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Pediatrics, Respiratory Distress Syndrome: Treatment & Medication
Updated: Sep 18, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Prehospital Care
Since the eventual severity of acute respiratory distress syndrome (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.
Emergency Department Care
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. However, early recognition of these signs and symptoms as well as recognition of the more common risk factors for developing ALI/ARDS can impact 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. Provided that 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.
Continuous positive airway pressure (CPAP) and bi-level 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, 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. 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 acute lung injury, 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.
- Once intubated, the following steps should be taken to minimize further lung injury:
- Peak inspiratory pressure (PIP): PIPs or plateau pressures generally should be maintained ideally no more than 30 cm H2 O. Because this may be difficult with volume-control ventilation, patients are alternatively managed with pressure-control ventilation. However, no data support pressure-control ventilation as being superior to volume-control ventilation. When using the latter, the National Institutes of Health (NIH) ARDS Network protocols include a target tidal volume of less than or equal to 6 mL/kg.
- Peak end-expiratory pressure (PEEP): Starting PEEP levels are typically 5 cm H2 O for normally compliant lungs. However, for poorly compliant lungs due to ALI/ARDS, PEEP levels can be increased aggressively to optimize oxygenation by increasing the mean airway pressure without increasing PIP (see above). Patients may require more deep sedation +/- paralysis for PEEP significantly greater than 10 cm H2 O. Furthermore, if it becomes clear that escalating PEEP levels significantly greater than 10 cm H2 O will be required to maintain adequate oxygenation, or despite "high" PEEP levels, oxygenation remains poor, changing to high-frequency oscillatory ventilation (HFOV) should be considered (see below).
- Inspiratory time (IT): Increasing IT may increase the mean airway pressure and thus improve oxygenation. In volume-control ventilation, this may also decrease PIP as long as I:E remains less than or equal to 1:1 or as long as no evidence of air-trapping is present.
- Respiratory rate (RR): RR normally should be set ideally to maintain normal arterial pH. However, RR should not be increased at the expense of exacerbating lung injury. Since 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 such as administering NaHCO3 and THAM may be used instead of increasing RR.
- FiO2: During the acute period, 100% FiO2 is typically administered to the patient, especially if the patient is hypoxic upon presentation. Although excessively high oxygen concentrations can result in increased oxygen free radicals production and subsequently lead to barotrauma independently, several hours of high oxygen concentration exposure is required for significant barotrauma effect. This time period would most likely exceed the duration of the patient's stay in the ED and, therefore, FiO2 weaning need not be addressed in most situations.
- High-frequency oscillatory ventilation (HFOV): Although less likely to be observed during the ALI phase or earlier ARDS phases, lung compliance may be already severely compromised, 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. However, this should be initiated in an ICU setting, since set-up would be more practical given nursing support needs, equipment and space, more invasive monitoring and vascular access, and anticipation for other potential 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.
- The need for pediatric critical care resources should be anticipated early.
Consultations
Consult a pediatric intensivist.
Medication
No specific drug therapy for ARDS exists, and many drugs relating to ARDS therapy will not be indicated during the early 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 carinii pneumonia. Meduri et al suggested late use of steroids to attenuate ARDS and improve survival.2 However, a larger, multicentered randomized controlled trial failed to demonstrate improved survival.3 In fact, an increased mortality rate was suggested in subgroups.
Inhaled nitric oxide 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.
Vasoactive agents
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 or inamrinone (formerly amrinone) may be chosen in this context because they increase cardiac output without producing significant pulmonary vasoconstriction.
Dobutamine (Dobutrex)
Sympathomimetic amine with stronger beta than alpha effects. 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.
Adult
2.5 mcg/kg/min IV initially; titrate to desired effect
Pediatric
5 mcg/kg/min IV initially; titrate to desired effect
Beta-adrenergic blockers antagonize effects; general anesthetics may increase toxicity; coadministration with diuretics may result in hypovolemia and decreased filling pressures
Documented hypersensitivity; idiopathic hypertrophic subaortic stenosis and atrial fibrillation or flutter
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Although unusual in children, following a myocardial infarction, use with extreme caution; hypovolemic state should be initiated before using this drug; arrhythmias
Milrinone (Primacor)
Positive inotrope and vasodilator with little chronotropic activity in a non–receptor-mediated mechanism. Induces peripheral vasodilation and provides inotropic support. Different in mode of action from either cardiac glycosides (digoxin) or catecholamines.
Adult
50 mcg/kg (0.05 mg/kg) IV loading dose, followed by 0.375-0.75 mcg/kg/min continuous IV infusion
Pediatric
50-75 mcg/kg (0.05-0.075 mg/kg) IV loading dose, followed by 0.25-0.75 mcg/kg/min continuous IV infusion
Coadministration with diuretics may result in hypovolemia and decrease in filling pressure; milrinone precipitates in presence of furosemide
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Monitor fluids, electrolyte changes, and renal function during therapy; excessive diuresis may increase potassium loss and predispose digitalized patients to arrhythmias; important to correct hypokalemia with potassium supplementation prior to treatment; patients showing excessive decreases in blood pressure should have infusion rates slowed or stopped; previous vigorous diuretic therapy has caused significant decreases in cardiac filling pressure, cautiously administer milrinone and monitor blood pressure, heart rate, and clinical symptomatology
Dopamine (Intropin)
Naturally occurring endogenous catecholamine that stimulates beta1-and alpha1-adrenergic and dopaminergic receptors in a dose-dependent fashion; stimulates release of norepinephrine.
In low doses (2-5 mcg/kg/min), acts on dopaminergic receptors in renal and splanchnic vascular beds, causing vasodilatation in these beds. In midrange doses (5-15 mcg/kg/min), acts on beta-adrenergic receptors to increase heart rate and contractility. In high doses (15-20 mcg/kg/min), acts on alpha-adrenergic receptors to increase systemic vascular resistance and raise BP.
After initiating therapy, increase dose by 1-4 mcg/kg/min q10-30min until optimal response is obtained. More than 50% of patients are satisfactorily maintained on doses less than 20 mcg/kg/min.
Adult
2-5 mcg/kg/min IV initially; not to exceed 50 mcg/kg/min
Pediatric
5 mcg/kg/min IV initially, titrate to desired effect
Catechol-o-methyltransferase (COMT) inhibitors may prolong effects of dopamine; beta-adrenergic blockers may antagonize peripheral vasoconstriction caused by high doses of dopamine; butyrophenones (eg, haloperidol) and phenothiazines can suppress dopaminergic renal and mesenteric vasodilation induced with low-dose dopamine infusion; concurrent administration of diuretic agents with low-dose dopamine may produce additive effects on urine flow; hypotension and bradycardia may occur with phenytoin; dopamine may decrease effects of phenytoin
Documented hypersensitivity; pheochromocytoma or ventricular fibrillation
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Closely monitor urine flow, cardiac output, pulmonary wedge pressure, and blood pressure during infusion; prior to infusion, correct hypovolemia with either whole blood or plasma, as indicated; monitoring central venous pressure or left ventricular filling pressure may be helpful in detecting and treating hypovolemia; patients who have received MAO inhibitors within 2 or 3 wk prior to administration of dopamine should receive initial doses no greater than 1/10 initial dose; ventricular arrhythmias and hypertension may occur when administering dopamine to patients receiving cyclopropane or halogenated hydrocarbon anesthetics
Epinephrine (Adrenalin)
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; higher doses predominantly activate alpha receptors.
Adult
1 mcg/min IV initially; not typically a first-line agent
Pediatric
0.02-0.05 mcg/kg/min IV initially; titrate to desired effect
Increases toxicity of beta- and alpha-blocking agents
Documented hypersensitivity; narrow- or shallow-angle glaucoma; aphakia
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in cardiac arrhythmias
Anti-inflammatory
Primarily used as an anti-inflammatory in this disease process.
Methylprednisolone (Solu-Medrol, Medrol)
Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability. For late-onset treatment, "refractory ARDS" defined as 7 days of mechanical ventilation without significant improvement.
Adult
Loading dose of 2 mg/kg IV, followed by 2 mg/kg/d IV divided q6h from days 1-14, then 1 mg/kg/d from days 15-21, then 0.5 mg/kg/d from days 22-28, 0.25 mg/kg/d on days 29-30, and finally 0.125 mg/kg/d on days 31-32
For patients extubated prior to day 14, skip to day 15 of treatment schedule and continue taper
Methylprednisolone tabs (Medrol) may be substituted when able to take PO
Pediatric
Administer as in adults
Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels of methylprednisolone; phenobarbital, phenytoin, and rifampin may decrease levels of methylprednisolone (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics; grapefruit juice increases prednisolone concentrations; methylprednisolone and cyclosporine mutually inhibit one another, resulting in increased plasma levels of each drug
Documented hypersensitivity; viral, fungal, or tubercular skin infections; administration of live or live-attenuated vaccine in patients receiving immunosuppressive doses of corticosteroids
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Peptic ulcer disease, ocular herpes simplex, untreated systemic infections, tuberculosis
More on Pediatrics, Respiratory Distress Syndrome |
| Overview: Pediatrics, Respiratory Distress Syndrome |
| Differential Diagnoses & Workup: Pediatrics, Respiratory Distress Syndrome |
 Treatment & Medication: Pediatrics, Respiratory Distress Syndrome |
| Follow-up: Pediatrics, Respiratory Distress Syndrome |
| Multimedia: Pediatrics, Respiratory Distress Syndrome |
| References |
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References
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Further Reading
Keywords
acute respiratory distress syndrome, ARDS, severe acute respiratory syndrome, SARS, acute lung injury, ALI, multiple organ failure syndrome, MOFS, respiratory distress syndrome in children
