Pediatric Acute Respiratory Distress Syndrome Treatment & Management

No treatment for acute respiratory distress syndrome (ARDS) is definitive. The cornerstone of management is impeccable intensive care. Early anticipatory management may avoid late complications and poor outcome. Treat the primary cause (eg, sepsis, pneumonia) if possible. As much as possible, minimizing the risk of multiple organ dysfunction syndrome (MODS) and ventilator-induced lung injury (VILI) is essential.

Critical aspects are maintaining nutrition and being cognizant of the risk of numerous complications in critically ill children, including sepsis, fluid overload, inappropriate levels of sedation, and neuromuscular blocking agents.

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.

Furthermore, an inability to adequately control for other therapies, specifically ventilation modalities, and the fact that most patients die from MODS or their precipitating illness confound the analysis and interpretation of data from many trials.

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.

Since the eventual severity of ARDS relates to the severity of the inciting event, prehospital care is likely to have the most impact by early recognition of associated risk factors and aggressive treatment to reversing respiratory and circulatory failure, potentially averting the onset of ARDS.

Children who ultimately develop ARDS more typically present in the emergency department (ED) without many of the signs and symptoms that fulfill the diagnostic criteria for acute lung injury (ALI) or ARDS. However, early recognition of these signs and symptoms as well as recognition of the more common risk factors for developing ALI/ARDS can influence the decision to initiate varying treatments for respiratory distress.

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.^[25] Noninvasive positive pressure ventilation and/or endotracheal intubation with mechanical ventilation is usually required in patients with clinical and radiographic evidence suggestive of worsening lung disease with a fraction of inspired oxygen (FiO₂) of greater than 50%. Striking a balance between the level of ventilator support necessary to provide a reasonable ventilation and oxygenation while minimizing VILI is one of the most active areas of research in critical care.

Noninvasive ventilation has been used early in ALI and ARDS to avoid endotracheal intubation.^[26] Published experience has largely been limited to the adults, and most patients with ARDS require endotracheal intubation for airway control and invasive mechanical ventilation.

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.

The main benefits of CPAP and BiPAP include improvement of oxygenation and work of breathing without the expense of inducing and maintaining sedation for intubation, since CPAP and BiPAP are relatively well tolerated by patients. Patients are also able to continue regulating their own minute ventilation.

More recently, Vapotherm (Vapotherm; Stevensville, MD) has become an option for delivering positive airway pressure and supplemental oxygen noninvasively, especially as a substitute for nasal CPAP in infants. Very few studies have been performed using this device.

Based on personal experience, the advantages of using the Vapotherm device or a similar high-flow, humidified nasal cannula device include easy set-up, easy access to the patient’s mouth, and better visualization of the patient’s face. The disadvantages include not being able to titrate, regulate, and measure pressures as precisely as with CPAP and BiPAP.

In the event that a patient requires intubation for ALI, it may be prudent to use a cuffed endotracheal tube regardless of the age of the patient. Traditionally, children younger than 8 years are intubated with uncuffed tubes. However, various lung conditions, such as ALI/ARDS, worsen lung compliance. Therefore, 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.

No gas exchange occurs in collapsed or 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.

Traditional ventilatory strategies maintained normal arterial blood gas (ABG) values, often at the cost of high tidal volumes and pressures and high morbidity and mortality rates. The strategy of open lung ventilation is based on the recognition that repetitive opening and closing of alveoli exacerbates lung injury and that there is often little harm associated with a high arterial carbon dioxide tension. This approach, termed the permissive hypercapnic strategy, may allow reductions in rate and peak inspiratory pressure (PIP), thereby limiting further barotrauma/volutrauma.

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.

Hickling et al gave one of the original descriptions of permissive hypercapnia, reporting an almost 80% reduction in mortality rates, though subsequent trials showed no benefit in reducing tidal volumes.^[27] 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 decreased the mortality rate (38% versus 71%).^[3]

The study by Amato et al was criticized for the high mortality rate in the control arm, but its results were confirmed by a multicenter study sponsored by the National Institutes of Health (NIH).^[28]

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%).

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.^[29]

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.^[30] The authors postulated that decreased levels of cytokines reflect reduced inflammation in organs other than the lungs, leading to a possible survival benefit.

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

Prophylactic application of PEEP has not been shown to improve outcome.^[31] As PEEP is increased, cardiac output may fall, and volume expansion or inotropic/pressor agents may be required.

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.

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. Randomized controlled trials have compared HFOV with conventional mechanical ventilation in pediatric and neonatal practice, with generally encouraging results. Although initial studies in neonates show no benefit, the strategy was less than optimal.

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.

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.

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.^[32] 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. Although no consensus regarding how to incorporate prone positioning into the care of a child with ARDS is available, it should still be attempted in a patient with profound hypoxemia.

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.^[33] 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.

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

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.^[34] 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.^{[35, 36, 37, 38]}

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%.^[39] 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.^[40]

Nitric oxide (NO) is a potent vasodilator, first described in 1989. Its use as a specific pulmonary vasodilator was first described almost a decade ago in neonates with persistent pulmonary hypertension. Subsequent trials confirmed the efficacy of inhaled NO (iNO) in this population, in whom iNO decreased the use of ECMO.

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. 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. Oxygenation benefits that occur while iNO diffuses to only relatively well-aerated parts of the lung lessen any local HPV. Other benefits may include decreased pulmonary edema while pulmonary pressures are reduced.

Although iNO often acutely improves oxygenation and, in the short term, allows weaning of FiO₂ and ventilatory parameters, not all patients respond and not all have a sustained response. An association exists between greater early response to iNO and improved clinical outcome.^[41]

Despite the potential benefits, no study has reported lasting advantage associated with iNO. 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). A systematic review and meta-analysis showed that although NO temporarily improves oxygenation, it does not improve survival and may cause harm in both children and adults.^[42]

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. Another confounder is that patients with ARDS are heterogeneous.

A multicenter study of the use of iNO (10-ppm dose) in children with acute hypoxic respiratory failure was reported. Although oxygenation acutely improved in the group treated with iNO, this change did not translate into a survival benefit.^[43] 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. However, this analysis has been criticized.^[44]

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).^{[45, 46]} A randomized trial in 1998 did not demonstrate a difference in outcome in a group treated with PLV compared with a group treated with cytomegalovirus (CMV).^[12]

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. Zapol et al did not demonstrate a benefit with ECMO, reporting a mortality rate of more than 90% in both control and ECMO groups.^[47]

Anecdotal reports and case series are numerous. They suggest that ECMO may be of benefit in children with severe ARDS unresponsive to maximal conventional therapy.

In 1996, Green et al reported data from a pediatric study, concluding that ECMO was associated with improved survival.^[48] This study had a number of limitations. It was not a controlled trial; instead, it was a retrospective collection of data from a large number of PICUs. Furthermore, conventional therapy was not uniform. An attempt at a definitive, randomized controlled trial was terminated when the overall mortality rate in pediatric ARDS decreased to such a degree that sufficient numbers of patients could not be recruited.

Numerous studies from the United Kingdom showed that the use of ECMO in neonates with respiratory failure was associated with improved outcomes.^{[11, 49, 50]} 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 is a relative contraindication.

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.

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. Limited data are available concerning this modality in the pediatric population.

Once the patient is intubated, several steps should be taken to minimize further lung injury.

Ideally, PIPs (or plateau pressures) generally should be maintained at no more than 30 cm water. Because this may be difficult with volume-control ventilation, patients may be managed with pressure-control ventilation instead; however, no data support pressure-control ventilation as being superior to volume-control ventilation. When the latter is used, the National Institutes of Health (NIH) ARDS Network protocols include a target tidal volume of less than or equal to 6 mL/kg.

Starting PEEP levels are typically 5 cm water for normally compliant lungs; however, for lungs that are poorly compliant because of ALI/ARDS, PEEP levels can be increased aggressively to optimize oxygenation by increasing the mean airway pressure without increasing PIP. Patients may require more deep sedation, with or without paralysis for PEEP significantly greater than 10 cm water.

Furthermore, if it becomes clear that escalating PEEP levels significantly greater than 10 cm water will be required to maintain adequate oxygenation, or if oxygenation remains poor despite apparently high PEEP levels, changing to HFOV should be considered.

Increasing the inspiratory time may increase the mean airway pressure and thus improve oxygenation. In volume-control ventilation, this may also decrease PIP, as long as the inspiratory-expiratory ratio (I:E) remains less than or equal to 1:1 or as long as no evidence of air-trapping is present.

Ideally, the respiratory rate (RR) should be set to maintain normal arterial pH; however, it should not be increased at the expense of exacerbating lung injury. Because relative hypercarbia has no significant deleterious effects beyond the context of intracranial hypertension, permissive hypercapnia is a common approach. However, severe acidemia may diminish other organ system functions. Therefore, other methods to avoid extreme acidosis (eg, administering NaHCO₃ and tris-hydroxymethyl aminomethane [THAM]) may be used instead of increasing RR.

During the acute period, an FiO₂ of 100% is typically administered, especially if the patient is hypoxic at presentation. Although excessively high oxygen concentrations can result in increased oxygen free radical production and subsequently lead to barotrauma independently, several hours of high oxygen concentration exposure is required for significant barotrauma effect. This period is likely to exceed the duration of the patient’s stay in the ED; therefore, FiO₂ weaning need not be addressed in most situations.

Although compromised lung compliance is less likely to be observed during the ALI phase or the earlier ARDS phases, it may already be severe by this point, and excessive PIP and/or PEEP settings may be needed just to meet adequate oxygenation needs. HFOV may provide superior lung protection in this scenario.

If used, HFOV should be initiated in an intensive care unit (ICU) setting; setup there would be more practical, given the nursing support needs, the equipment and space requirements, the more invasive monitoring and vascular access used, and the potential for other complications that are beyond the scope of this discussion.

Regardless of the patient’s mechanical ventilation needs, an expedient transfer to the PICU may be prudent. In general, the need for pediatric critical care resources should be anticipated early.

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.^[51] Patients received methylprednisolone or placebo for 32 days. Nonresponders were given the alternative treatment on day 10. Those receiving steroids had reduced lung injury and multiorgan dysfunction scores, were extubated more frequently, and had significantly lower hospital mortality rates (12% vs 62%). Rates of infection did not differ between the groups.

Similar data in the pediatric population are not available. Some centers begin steroid therapy on days 7-10 of mechanical ventilation. The use of steroids for the fibroproliferative phase of ARDS in the pediatric population is extrapolated from this study.

In contrast with the results of Meduri et al, a larger, multicentered randomized controlled trial failed to demonstrate improved survival.^[52] In fact, an increased mortality rate was suggested in subgroups.

A multicenter trial of corticosteroids for persistent ARDS in adults showed increased number of ventilator and shock-free days but also showed increased 60-day and 180-day mortality rates for patients whose therapy started 14 or more days after the onset of ARDS.^[28]

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

Steroids may be indicated as part of the treatment for the underlying etiology of ARDS (eg, ARDS secondary to Pneumocystis jiroveci infection).

A subgroup of patients with ARDS with marked eosinophilia in their peripheral blood or bronchoalveolar fluid may benefit from steroid therapy.

Steroid use may contribute to prolonged weakness after ARDS. Care should be taken to minimize concomitant neuromuscular blockade.

Prevention of the numerous complications associated with intensive care is paramount in patients with ARDS. Have a high index of suspicion for nosocomial infections, specifically line-related bacteremia and ventilator-associated pneumonia. Continue aggressive nutrition to maintain anabolism or at least to prevent catabolism. Use neuromuscular blockers judiciously, especially in conjunction with steroids, to minimize the risk of myopathy and long-term weakness. In the event of a pneumothorax, placement of a chest tube is usually mandatory.

Meticulous attention to fluid balance is essential because excess body water may further increase ventilator requirements because of increased parenchymal water and chest-wall edema, which decrease pulmonary and total chest compliance. Furthermore, alveolar water may reduce oxygen diffusion across the alveolar membrane. Judicious use of diuretics may be necessary, as is early renal replacement therapy (eg, hemofiltration, hemodialysis, peritoneal dialysis) if renal failure leads to difficulties in maintaining fluid balance.

Critically ill children may require sedation and neuromuscular blockade. Hence, it may be necessary to prevent joint contractures. Early occupational/physical therapy is essential in preventing these complications.

Many institutions, as part of their standard of care for children treated with HFOV, require that earplugs be placed to reduce both discomfort and the risk of permanent hearing loss resulting from HFOV.

Placement of a semipermanent line (eg, a peripherally inserted central catheter [PICC]) may help reduce nosocomial infections in at-risk children by allowing the removal of large-caliber central venous catheters.

Bronchodilators may be beneficial in cases of ARDS complicated by reactive airway disease.

All children should receive prophylaxis for stress ulcers.

Many predictors of extubation success have been published; however, clinicians often use clinical judgment to determine a patients’ readiness for extubation. To date, no data specifically describe predictive parameters in children with ARDS. Indices used to predict successful extubation include the rapid, shallow breathing index (RSBI); the compliance, resistance, oxygenation, and pressure (CROP) index; and ratio of tidal volume to dead space (Vd/Vt).

Regardless of the method used, all candidates for extubation should have a leak around their endotracheal tube (ie, at a reasonable airway pressure), and they should be able to maintain their own airway (ie, good cough and gag reflex). Patients must not be dependent on suctioning through their endotracheal tube. The level of sedation must not be excessive. If no air leak is present around the endotracheal tube, consider deferring extubation and administering steroids to reduce airway edema.

Once extubated, patients may require further support of their breathing. Options include CPAP, BiPAP, supplemental oxygen, heliox, or reintubation.

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).

Administration of a formula supplemented with eicosapentaenoic acid, gamma-linolenic acid, and antioxidants is associated with reduced pulmonary neutrophil recruitment, improved gas exchange, decreased requirement for mechanical ventilation, reduced length of ICU stay, and fewer new organ failures.

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.

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.