-36. [Medline].

  23. Panoskaltsis-Mortari A, Griese M, Madtes DK, Belperio JA, Haddad IY, Folz RJ, et al. An official American Thoracic Society research statement: noninfectious lung injury after hematopoietic stem cell transplantation: idiopathic pneumonia syndrome. Am J Respir Crit Care Med. 2011 May 1. 183(9):1262-79. [Medline].

  24. Li G, Malinchoc M, Cartin-Ceba R, Venkata CV, Kor DJ, Peters SG, et al. Eight-year trend of acute respiratory distress syndrome: a population-based study in Olmsted County, Minnesota. Am J Respir Crit Care Med. 2011 Jan 1. 183 (1):59-66. [Medline].

  25. Luhr OR, Antonsen K, Karlsson M, Aardal S, Thorsteinsson A, Frostell CG, et al. Incidence and mortality after acute respiratory failure and acute respiratory distress syndrome in Sweden, Denmark, and Iceland. The ARF Study Group. Am J Respir Crit Care Med. 1999 Jun. 159 (6):1849-61. [Medline].

  26. Bersten AD, Edibam C, Hunt T, Moran J, Australian and New Zealand Intensive Care Society Clinical Trials Group. Incidence and mortality of acute lung injury and the acute respiratory distress syndrome in three Australian States. Am J Respir Crit Care Med. 2002 Feb 15. 165 (4):443-8. [Medline].

  27. Rubenfeld GD, Caldwell E, Peabody E, Weaver J, Martin DP, Neff M, et al. Incidence and outcomes of acute lung injury. N Engl J Med. 2005 Oct 20. 353 (16):1685-93. [Medline].

  28. Zhu YF, Xu F, Lu XL, Wang Y, Chen JL, Chao JX, et al. Mortality and morbidity of acute hypoxemic respiratory failure and acute respiratory distress syndrome in infants and young children. Chin Med J (Engl). 2012 Jul. 125 (13):2265-71. [Medline].

  29. López-Fernández Y, Azagra AM, de la Oliva P, Modesto V, Sánchez JI, Parrilla J, et al. Pediatric Acute Lung Injury Epidemiology and Natural History study: Incidence and outcome of the acute respiratory distress syndrome in children. Crit Care Med. 2012 Dec. 40 (12):3238-45. [Medline].

  30. Kneyber MC, Brouwers AG, Caris JA, Chedamni S, Plötz FB. Acute respiratory distress syndrome: is it underrecognized in the pediatric intensive care unit?. Intensive Care Med. 2008 Apr. 34 (4):751-4. [Medline].

  31. Zimmerman JJ, Akhtar SR, Caldwell E, Rubenfeld GD. Incidence and outcomes of pediatric acute lung injury. Pediatrics. 2009 Jul. 124 (1):87-95. [Medline].

  32. Bindl L, Dresbach K, Lentze MJ. Incidence of acute respiratory distress syndrome in German children and adolescents: a population-based study. Crit Care Med. 2005 Jan. 33 (1):209-312. [Medline].

  33. Moss M, Bucher B, Moore FA, Moore EE, Parsons PE. The role of chronic alcohol abuse in the development of acute respiratory distress syndrome in adults. JAMA. 1996 Jan 3. 275 (1):50-4. [Medline].

  34. Moazed F, Calfee CS. Environmental risk factors for acute respiratory distress syndrome. Clin Chest Med. 2014 Dec. 35 (4):625-37. [Medline].

  35. Calfee CS, Matthay MA, Eisner MD, Benowitz N, Call M, Pittet JF, et al. Active and passive cigarette smoking and acute lung injury after severe blunt trauma. Am J Respir Crit Care Med. 2011 Jun 15. 183 (12):1660-5. [Medline].

  36. Meyer NJ, Christie JD. Genetic heterogeneity and risk of acute respiratory distress syndrome. Semin Respir Crit Care Med. 2013 Aug. 34 (4):459-74. [Medline].

  37. Matthay MA, Ware LB, Zimmerman GA. The acute respiratory distress syndrome. J Clin Invest. 2012 Aug. 122 (8):2731-40. [Medline].

  38. Gao L, Barnes KC. Recent advances in genetic predisposition to clinical acute lung injury. Am J Physiol Lung Cell Mol Physiol. 2009 May. 296 (5):L713-25. [Medline].

  39. Wei Y, Wang Z, Su L, Chen F, Tejera P, Bajwa EK, et al. Platelet count mediates the contribution of a genetic variant in LRRC16A to ARDS risk. Chest. 2015 Mar. 147 (3):607-17. [Medline].

  40. Reilly JP, Christie JD. Linking genetics to ARDS pathogenesis: the role of the platelet. Chest. 2015 Mar. 147 (3):585-6. [Medline].

  41. Sheu CC, Zhai R, Su L, Tejera P, Gong MN, Thompson BT, et al. Sex-specific association of epidermal growth factor gene polymorphisms with acute respiratory distress syndrome. Eur Respir J. 2009 Mar. 33 (3):543-50. [Medline].

  42. Brun-Buisson C, Minelli C, Bertolini G, Brazzi L, Pimentel J, Lewandowski K, et al. Epidemiology and outcome of acute lung injury in European intensive care units. Results from the ALIVE study. Intensive Care Med. 2004 Jan. 30 (1):51-61. [Medline].

  43. Erickson SE, Shlipak MG, Martin GS, Wheeler AP, Ancukiewicz M, Matthay MA, et al. Racial and ethnic disparities in mortality from acute lung injury. Crit Care Med. 2009 Jan. 37 (1):1-6. [Medline].

  44. Moss M, Mannino DM. Race and gender differences in acute respiratory distress syndrome deaths in the United States: an analysis of multiple-cause mortality data (1979- 1996). Crit Care Med. 2002 Aug. 30 (8):1679-85. [Medline].

  45. Stephane Dauger, Philippe Durand, Etinne Javouey and Jean-Christophe Mercier. Acute Respiratory Distress Syndrome in Children. Pediatric Critical Care. Fourth edition. Philadelphia, PA 19103-2899.: Elsevier Saunders. Copyright 2011 by Mosby, Inc; 2011. 706-716.

  46. Visser LH. Critical illness polyneuropathy and myopathy: clinical features, risk factors and prognosis. Eur J Neurol. 2006 Nov. 13 (11):1203-12. [Medline].

  47. Murray MJ, Brull SJ, Bolton CF. Brief review: Nondepolarizing neuromuscular blocking drugs and critical illness myopathy. Can J Anaesth. 2006 Nov. 53 (11):1148-56. [Medline].

  48. Gattinoni L, Bombino M, Pelosi P, Lissoni A, Pesenti A, Fumagalli R, et al. Lung structure and function in different stages of severe adult respiratory distress syndrome. JAMA. 1994 Jun 8. 271 (22):1772-9. [Medline].

  49. Goodman LR, Fumagalli R, Tagliabue P, Tagliabue M, Ferrario M, Gattinoni L, et al. Adult respiratory distress syndrome due to pulmonary and extrapulmonary causes: CT, clinical, and functional correlations. Radiology. 1999 Nov. 213 (2):545-52. [Medline].

  50. Gorini M, Ginanni R, Villella G, Tozzi D, Augustynen A, Corrado A. Non-invasive negative and positive pressure ventilation in the treatment of acute on chronic respiratory failure. Intensive Care Med. 2004 May. 30 (5):875-81. [Medline].

  51. Zhao X, Huang W, Li J, Liu Y, Wan M, Xue G, et al. Noninvasive Positive-Pressure Ventilation in Acute Respiratory Distress Syndrome in Patients With Acute Pancreatitis: A Retrospective Cohort Study. Pancreas. 2016 Jan. 45 (1):58-63. [Medline].

  52. Antonelli M, Conti G, Esquinas A, Montini L, Maggiore SM, Bello G, et al. A multiple-center survey on the use in clinical practice of noninvasive ventilation as a first-line intervention for acute respiratory distress syndrome. Crit Care Med. 2007 Jan. 35 (1):18-25. [Medline].

  53. Uçgun I, Yildirim H, Metintaş M, Güntülü AK. The efficacy of non-invasive positive pressure ventilation in ARDS: a controlled cohort study. Tuberk Toraks. 2010. 58 (1):16-24. [Medline].

  54. Teague WG. Noninvasive ventilation in the pediatric intensive care unit for children with acute respiratory failure. Pediatr Pulmonol. 2003 Jun. 35 (6):418-26. [Medline].

  55. Essouri S, Chevret L, Durand P, Haas V, Fauroux B, Devictor D. Noninvasive positive pressure ventilation: five years of experience in a pediatric intensive care unit. Pediatr Crit Care Med. 2006 Jul. 7 (4):329-34. [Medline].

  56. Bernet V, Hug MI, Frey B. Predictive factors for the success of noninvasive mask ventilation in infants and children with acute respiratory failure. Pediatr Crit Care Med. 2005 Nov. 6 (6):660-4. [Medline].

  57. Yañez LJ, Yunge M, Emilfork M, Lapadula M, Alcántara A, Fernández C, et al. A prospective, randomized, controlled trial of noninvasive ventilation in pediatric acute respiratory failure. Pediatr Crit Care Med. 2008 Sep. 9 (5):484-9. [Medline].

  58. Pancera CF, Hayashi M, Fregnani JH, Negri EM, Deheinzelin D, de Camargo B. Noninvasive ventilation in immunocompromised pediatric patients: eight years of experience in a pediatric oncology intensive care unit. J Pediatr Hematol Oncol. 2008 Jul. 30 (7):533-8. [Medline].

  59. Perry SA, Kesser KC, Geller DE, Selhorst DM, Rendle JK, Hertzog JH. Influences of cannula size and flow rate on aerosol drug delivery through the Vapotherm humidified high-flow nasal cannula system. Pediatr Crit Care Med. 2013 Jun. 14 (5):e250-6. [Medline].

  60. Mercat A, Richard JC, Vielle B, Jaber S, Osman D, Diehl JL, et al. Positive end-expiratory pressure setting in adults with acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA. 2008 Feb 13. 299 (6):646-55. [Medline].

  61. Ranieri VM, Suter PM, Tortorella C, De Tullio R, Dayer JM, Brienza A, et al. Effect of mechanical ventilation on inflammatory mediators in patients with acute respiratory distress syndrome: a randomized controlled trial. JAMA. 1999 Jul 7. 282 (1):54-61. [Medline].

  62. Amato MB, Barbas CS, Medeiros DM, Magaldi RB, Schettino GP, Lorenzi-Filho G, et al. Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med. 1998 Feb 5. 338 (6):347-54. [Medline].

  63. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med. 2000 May 4. 342 (18):1301-8. [Medline].

  64. Petrucci N, De Feo C. Lung protective ventilation strategy for the acute respiratory distress syndrome. Cochrane Database Syst Rev. 2013 Feb 28. 2:CD003844. [Medline].

  65. Hickling KG, Henderson SJ, Jackson R. Low mortality associated with low volume pressure limited ventilation with permissive hypercapnia in severe adult respiratory distress syndrome. Intensive Care Med. 1990. 16 (6):372-7. [Medline].

  66. Lunkenheimer PP, Rafflenbeul W, Keller H, Frank I, Dickhut HH, Fuhrmann C. Application of transtracheal pressure oscillations as a modification of "diffusing respiration". Br J Anaesth. 1972 Jun. 44 (6):627. [Medline].

  67. High-frequency oscillatory ventilation compared with conventional mechanical ventilation in the treatment of respiratory failure in preterm infants. The HIFI Study Group. N Engl J Med. 1989 Jan 12. 320 (2):88-93. [Medline].

  68. Ferguson ND, Cook DJ, Guyatt GH, Mehta S, Hand L, Austin P, et al. High-frequency oscillation in early acute respiratory distress syndrome. N Engl J Med. 2013 Feb 28. 368 (9):795-805. [Medline].

  69. Young D, Lamb SE, Shah S, MacKenzie I, Tunnicliffe W, Lall R, et al. High-frequency oscillation for acute respiratory distress syndrome. N Engl J Med. 2013 Feb 28. 368 (9):806-13. [Medline].

  70. Arnold JH, Hanson JH, Toro-Figuero LO, Gutiérrez J, Berens RJ, Anglin DL. Prospective, randomized comparison of high-frequency oscillatory ventilation and conventional mechanical ventilation in pediatric respiratory failure. Crit Care Med. 1994 Oct. 22 (10):1530-9. [Medline].

  71. Gupta P, Green JW, Tang X, Gall CM, Gossett JM, Rice TB, et al. Comparison of high-frequency oscillatory ventilation and conventional mechanical ventilation in pediatric respiratory failure. JAMA Pediatr. 2014 Mar. 168 (3):243-9. [Medline].

  72. Adhikari NK, Burns KE, Friedrich JO, Granton JT, Cook DJ, Meade MO. Effect of nitric oxide on oxygenation and mortality in acute lung injury: systematic review and meta-analysis. BMJ. 2007 Apr 14. 334 (7597):779. [Medline].

  73. Curley MA, Hibberd PL, Fineman LD, Wypij D, Shih MC, Thompson JE, et al. Effect of prone positioning on clinical outcomes in children with acute lung injury: a randomized controlled trial. JAMA. 2005 Jul 13. 294 (2):229-37. [Medline].

  74. Papazian L, Forel JM, Gacouin A, Penot-Ragon C, Perrin G, Loundou A, et al. Neuromuscular blockers in early acute respiratory distress syndrome. N Engl J Med. 2010 Sep 16. 363 (12):1107-16. [Medline].

  75. Willson DF, Chess PR, Notter RH. Surfactant for pediatric acute lung injury. Pediatr Clin North Am. 2008 Jun. 55 (3):545-75, ix. [Medline].

  76. Anzueto A, Baughman RP, Guntupalli KK, Weg JG, Wiedemann HP, Raventós AA, et al. Aerosolized surfactant in adults with sepsis-induced acute respiratory distress syndrome. Exosurf Acute Respiratory Distress Syndrome Sepsis Study Group. N Engl J Med. 1996 May 30. 334 (22):1417-21. [Medline].

  77. Czaja AS. A critical appraisal of a randomized controlled trial: Willson et al: Effect of exogenous surfactant (calfactant) in pediatric acute lung injury (JAMA 2005, 293: 470-476). Pediatr Crit Care Med. 2007 Jan. 8 (1):50-3. [Medline].

  78. Luchetti M, Ferrero F, Gallini C, Natale A, Pigna A, Tortorolo L, et al. Multicenter, randomized, controlled study of porcine surfactant in severe respiratory syncytial virus-induced respiratory failure. Pediatr Crit Care Med. 2002 Jul. 3 (3):261-268. [Medline].

  79. Walmrath D, Günther A, Ghofrani HA, Schermuly R, Schneider T, Grimminger F, et al. Bronchoscopic surfactant administration in patients with severe adult respiratory distress syndrome and sepsis. Am J Respir Crit Care Med. 1996 Jul. 154 (1):57-62. [Medline].

  80. Willson DF, Thomas NJ, Markovitz BP, Bauman LA, DiCarlo JV, Pon S, et al. Effect of exogenous surfactant (calfactant) in pediatric acute lung injury: a randomized controlled trial. JAMA. 2005 Jan 26. 293 (4):470-6. [Medline].

  81. Thomas NJ, Hollenbeak CS, Lucking SE, Willson DF. Cost-effectiveness of exogenous surfactant therapy in pediatric patients with acute hypoxemic respiratory failure. Pediatr Crit Care Med. 2005 Mar. 6 (2):160-5. [Medline].

  82. Furchgott RF, Jothianandan D. Endothelium-dependent and -independent vasodilation involving cyclic GMP: relaxation induced by nitric oxide, carbon monoxide and light. Blood Vessels. 1991. 28 (1-3):52-61. [Medline].

  83. Goldman AP, Tasker RC, Hosiasson S, Henrichsen T, Macrae DJ. Early response to inhaled nitric oxide and its relationship to outcome in children with severe hypoxemic respiratory failure. Chest. 1997 Sep. 112 (3):752-8. [Medline].

  84. Bronicki RA, Fortenberry J, Schreiber M, Checchia PA, Anas NG. Multicenter randomized controlled trial of inhaled nitric oxide for pediatric acute respiratory distress syndrome. J Pediatr. 2015 Feb. 166 (2):365-9.e1. [Medline].

  85. Bohn D. Nitric oxide in acute hypoxic respiratory failure: from the bench to the bedside and back again. J Pediatr. 1999 Apr. 134 (4):387-9. [Medline].

  86. Dobyns EL, Cornfield DN, Anas NG, Fortenberry JD, Tasker RC, Lynch A, et al. Multicenter randomized controlled trial of the effects of inhaled nitric oxide therapy on gas exchange in children with acute hypoxemic respiratory failure. J Pediatr. 1999 Apr. 134 (4):406-12. [Medline].

  87. Hirschl RB, Conrad S, Kaiser R, Zwischenberger JB, Bartlett RH, Booth F, et al. Partial liquid ventilation in adult patients with ARDS: a multicenter phase I-II trial. Adult PLV Study Group. Ann Surg. 1998 Nov. 228 (5):692-700. [Medline].

  88. Fedora M, Nekvasil R, Seda M, Klimovic M, Dominik P. Partial liquid ventilation in the therapy of pediatric acute respiratory distress syndrome. Bratisl Lek Listy. 1999 Sep. 100 (9):481-5. [Medline].

  89. Galvin IM, Steel A, Pinto R, Ferguson ND, Davies MW. Partial liquid ventilation for preventing death and morbidity in adults with acute lung injury and acute respiratory distress syndrome. Cochrane Database Syst Rev. 2013 Jul 23. 7:CD003707. [Medline].

  90. Zapol WM, Snider MT, Hill JD, Fallat RJ, Bartlett RH, Edmunds LH, et al. Extracorporeal membrane oxygenation in severe acute respiratory failure. A randomized prospective study. JAMA. 1979 Nov 16. 242 (20):2193-6. [Medline].

  91. Gray BW, Haft JW, Hirsch JC, Annich GM, Hirschl RB, Bartlett RH. Extracorporeal life support: experience with 2,000 patients. ASAIO J. 2015 Jan-Feb. 61 (1):2-7. [Medline].

  92. Green TP, Timmons OD, Fackler JC, Moler FW, Thompson AE, Sweeney MF. The impact of extracorporeal membrane oxygenation on survival in pediatric patients with acute respiratory failure. Pediatric Critical Care Study Group. Crit Care Med. 1996 Feb. 24 (2):323-9. [Medline].

  93. Brown KL, Walker G, Grant DJ, Tanner K, Ridout DA, Shekerdemian LS, et al. Predicting outcome in ex-premature infants supported with extracorporeal membrane oxygenation for acute hypoxic respiratory failure. Arch Dis Child Fetal Neonatal Ed. 2004 Sep. 89 (5):F423-7. [Medline].

  94. Petrou S, Edwards L, UK Collaborative ECMO Trial. Cost effectiveness analysis of neonatal extracorporeal membrane oxygenation based on four year results from the UK Collaborative ECMO Trial. Arch Dis Child Fetal Neonatal Ed. 2004 May. 89 (3):F263-8. [Medline].

  95. Bennett CC, Johnson A, Field DJ, Elbourne D, UK Collaborative ECMO Trial Group. UK collaborative randomised trial of neonatal extracorporeal membrane oxygenation: follow-up to age 4 years. Lancet. 2001 Apr 7. 357 (9262):1094-6. [Medline].

  96. Romay E, Ferrer R. Extracorporeal CO2 removal: Technical and physiological fundaments and principal indications. Med Intensiva. 2015 Sep 29. [Medline].

  97. Meduri GU, Headley AS, Golden E, Carson SJ, Umberger RA, Kelso T, et al. Effect of prolonged methylprednisolone therapy in unresolving acute respiratory distress syndrome: a randomized controlled trial. JAMA. 1998 Jul 8. 280 (2):159-65. [Medline].

  98. Steinberg KP, Hudson LD, Goodman RB, Hough CL, Lanken PN, Hyzy R, et al. Efficacy and safety of corticosteroids for persistent acute respiratory distress syndrome. N Engl J Med. 2006 Apr 20. 354 (16):1671-84. [Medline].

  99. Tang BM, Craig JC, Eslick GD, Seppelt I, McLean AS. Use of corticosteroids in acute lung injury and acute respiratory distress syndrome: a systematic review and meta-analysis. Crit Care Med. 2009 May. 37 (5):1594-603. [Medline].

  100. Yehya N, Servaes S, Thomas NJ, Nadkarni VM, Srinivasan V. Corticosteroid exposure in pediatric acute respiratory distress syndrome. Intensive Care Med. 2015 Sep. 41 (9):1658-66. [Medline].

  101. Kangelaris KN, Sapru A, Calfee CS, Liu KD, Pawlikowska L, Witte JS, et al. The association between a Darc gene polymorphism and clinical outcomes in African American patients with acute lung injury. Chest. 2012 May. 141 (5):1160-9. [Medline].

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.
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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