Pediatric Acute Respiratory Distress Syndrome Medication

Updated: Nov 23, 2016
  • Author: Prashant Purohit, MD; Chief Editor: Timothy E Corden, MD  more...
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Medication

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.

Routine use of corticosteroids is not recommended at this time by PALICC. It might be beneficial to use in patients with ARDS associated with Pneumocystis jiroveci (previously 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. Based on current evidence, it can be used in patients with severe PARDS, and in cases to bridge to ECLS/ECMO.

Evidence is insufficient at this stage to recommend use of exogenous surfactant. 

Discussion provided below is brief. Detailed discussion of these medication is beyond the scope for the topic of Pediatric ARDS. 

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Adrenergic Agonist Agents

Class Summary

Adrenergic agonist agents are used to increase cardiac output and improve hemodynamics induced by various mechanism including elevated mean airway pressures from mechanical ventilation, sedation, multi organ failure etc. These agents should be administered via central line. 

Dobutamine

Dobutamine is a sympathomimetic agent with predominant beta one agonist followed by beta 2 and than alpha agonist. It provides inotropy, chronotropy and systemic vasodilation. Adverse effects include tachycardia, increased myocardial oxygen requirement and so can exacerbate myocardial ischemia.

Dopamine

In low doses (2-5 µg/kg/min), dopamine acts on dopaminergic receptors in renal and splanchnic vascular beds, potentially causing vasodilatation in these beds. In the doses 5-15 µg/kg/min, it acts on beta-adrenergic receptors creating inotropy and chronotropy. At high doses (15-20 µg/kg/min), it acts on alpha-adrenergic receptors to increase systemic vascular resistance. Higher doses have been associated with risks of arrhythmia and local tissue necrosis. 

Epinephrine (Adrenalin)

Epinephrine stimulated beta 1 and produces inotropy and chronotropy. At lower doses, it causes peripheral vascular dilatation from beta-2 effects. Beta2-agonist effects also include bronchodilatation. At higher doses, it predominantly activate alpha receptors and causes peripheral vasoconstriction. 

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Phosphodiesterase Enzyme Inhibitors

Class Summary

These agents increase cellular levels of cAMP, which results in a positive inotropic effect, peripheral vasodilatation and increased cardiac output. Milrinone is commonly used phosphodiesterase inhibitor. 

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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. As discussed previously, current evidence is insufficient for use of corticosteroids in PARDS patients. 

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Lung Surfactants

Class Summary

Exogenous surfactant can be helpful in treating airspace disease (eg, respiratory distress syndrome [RDS] in neonates). Surfactant dysfunction is well known pathophysiology in pediatric ARDS patients. However, current evidence is insufficient to use exogenous surfactant in pediatric ARDS patients. 

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