Pediatric Acute Respiratory Distress Syndrome Medication

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

Medication Summary

No specific drug therapy for acute respiratory distress syndrome (ARDS) exists, and many drugs relating to ARDS therapy will not be indicated during the early emergency department (ED) intervention period beyond supportive care. However, as a sequela to intubation and mechanical ventilation, high mean airway pressures for poor oxygenation may compromise cardiac output and may require fluid resuscitation and the initiation of vasoactive agents.

Corticosteroids have been used empirically and in numerous clinical trials. Early use of steroids has not yielded any significant impact on attenuation or survival outcome, except for patients at risk for fat embolism and patients with AIDS and Pneumocystis jiroveci (carinii) pneumonia.

Inhaled nitric oxide (iNO) has produced short-term physiologic improvements in ventilation-perfusion matching and intrapulmonary shunting; however, no randomized clinical studies have documented improved patient outcome. Of prognostic value, a poor early response to inhaled nitric oxide is associated with death.

Administration of exogenous surfactant has many theoretical benefits, as demonstrated in vitro. However, studies of various surfactants and different modes of delivery in adults have not yielded a consensus regarding the efficacy of surfactant in ARDS.

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Adrenergic Agonist Agents

Class Summary

Adrenergic agonist agents are used to increase cardiac output and improve hypotension induced by elevated mean airway pressures from mechanical ventilation. Increases in pulmonary vascular resistance may also be seen in ARDS, which may result in increased right ventricular work. Adequate cardiac output depends on the ability of the right ventricle to increase stroke work. Dobutamine may be chosen in this context because they increase cardiac output without producing significant pulmonary vasoconstriction.

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Dobutamine

 

Dobutamine is a sympathomimetic amine with stronger beta than alpha effects. It produces systemic vasodilation and increases the inotropic state. Vasopressors augment the coronary and cerebral blood flow during the low-flow state associated with shock. Sympathomimetic amines with both alpha- and beta-adrenergic effects are indicated in cardiogenic shock.

Dopamine and dobutamine are the drugs of choice to improve cardiac contractility, with dopamine the preferred agent in hypotensive patients.

Higher dosages may cause an increase in heart rate, exacerbating myocardial ischemia.

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Dopamine (Intropin)

 

Dopamine is a naturally occurring endogenous catecholamine that stimulates beta1-and alpha1-adrenergic and dopaminergic receptors in a dose-dependent fashion; it stimulates release of norepinephrine.

In low doses (2-5 µg/kg/min), dopamine acts on dopaminergic receptors in renal and splanchnic vascular beds, causing vasodilatation in these beds. In midrange doses (5-15 µg/kg/min), it acts on beta-adrenergic receptors to increase heart rate and contractility. In high doses (15-20 µg/kg/min), it acts on alpha-adrenergic receptors to increase systemic vascular resistance and raise BP.

After initiating therapy, increase the dose by 1-4 µg/kg/min q10-30min until optimal response is obtained. More than 50% of patients are satisfactorily maintained on doses less than 20 µg/kg/min.

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Epinephrine (Adrenalin)

 

Epinephrine is used for hypotension refractory to dopamine. Alpha-agonist effects include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta2-agonist effects include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects. Adrenergic receptor activity tends to be dose-related: lower doses predominantly activate beta receptors, whereas higher doses predominantly activate alpha receptors.

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Phosphodiesterase Enzyme Inhibitors

Class Summary

These agents increase cellular levels of cAMP, which results in a positive inotropic effect and cardiac output. They also have pulmonary vasodilator effects. Inamrinone (formerly amrinone) may be chosen in this context because they increase cardiac output without producing significant pulmonary vasoconstriction.

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Inamrinone

 

Inamrinone is a positive inotrope and vasodilator with little chronotropic activity in a non–receptor-mediated mechanism. It induces peripheral vasodilation and provides inotropic support. It is different in its mode of action from either cardiac glycosides (digoxin) or catecholamines.

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Adrenal Corticosteroids

Class Summary

Corticosteroids have anti-inflammatory and immunosuppressive properties. They cause profound and varied metabolic effects, and they modify the body’s immune response to diverse stimuli. They are primarily used as anti-inflammatories in ARDS.

As discussed previously, data suggest that the use of corticosteroids may be beneficial in patients with severe ARDS. To the authors’ knowledge, no large blinded multicenter trial has been performed. Although anecdotal, the suggested regimen may be therapeutic in children; however, no trials have been conducted to evaluate their use in children with ARDS.

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Methylprednisolone (Solu-Medrol)

 

Methylprednisolone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability. Its mechanism of action in ARDS is unknown. By virtue of anti-inflammatory effects, host fibrotic response is presumably dampened, allowing salvage of viable lung tissue. It is used for late-onset treatment, "refractory ARDS" defined as 7 days of mechanical ventilation without significant improvement.

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Lung Surfactants

Class Summary

Exogenous surfactant can be helpful in treating airspace disease (eg, respiratory distress syndrome [RDS]). If administered under carefully controlled conditions, surfactant may also be helpful in other conditions (eg, meconium aspiration syndrome [MAS]), though it is not yet approved for this indication. After inhaled administration, surface tension is reduced, and alveoli are stabilized, decreasing the work of breathing and increasing lung compliance.

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Calfactant (Infasurf)

 

Calfactant is a natural calf lung extract containing phospholipids, fatty acids, and surfactant-associated proteins B (260 µg/mL) and C (390 µg/mL). Decreases in surfactant levels and function are commonly observed in ARDS. Evidence suggests that surfactant use may be beneficial in children with ARDS by reducing mortality and ventilator-dependent days. Young children with ARDS due to a primary pulmonary insult may be the most likely to benefit from exogenous surfactant.

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Beractant (Survanta)

 

Beractant mimics the surface tension–lowering properties of natural lung surfactant. It contains colfosceril palmitate, cetyl alcohol, and tyloxapol.

This surfactant prevents alveoli from collapsing during expiration by lowering the surface tension between air and alveolar surfaces.

Beractant is used for prophylaxis of respiratory distress syndrome (RDS) in premature infants with birthweight of less than 1350 grams or RDS in premature infants with birthweight of greater than 1350 grams who have evidence of pulmonary immaturity.

It is for intratracheal administration only.

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Poractant alfa (Curosurf)

 

Poractant mimics the surface tension–lowering properties of natural lung surfactant. Contains colfosceril palmitate, cetyl alcohol, and tyloxapol.

This surfactant prevents alveoli from collapsing during expiration by lowering the surface tension between air and alveolar surfaces.

Poractant is used for prophylaxis of respiratory distress syndrome (RDS) in premature infants. It is for intratracheal administration only.

Bovine lipid extract surfactant

 

This agent replaces deficient or ineffective endogenous lung surfactant in neonates with RDS. It prevents the alveoli from collapsing during expiration by lowering the surface tension between air and alveolar surfaces.

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Contributor Information and Disclosures
Author

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

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

Disclosure: Nothing to disclose.

Coauthor(s)

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

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

Disclosure: Nothing to disclose.

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

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

Disclosure: Nothing to disclose.

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

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

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

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

Disclosure: Nothing to disclose.

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

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

Disclosure: Nothing to disclose.

Chief Editor

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

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

Disclosure: Nothing to disclose.

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