eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Neonatology

Bronchopulmonary Dysplasia: Treatment & Medication

Author: Namasivayam Ambalavanan, MD, MBBS, Associate Professor, Division of Neonatology, Departments of Pediatrics, Cell Biology, and Pathology, University of Alabama School of Medicine
Coauthor(s): Thomas D Soltau, MD,, Assistant Professor, Department of Pediatrics, Division of Neonatology, University of Alabama School of Medicine
Contributor Information and Disclosures

Updated: Nov 9, 2009

Treatment

Medical Care

Mechanical ventilation

In most cases of bronchopulmonary dysplasia (BPD), respiratory distress syndrome is diagnosed and treated. The mainstay for treating RDS has been surfactant replacement with oxygen supplementation, continuous positive airway pressure (CPAP), and mechanical ventilation. The treatment necessary to recruit alveoli and prevent atelectasis in the immature lung may cause lung injury and activate the inflammatory cascade.

Trauma secondary to positive pressure ventilation (PPV) is generally referred to as barotrauma. With the recent focus on a ventilation strategy involving low versus high tidal volume, some investigators have adopted the term volutrauma. Volutrauma suggests the occurrence of lung injury secondary to excessive tidal volume from PPV.

The severity of lung immaturity, the fetal milieu, and the effects of surfactant deficiency determine the need for PPV, surfactant supplementation, and resultant barotrauma or volutrauma. With severe lung immaturity, the total number of alveoli is reduced, increasing the positive pressure transmitted to distal terminal bronchioles. In the presence of surfactant deficiency, surface tension forces are increased. Some compliant alveoli may become hyperinflated, whereas other saccules with increased surface tension remain collapsed. With increasing PPV to recruit alveoli and improve gas exchange, the compliant terminal bronchiole and alveolar ducts may rupture, leaking air into the interstitium, with resultant pulmonary interstitial emphysema (PIE). The occurrence of PIE greatly increases the risk of bronchopulmonary dysplasia.

Many modes of ventilation and many ventilator strategies have been studied to potentially reduce lung injury, such as synchronized intermittent mechanical ventilation (SIMV), high-frequency jet ventilation (HFJV), and high-frequency oscillatory ventilation (HFOV). Results have been mixed, although some theoretical benefits are associated with these alternative modes of ventilation. Although shorter duration of mechanical ventilation has been demonstrated in some trials of SIMV, most trials have not had a large enough sample size to demonstrate a reduction in bronchopulmonary dysplasia. Systematic reviews suggest that optimal use of conventional ventilation may be as effective as HFOV in improving pulmonary outcomes. Regardless of the high-frequency strategy used, avoidance of hypocarbia and optimization of alveolar recruitment may decrease the risk of bronchopulmonary dysplasia and associated of neurodevelopmental abnormalities.

PPV with various forms of nasal CPAP has been reported to decrease injury to the developing lung and may reduce the development of bronchopulmonary dysplasia. In general, centers that use "gentler ventilation" with more CPAP and less intubation, surfactant, and indomethacin had the lowest rates of bronchopulmonary dysplasia.

Oxygen and PPV frequently are life-saving in extremely preterm infants. However, early and aggressive CPAP may eliminate the need for PPV and exogenous surfactant or facilitate weaning from PPV. Some recommend brief periods of intubation primarily for the administration of exogenous surfactant quickly followed by extubation and nasal CPAP to minimize the need for prolonged PPV. This strategy may be most effective in infants without severe RDS, such as many infants with birth weights of 1000-1500 g. In infants who require oxygen and PPV, careful and meticulous treatment can minimize oxygen toxicity and lung injury. Optimal levels include a pH level of 7.2-7.3, a partial pressure of carbon dioxide (pCO2) of 45-55 mm Hg, and a partial pressure of oxygen (pO2) level of 50-70 mm Hg (with oxygen saturation at 87-92%).

Assessment of blood gases requires arterial, venous, or capillary blood samples. As a result, indwelling arterial lines are often inserted early in the acute management of RDS. Samples obtained from these lines provide the most accurate information about pulmonary function. Arterial puncture may not provide completely accurate samples because of patient agitation and discomfort. Capillary blood gas results, if samples are properly obtained, may be correlated with arterial values; however, capillary samples may widely vary, and results for carbon dioxide are poorly correlated. Following trends in transcutaneous PO2 andP CO2 may reduce the need for frequent blood gas measurements.

Weaning from mechanical ventilation and oxygen is often difficult in infants with moderate-to-severe bronchopulmonary dysplasia, and few criteria are defined to enhance the success of extubation. When tidal volumes are adequate and respiratory rates are low, a trial of extubation and nasal CPAP may be indicated. Atrophy and fatigue of the respiratory muscles may lead to atelectasis and extubation failure. A trial of endotracheal CPAP before extubation is controversial because of the increased work of breathing and airway resistance.

Optimization of methylxanthines and diuretics and adequate nutrition may facilitate weaning the infant from mechanical ventilation. Meticulous primary nursing care is essential to ensure airway patency and facilitate extubation. Prolonged and repeated intubations, as well as mechanical ventilation, may be associated with severe upper airway abnormalities, such as vocal cord paralysis, subglottic stenosis, and laryngotracheomalacia. Bronchoscopic evaluation should be considered in infants with bronchopulmonary dysplasia in whom extubation is repeatedly unsuccessful. Surgical interventions (cricoid splitting, tracheostomy) to address severe structural abnormalities are used less frequently today than in the past.

Oxygen therapy

Oxygen can accept electrons in its outer ring to form free radicals. Oxygen free radicals can cause cell-membrane destruction, protein modification, and DNA abnormalities. Compared with fetuses, neonates live in a relatively oxygen-rich environment. Oxygen is ubiquitous and necessary for extrauterine survival. All mammals have antioxidant defenses to mitigate injury due to oxygen free radicals. However, neonates have a relative deficiency in antioxidant enzymes.

The major antioxidant enzymes in humans are superoxide dismutase, glutathione peroxidase, and catalase. Activity of antioxidant enzymes tend to increase during the last trimester of pregnancy, similar to surfactant production, alveolarization, and development of the pulmonary vasculature. Increases in alveolar size and number, surfactant production, and antioxidant enzymes prepare the fetus for transition from a relatively hypoxic intrauterine environment to a relatively hyperoxic extrauterine environment. Preterm birth exposes the neonate to high oxygen concentrations, increasing the risk of injury due to oxygen free radical.

Animal and human studies of supplemental superoxide dismutase and catalase supplementation have shown reduced cell damage, increased survival, and possible prevention of lung injury. Evidence of oxidation of lipids and proteins has been found in neonates who develop bronchopulmonary dysplasia. Supplementation with superoxide dismutase in ventilated preterm infants with RDS substantially reduced in readmissions compared with placebo-treated control subjects. Further trials are currently under way to examine the effects of supplementation with superoxide dismutase in preterm infants at high risk for bronchopulmonary dysplasia.

Ideal oxygen saturation for term or preterm neonates of various gestational ages has not been definitively determined. In practice, many clinicians have adopted conservative oxygen saturation parameters (ie, 87-92%). A delicate balance to optimally promote neonatal pulmonary (alveolar and vascular) and retinal vascular homeostasis is noted. In the Supplemental Therapeutic Oxygen for Prethreshold Retinopathy of Prematurity (STOP-ROP) trial to reduce severe retinopathy of prematurity (ROP), oxygen saturations of more than 95% minimally affected retinopathy but increased the risk for pneumonia or bronchopulmonary dysplasia.

The normal oxygen requirement of a preterm infant is unknown. Pulmonary hypertension and cor pulmonale may result from chronic hypoxia and lead to airway remodeling in infants with severe bronchopulmonary dysplasia. Oxygen is a potent pulmonary vasodilator that stimulates the production of nitric oxide (NO). NO causes smooth muscle cells to relax by activating cyclic guanosine monophosphate. Currently, pulse oximetry is the mainstay of noninvasive monitoring of oxygenation.

Repeated episodes of desaturation and hypoxia may occur in infants with bronchopulmonary dysplasia receiving mechanical ventilation as a result of decreased respiratory drive, altered pulmonary mechanics, excessive stimulation, bronchospasm, and forced exhalation efforts. Forced exhalation efforts due to infant agitation may cause atelectasis and recurrent hypoxic episodes. Hyperoxia may overwhelm the neonate's relatively deficient antioxidant defenses and worsen bronchopulmonary dysplasia. The patient's oxygen requirements are frequently increased during stressful procedures and feedings. Some NICUs have adopted a conservative oxygen saturation policy of maintaining saturations of 88-94%. Caregivers are more likely to follow wide guidelines for ranges of oxygen saturation than narrow ones. Some infants, especially those living at high altitudes, may require oxygen therapy for many months.

Transfusion of packed RBCs may increase oxygen-carrying capacity in preterm infants who have anemia (hematocrit <30% [0.30]), but transfusion may further increase complication rates. The ideal hemoglobin level in critically ill neonates is not well established. Hemoglobin levels are not well correlated with oxygen transport, although it has been shown that oxygen content and systemic oxygen transport increased and that oxygen consumption and requirements decreased in infants with bronchopulmonary dysplasia after blood transfusion.

The need for multiple transfusions and donor exposures can be minimized by using iron supplementation, a reduction in phlebotomy requirements, and by use of erythropoietin administration.

Treatment of inflammation

 Elevated levels of interleukin-6 and placental growth factor in the umbilical venous blood of preterm neonates are associated with increased incidence of bronchopulmonary dysplasia. This inflammation likely affects alveolarization and vascularization of the pulmonary system of the second-trimester fetus.

Fetal sheep exposed to inflammatory mediators or endotoxin develop inflammation and abnormal lung development. Activation of inflammatory mediators has been demonstrated in humans and animal models of acute lung injury. Activation of leukocytes after cell injury caused by oxygen free radicals, barotrauma, infection, and other stimuli may begin the process of destruction and abnormal lung repair that results in acute lung injury then bronchopulmonary dysplasia.

Radiolabeled activated leukocytes have been recovered by means of bronchoalveolar lavage (BAL) in preterm neonates receiving oxygen and PPV. These leukocytes, as well as lipid byproducts of cell-membrane destruction, activate the inflammatory cascade and are metabolized to arachidonic acid and lysoplatelet factor. Lipoxygenase catabolizes arachidonic acid, resulting in the production of cytokines and leukotrienes. Cyclooxygenase may also metabolize these byproducts to produce thromboxane, prostaglandin, or prostacyclin. All of these substances have potent vasoactive and inflammatory properties. levels of these substances are elevated in the first days of life, as measured in tracheal aspirates of preterm infants who subsequently develop bronchopulmonary dysplasia.

Metabolites of arachidonic acid, lysoplatelet factor, prostaglandin, and prostacyclin may cause vasodilatation, increase capillary permeability with subsequent albumin leakage, and inhibit surfactant function. This effects increase oxygenation and ventilation requirements and potentially increase rates of bronchopulmonary dysplasia Activation of transcription factors such as nuclear factor-kappa B in early postnatal life is associated with death or bronchopulmonary dysplasia.

Collagenase and elastase are released from activated neutrophils. These enzymes may directly destroy lung tissue because hydroxyproline and elastin (breakdown products of collagen and elastin) have been recovered in the urine of preterm infants who develop bronchopulmonary dysplasia.

Alpha1-proteinase inhibitor mitigates the action of elastases and is activated by oxygen free radicals. Increased activity and decreased function of alpha1-proteinase inhibitor may worsen lung injury in neonates. A decrease in bronchopulmonary dysplasia and in the need for continued ventilator support is found in neonates given supplemental alpha1-proteinase inhibitor.

All of these findings suggest the fetal inflammatory response effects pulmonary development and substantially contributes to the development of bronchopulmonary dysplasia. The self-perpetuating cycle of lung injury is accentuated in the extremely preterm neonate with immature lungs.

Management of infection

 Maternal cervical colonization and/or colonization in the neonate with Ureaplasma urealyticum has been implicated in the development of bronchopulmonary dysplasia. Viscardi and colleagues found that persistent lung infection with U urealyticum may contribute to chronic inflammation and early fibrosis in the preterm lung, leading to pathology consistent with clinically significant bronchopulmonary dysplasia.13

Systematic reviews have concluded that infection with U urealyticum is associated with increased rates of bronchopulmonary dysplasia. Infection—either antenatal chorioamnionitis and funisitis or postnatal infection—may activate the inflammatory cascade and damage the preterm lung, resulting in bronchopulmonary dysplasia. In fact, any clinically significant episode of sepsis in the vulnerable preterm neonate greatly increases his or her risk of bronchopulmonary dysplasia, especially if the infection increases the baby's requirement for oxygen and mechanical ventilation.

Future management

Future management of bronchopulmonary dysplasia will involve strategies that emphasize prevention. Because few accepted therapies currently prevent bronchopulmonary dysplasia, many therapeutic modalities (eg, mechanical ventilation, oxygen therapy, nutritional support, medication) are used to treat bronchopulmonary dysplasia. Practicing neonatologists have observed reduced severities of bronchopulmonary dysplasia in the postsurfactant era. Maintaining PPV and oxygen therapy for longer than 4 months and discharging patients to facilities for prolonged mechanical ventilation is now unusual.

Consultations

Infants with bronchopulmonary dysplasia have multisystem involvement. Therefore, various pediatric subspecialists should be consulted: cardiologist, pulmonologist, gastroenterologist, developmentalist, ophthalmologist, neurologist, physical therapist, and nutritionist.

Pharmacists who have specialized in pediatrics and neonatal care are invaluable in guiding therapy and providing in-patient and outpatient support for these fragile infants. They may also assist with ongoing care after patients are discharged from the hospital.

Diet

Infants with bronchopulmonary dysplasia have increased energy requirements. Early parenteral nutrition is often used to ameliorate the catabolic state of the preterm infant, although excessive fluid administration (and failure to lose weight) in the first week of life may increase the risk for patent ductus arteriosus (PDA) and bronchopulmonary dysplasia. Maximizing the patient's intake of protein, carbohydrates, fat, vitamins, and trace metals is critical to prevent further lung injury and augment tissue repair. However, excessive administration of non-nitrogen calories should be avoided because this may lead to excessive formation of carbon dioxide and complicate weaning.

Antioxidant enzymes may protect the lung and help prevent or mitigate bronchopulmonary dysplasia. In preterm neonates, deficiency of trace element such as copper, zinc, and manganese may predispose them to lung injury, and supplementation may provide protection.

Vitamins A and E are nutritional antioxidants that may help prevent lipid peroxidation and maintain cell integrity. However, supplementation of vitamin E in preterm neonates does not prevent bronchopulmonary dysplasia. Preterm neonates may be deficient in vitamin A, and many trials of vitamin A supplementation to prevent bronchopulmonary dysplasia in preterm infants have been completed. Data from meta-analyses reported in a Cochrane Database review of vitamin A supplementation indicate that vitamin A supplementation reduces the risk of bronchopulmonary dysplasia in premature neonates.

Extremely preterm infants may require large amounts of free water because of increased insensible water loss through their thin, immature skin. Excessive administration of fluid increases the risk of symptomatic PDA and pulmonary edema (PE). The increased ventilator settings and oxygen requirements necessary to treat PDA and PE may worsen pulmonary injury and increase the risk of bronchopulmonary dysplasia. Early PDA treatment may improve pulmonary function but does not affect the incidence of bronchopulmonary dysplasia. A retrospective study by Oh et al revealed that lowered fluid intake soon after birth helped reduce the risk of death and oxygen requirement at 36 weeks' corrected gestational age.14

Protein and fat supplementation is progressively increased to provide approximately 3-3.5 g/kg/day. Rapid and early administration of high concentrations of lipids may possibly worsen bronchopulmonary dysplasia by depleting pulmonary vascular lipid. Excessive glucose loads may increase oxygen consumption, the respiratory drive, and glucosuria. Calcium and phosphorus requirements are greatly increased in preterm infants. Most mineral stores in the fetus are collected during the third trimester, leaving the extremely preterm infant deficient in calcium and phosphorus and at increased risk of rickets. Furosemide therapy and limited intravenous administration of calcium may worsen bone mineralization and cause secondary hyperparathyroidism.

Vitamin A supplementation decreases the incidence of bronchopulmonary dysplasia. Supplementation of trace minerals (eg, copper, zinc, manganese) are needed because they are essential cofactors in antioxidant enzymes.

Early insertion of percutaneous central venous lines may aid the administration of parenteral nutrition.

Early enteral feeding of small amounts (even if umbilical lines are in place) followed by slow, steady increases in volume appears to optimize tolerance of feeds and nutritional support. The most immature and unstable preterm infant often has a difficult transition to complete enteral nutrition. Frequent interruption of feedings because of intolerance or illness can complicate the care of patients. Enteral feedings of breast milk provides the best nutrition while preventing feeding complications (eg, sepsis, necrotizing enterocolitis). The energy content of expressed breast milk and formulas can be enhanced to increase energy intake while minimizing fluid intake. Infants may require 120-150 kcal/kg/day to gain weight.

Diuretics are often used to treat fluid overload, but initially avoiding excessive fluid administration is preferred.

Postnatal growth failure is common and may have considerable effects on long-term developmental outcomes. Strategies to optimize postnatal weight gain are important to improve pulmonary, retinal, and neurologic development.

Medication

Many drug therapies are used to treat infants with severe bronchopulmonary dysplasia (BPD). The efficacy, exact mechanisms of action, and potential adverse effects of these drugs have not been definitively established. A study group from the NICHD and US Food and Drug Administration (FDA) reviewed many of the drugs used to prevent and treat bronchopulmonary dysplasia. Walsh and colleagues concluded that detailed analyses of many of these treatments, as well as long-term follow-up, are needed.15

Vitamin A supplementation

Seven trials of vitamin A supplementation in preterm neonates to prevent bronchopulmonary dysplasia were analyzed for the Cochrane Collaborative Neonatal review. Vitamin A supplementation reduced bronchopulmonary dysplasia and death at 36 weeks' postmenstrual age. However, the need for frequent intramuscular injections in extremely premature infants has precluded widespread use of this therapy.

Diuretics

Furosemide (Lasix) is the treatment of choice for fluid overload in infants with bronchopulmonary dysplasia. It is a loop diuretic that improves clinical pulmonary status and function and decreases pulmonary vascular resistance. Daily or alternate-day furosemide therapy may facilitate weaning from positive pressure ventilation (PPV), oxygenation, or both. Adverse effects of long-term therapy are frequent and include hyponatremia, hypokalemia, contraction alkalosis, hypocalcemia, hypercalciuria, renal stones, nephrocalcinosis, and ototoxicity. Careful parenteral and enteral nutritional supplementation is required to maximize the benefits instead of exacerbating the adverse effects. In patients with mild hyponatremia or hypokalemia, supplementation with potassium chloride is favored over supplementation with sodium chloride.

Thiazide diuretics plus aldosterone inhibitors (eg, spironolactone [Aldactone]) have also been used in infants with bronchopulmonary dysplasia. In several trials of infants with bronchopulmonary dysplasia, thiazide diuretics combined with spironolactone increased urine output with or without improvement in pulmonary mechanics. Hoffman et al reported that spironolactone did not reduce the need for supplemental electrolytes in preterm infants with bronchopulmonary dysplasia.16 To the present authors' knowledge, long-term studies to compare the efficacy of furosemide with those of thiazide and spironolactone therapy have not been performed.

Bronchodilators

Albuterol is a specific beta2-agonist used to treat bronchospasm in infants with bronchopulmonary dysplasia. Albuterol may improve lung compliance by decreasing airway resistance by relaxing smooth muscle cell. Changes in pulmonary mechanics may last as long as 4-6 hours. Adverse effects include increased blood pressure (BP) and heart rate. Ipratropium bromide is a muscarinic antagonist that is related to atropine; however, it may have bronchodilator effects more potent than those of albuterol. Improvements in pulmonary mechanics were demonstrated in patients with bronchopulmonary dysplasia after they received ipratropium bromide by inhalation. Combined therapy with albuterol and ipratropium bromide may be more effective than either agent alone. Few adverse effects are noted.

Methylxanthines are used to increase respiratory drive, decrease apnea, and improve diaphragmatic contractility. These substances may also decrease pulmonary vascular resistance and increase lung compliance in infants with bronchopulmonary dysplasia, probably by directly causing smooth muscle to relax. Methylxanthines also have diuretic effects. All of these effects may increase success in weaning patients from mechanical ventilation.

Synergy between theophylline and diuretics has been demonstrated. Theophylline has a half-life of 30-40 hours. It is metabolized primarily to caffeine in the liver and may result in adverse effects such as increase in heart rate, gastroesophageal reflux, agitation, and seizures. The half-life of caffeine is approximately 90-100 hours, and caffeine is excreted unchanged in the urine. Both agents are available in intravenous and enteral formulations. Caffeine has fewer adverse effects than theophylline. Schmidt and colleagues reported that the early use of caffeine to treat apnea of prematurity appeared to reduce ventilatory requirements and that it may decrease the incidence of bronchopulmonary dysplasia.17

Corticosteroids

Systemic and inhaled corticosteroids have been studied extensively in preterm infants to prevent and treat bronchopulmonary dysplasia.

Dexamethasone is the primary systemic synthetic corticosteroid studied in preterm neonates. Dexamethasone has many pharmacologic benefits but clinically significant adverse effects. This drug stabilizes cell and lysosomal membranes, increases surfactant synthesis, increases serum vitamin A concentration, inhibits prostaglandin and leukotriene, decreases pulmonary edema (PE), breaks down granulocyte aggregates, and improves pulmonary microcirculation. Its adverse effects are hyperglycemia, hypertension, weight loss, GI bleeding or perforation, cerebral palsy, adrenal suppression, and death.

Many researchers have evaluated the effects of early administration of dexamethasone to prevent bronchopulmonary dysplasia, often demonstrating short-term improvements in clinical outcome. However, Papile and associates reported that early use of dexamethasone during the first 2 weeks of life did not prevent bronchopulmonary dysplasia and may worsen neurologic outcome.18 Infants who received a combination of dexamethasone and indomethacin were at increased risk of spontaneous intestinal perforation. Neurodevelopmental follow-up studies of infants treated with prolonged and high-dose dexamethasone suggest that, though this therapy improves short-term pulmonary outcome, long-term outcome appears to considerably worsen. Recent studies, including a Cochrane review, have demonstrated that low-dose, short-term therapy improved pulmonary and neurodevelopmental outcomes.

Studies of inhaled glucocorticoid therapy have suggested that the only beneficial effect was a reduction in the use of systemic corticosteroids in infants receiving inhaled steroids. However, concerns about systemic absorption (hypertension), associated complications, drug delivery, and current restrictions on systemic dexamethasone use may eliminate the need for this therapeutic approach. The routine use of dexamethasone in infants with bronchopulmonary dysplasia is not currently recommended. The American Academy of Pediatrics and the Canadian Society of Pediatrics do not advocate the routine use of corticosteroids in preterm neonates to treat bronchopulmonary dysplasia.19,20 Despite these recommendations, dexamethasone is still used in carefully selected patients who have substantially increased ventilatory requirements at about 1 month of age.

Vasodilators

Inhaled NO (iNO) is a short-acting gas that relaxes the pulmonary vasculature. It may also act as an anti-inflammatory agent at low concentrations.

Multiple randomized controlled trials of iNO in preterm infants have been performed using varying entry criteria and outcomes. The results are mixed. Although certain selected subgroups may benefit, whether the sickest and smallest infants at greatest risk of bronchopulmonary dysplasia benefit from iNO remains unclear.

Diuretics

Diuretics promote excretion of water and electrolytes by the kidneys. They are used to treat heart failure or hepatic, renal, or pulmonary disease when sodium and water retention results in edema or ascites.


Furosemide (Lasix)

DOC for fluid overload in infants with BPD. Loop diuretic. Therapy qd or qod improves respiratory function and may facilitate weaning from PPV, oxygen, or both. Increases excretion of water by interfering with chloride-binding cotransport system, which in turn inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule.

Adult

Indication not applicable

Pediatric

0.5-2 mg/kg/dose PO/IV bid-qod (qd in infants <31 wk postconceptual age)

Antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to increase with coadministration of aminoglycosides; may enhance anticoagulant activity of warfarin when taken concurrently

Documented hypersensitivity; hepatic coma; anuria; state of severe electrolyte depletion

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

Hearing loss of various degrees may occur; observe for hyponatremia, hypokalemia, contraction alkalosis, hypocalcemia, hypercalciuria, cholelithiasis, renal stones, nephrocalcinosis, and ototoxicity; potassium chloride supplementation favored over sodium chloride supplementation in mild hyponatremia or hypokalemia

Bronchodilators

Bronchodilators decrease muscle tone in both the small and large airways in the lungs, increasing ventilation. This category includes beta-adrenergic agents, methylxanthines, and anticholinergics.


Albuterol (Proventil, Ventolin)

Specific beta2-agonist used to treat bronchospasm in infants with BPD. May improve lung compliance by decreasing airway resistance secondary to smooth muscle cell relaxation. With current strategies for aerosol administration, exactly how much is delivered to airways and lungs of infants with BPD (especially if ventilator dependent) is unclear. Because clinically significant smooth muscle relaxation does not appear to occur in first few weeks of life, do not start aerosol therapy before this time unless patient has profound respiratory illness.

Adult

Indication not applicable

Pediatric

0.1-0.2 mg (0.02-0.04 mL of 0.5% solution diluted with 1-2 mL 0.45-0.9% NaCl) per kg/dose inhaled by nebulizer q4-6h

Beta-blockers antagonize effects; inhaled ipratropium may increase duration of bronchodilatation; cardiovascular effects may increase with MAOIs, inhaled anesthetics, tricyclic antidepressants, or sympathomimetic agents

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

May cause tachycardia or reflex bronchospasm; changes in pulmonary mechanics may last as long as 4-6 h; adverse effects include increased BP and heart rate; tolerance may develop with prolonged use


Caffeine citrate (Cafcit)

CNS stimulant used to treat infants with apnea of prematurity and infants with BPD. Caffeine may facilitate weaning from ventilator.

Adult

Indication not applicable

Pediatric

Loading dose: 20 mg/kg PO/IV
Maintenance dose: 5 mg/kg/d PO/IV

Caution with cardiovascular, renal, or hepatic dysfunction; may act synergistically with diuretics; additive positive inotropic and chronotropic effects with beta-agonists; cimetidine and fluconazole decrease clearance

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 cardiovascular, renal, or hepatic dysfunction; monitor levels at least weekly; long half-life of 100 h; therapeutic levels 10-20 mcg/mL; very high levels may alter seizure threshold; may worsen gastroesophageal reflux


Theophylline (Elixophyllin, Theo-Dur)

Systemic bronchodilator. Used to treat apnea of prematurity. May improve contractility of skeletal muscle and decrease diaphragmatic fatigue in infants with BPD. May facilitate weaning infant with BPD from continuous mechanical ventilation.
Monitor serum levels and adjust on basis of infant's response; therapeutic levels approximately 5-12 mcg/mL. IV dose based on theophylline equivalent.

Adult

Indication not applicable

Pediatric

Loading dose: 3-5 mg/kg PO/IV
Maintenance dose: 1-3 mg/kg/d PO/IV divided q8-12h

Drugs that induce or inhibit hepatic cytochrome P450 (CYP) may affect levels; aminoglutethimide, barbiturates, carbamazepine, ketoconazole, loop diuretics, charcoal, hydantoins, phenobarbital, phenytoin, rifampin, isoniazid, and sympathomimetics may decrease effects; effects may increase with allopurinol, beta-blockers, corticosteroids, thyroid hormones, ephedrine, carbamazepine, cimetidine, erythromycin, macrolides, propranolol, and interferon

Documented hypersensitivity; uncontrolled arrhythmias; hyperthyroidism; uncontrolled seizure disorders

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 hypertension, tachyarrhythmias, hyperthyroidism, or compromised cardiac function; do not inject IV solution faster than 25 mg/min; patients with PE or liver dysfunction are at increased risk of toxicity because of reduced drug clearance; may worsen gastroesophageal reflux; may lower seizure threshold at high levels


Ipratropium bromide (Atrovent)

Muscarinic antagonist with potent bronchodilating effects. May improve pulmonary mechanics in infants with BPD. Inhaled drug poorly absorbed systemically.

Adult

Indication not applicable

Pediatric

0.025-0.08 mg/kg inhaled by nebulizer q6h (dilute in 1.5-2 mL 0.9% NaCl)

Drugs with anticholinergic properties (eg, dronabinol) may increase toxicity; albuterol increases effects

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

Not indicated for acute episodes of bronchospasm; caution in narrow-angle glaucoma, prostatic hypertrophy, and bladder neck obstruction

Corticosteroids

Corticosteroids are produced by the adrenal gland. Mineralocorticoids are produced in the adrenal medulla and primarily affect fluid and electrolyte balance. Glucocorticoids possess strong anti-inflammatory properties and affect the metabolism of many tissues.


Dexamethasone (Decadron)

Stabilizes cell and lysosomal membranes, increases surfactant synthesis, increases serum vitamin A concentration, inhibits prostaglandin and leukotriene, breaks down granulocyte aggregates, and improves pulmonary microcirculation. Has many pharmacologic benefits but clinically significant adverse effects: hyperglycemia, hypertension, weight loss, GI bleeding or perforation, cerebral palsy, adrenal suppression, and death.

Adult

Indication not applicable

Pediatric

0.15-0.25 mg/kg/d PO/IV divided bid; wean over 5-7 d; safe and effective dose ranges for neonates not definitively established.

Coadministration of barbiturates, phenytoin, and rifampin decrease effects; decreases effect of salicylates and vaccines used for immunization

Documented hypersensitivity; active bacterial or fungal infection

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

Routine use in infants with BPD not recommended unless severe pulmonary disease present because of possible detrimental long-term effects on neurologic outcome and increased risk of multiple complications, including severe infections; monitor adrenal insufficiency when tapering; abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteoporosis, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, myasthenia gravis, growth suppression, and infections are possible complications of glucocorticoid use

Vitamin

Preterm infants are deficient in vitamin A.


Vitamin A (Palmitate-A 5000)

Intramuscular vitamin A supplementation reduces incidence of BPD. Firm dosing guidelines not established.

Adult

Indication not applicable

Pediatric

5000 IU IM 3 times per wk for 4 wk

Cholestyramine, neomycin, and mineral oil may decrease enteral absorption

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Pregnancy category X if dose exceeds RDA recommendation; monitor for toxicity if dose >25,000 U/d; parenteral vitamin A in low birth low-birth-weight infants may be associated with thrombocytopenia, renal dysfunction, hepatomegaly, cholestasis, ascites, hypotension, and metabolic acidosis (E-Ferol syndrome)

More on Bronchopulmonary Dysplasia

Overview: Bronchopulmonary Dysplasia
Differential Diagnoses & Workup: Bronchopulmonary Dysplasia
Treatment & Medication: Bronchopulmonary Dysplasia
Follow-up: Bronchopulmonary Dysplasia
Multimedia: Bronchopulmonary Dysplasia
References
[ CLOSE WINDOW ]

References

  1. Northway WH Jr, Rosan RC, Porter DY. Pulmonary disease following respirator therapy of hyaline-membrane disease. Bronchopulmonary dysplasia. N Engl J Med. Feb 16 1967;276(7):357-68. [Medline].

  2. Bancalari E, Abdenour GE, Feller R, Gannon J. Bronchopulmonary dysplasia: clinical presentation. J Pediatr. Nov 1979;95(5 Pt 2):819-23. [Medline].

  3. Shennan AT, Dunn MS, Ohlsson A, et al. Abnormal pulmonary outcomes in premature infants: prediction from oxygen requirement in the neonatal period. Pediatrics. Oct 1988;82(4):527-32. [Medline].

  4. Jobe AH, Bancalari E. Bronchopulmonary dysplasia. Am J Respir Crit Care Med. Jun 2001;163(7):1723-9. [Medline].

  5. Walsh MC, Yao Q, Gettner P, et al. Impact of a physiologic definition on bronchopulmonary dysplasia rates. Pediatrics. Nov 2004;114:1305-11. [Medline].

  6. Ambalavanan N, Carlo WA. Bronchopulmonary dysplasia: new insights. Clin Perinatol. Sept 2004;31:613-28. [Medline].

  7. Kresch MJ, Clive JM. Meta-analyses of surfactant replacement therapy of infants with birth weights less than 2000 grams. J Perinatol. Jul-Aug 1998;18(4):276-83. [Medline].

  8. Van Marter LJ, Allred EN, Pagano M, et al. Do clinical markers of barotrauma and oxygen toxicity explain interhospital variation in rates of chronic lung disease? The Neonatology Committee for the Developmental Network. Pediatrics. Jun 2000;105(6):1194-201. [Medline].

  9. Weinstein MR, Oh W. Oxygen consumption in infants with bronchopulmonary dysplasia. J Pediatr. Dec 1981;99(6):958-61. [Medline].

  10. Jobe AJ. The new BPD: an arrest of lung development. Pediatr Res. Dec 1999;46(6):641-3. [Medline].

  11. Kim BI, Lee HE, Choi CW, et al. Increase in cord blood soluble E-selectin and tracheal aspirate neutrophils at birth and the development of new bronchopulmonary dysplasia. J Perinat Med. 32(3):282-7. [Medline].

  12. [Best Evidence] Borghesi A, Massa M, Campanelli R, et al. Circulating endothelial progenitor cells in preterm infants with bronchopulmonary dysplasia. Am J Respir Crit Care Med. Sep 15 2009;180(6):540-6. [Medline].

  13. Viscardi RM, Muhumuza CK, Rodriguez A, et al. Inflammatory markers in intrauterine and fetal blood and cerebrospinal fluid compartments are associated with adverse pulmonary and neurologic outcomes in preterm infants. Pediatr Res. 55(6):1009-17. [Medline].

  14. Oh W, Poindexter BB, Perritt R, Lemons JA, Bauer CR, Ehrenkranz RA. Association between fluid intake and weight loss during the first ten days of life and risk of bronchopulmonary dysplasia in extremely low birth weight infants. J Pediatr. Dec 2005;147(6):786-90. [Medline].

  15. Walsh MC, Szefler S, Davis J, et al. Summary proceedings from the bronchopulmonary dysplasia group. Pediatrics. Mar 2006;117(3 Pt 2):S52-6. [Medline].

  16. Hoffman DJ, Gerdes JS, Abbasi S. Pulmonary function and electrolyte balance following spironolactone treatment in preterm infants with chronic lung disease: a double-blind, placebo-controlled, randomized trial. J Perinatol. Jan-Feb 2000;20(1):41-5. [Medline].

  17. [Best Evidence] Schmidt B, Roberts RS, Davis P, et al. Caffeine therapy for apnea of prematurity. N Engl J Med. May 18 2006;354(20):2112-21. [Medline].

  18. Papile LA, Tyson JE, Stoll BJ, et al. A multicenter trial of two dexamethasone regimens in ventilator-dependent premature infants. N Engl J Med. Apr 16 1998;338(16):1112-8. [Medline].

  19. [Guideline] AAP. Prevention of respiratory syncytial virus infections: indications for the use of palivizumab and update on the use of RSV-IGIV. American Academy of Pediatrics Committee on Infectious Diseases and Committee of Fetus and Newborn. Pediatrics. Nov 1998;102(5):1211-6. [Medline].

  20. [Guideline] AAP. Revised indications for the use of palivizumab and respiratory syncytial virus immune globulin intravenous for the prevention of respiratory syncytial virus infections. Pediatrics. Dec 2003;112(6 Pt 1):1442-6. [Medline].

  21. Hakulinen AL, Heinonen K, Lansimies E, Kiekara O. Pulmonary function and respiratory morbidity in school-age children born prematurely and ventilated for neonatal respiratory insufficiency. Pediatr Pulmonol. 1990;8(4):226-32. [Medline].

  22. Northway WH Jr. Bronchopulmonary dysplasia: twenty-five years later. Pediatrics. May 1992;89(5 Pt 1):969-73. [Medline].

  23. Bader D, Ramos AD, Lew CD, et al. Childhood sequelae of infant lung disease: exercise and pulmonary function abnormalities after bronchopulmonary dysplasia. J Pediatr. May 1987;110(5):693-9. [Medline].

  24. Blayney M, Kerem E, Whyte H, O'Brodovich H. Bronchopulmonary dysplasia: improvement in lung function between 7 and 10 years of age. J Pediatr. Feb 1991;118(2):201-6. [Medline].

  25. Abman SH. Bronchopulmonary dysplasia: "a vascular hypothesis". Am J Respir Crit Care Med. Nov 15 2001;164(10 Pt 1):1755-6. [Medline].

  26. Abman SH, Wolfe RR, Accurso FJ, et al. Pulmonary vascular response to oxygen in infants with severe bronchopulmonary dysplasia. Pediatrics. Jan 1985;75(1):80-4. [Medline].

  27. Ackerman NB Jr, Coalson JJ, Kuehl TJ, et al. Pulmonary interstitial emphysema in the premature baboon with hyaline membrane disease. Crit Care Med. Jun 1984;12(6):512-6. [Medline].

  28. Aliakbar S, Brown PR, Bidwell D, Nicolaides KH. Human erythrocyte superoxide dismutase in adults, neonates, and normal, hypoxaemic, anaemic, and chromosomally abnormal fetuses. Clin Biochem. Apr 1993;26(2):109-15. [Medline].

  29. Alverson DC, Isken VH, Cohen RS. Effect of booster blood transfusions on oxygen utilization in infants with bronchopulmonary dysplasia. J Pediatr. Oct 1988;113(4):722-6. [Medline].

  30. Ambalavanan N, Tyson JE, Kennedy KA, et al. Vitamin A supplementation for extremely low birth weight infants: outcome at 18 to 22 months. Pediatrics. Mar 2005;115(3):e249-54. [Medline].

  31. Aquino SL, Schechter MS, Chiles C, et al. High-resolution inspiratory and expiratory CT in older children and adults with bronchopulmonary dysplasia. AJR Am J Roentgenol. Oct 1999;173(4):963-7. [Medline].

  32. Aranda JV, Turmen T. Methylxanthines in apnea of prematurity. Clin Perinatol. Mar 1979;6(1):87-108. [Medline].

  33. Athavale K, Claure N, D'Ugard C, et al. Acute effects of inhaled nitric oxide on pulmonary and cardiac function in preterm infants with evolving bronchopulmonary dysplasia. J Perinatol. 24(12):769-74. [Medline].

  34. Bagchi A, Viscardi RM, Taciak V, et al. Increased activity of interleukin-6 but not tumor necrosis factor-alpha in lung lavage of premature infants is associated with the development of bronchopulmonary dysplasia. Pediatr Res. Aug 1994;36(2):244-52. [Medline].

  35. Ballard RA, Truog WE, Cnaan A, et al. Inhaled nitric oxide in preterm infants undergoing mechanical ventilation. N Engl J Med. 355(4):343-53. [Medline].

  36. Bancalari E, Sosenko I. Pathogenesis and prevention of neonatal chronic lung disease: recent developments. Pediatr Pulmonol. 1990;8(2):109-16. [Medline].

  37. Banks BA, Seri I, Ischiropoulos H, et al. Changes in oxygenation with inhaled nitric oxide in severe bronchopulmonary dysplasia. Pediatrics. Mar 1999;103(3):610-8. [Medline].

  38. Barth H. Comments on the paper by P. Jurgens, D. Dolif and G Fondalinski: "Comparative nutritional studies using 4 L-amino-acid solutions in 25 adults with healthy metabolism under conditions of total parenteral feeding (Infusionstherapie 5:141-54, 1978) [in German]. Infusionsther Klin Ernahr. 5(5):306-7. [Medline].

  39. Batsakis JG, Aronsohn RS, Walker WA, Barnes B. Serum albumin. A CAP survey. Am J Clin Pathol. Jul 1976;66(1):238-43. [Medline].

  40. Berman W Jr, Yabek SM, Dillon T, et al. Evaluation of infants with bronchopulmonary dysplasia using cardiac catheterization. Pediatrics. Nov 1982;70(5):708-12. [Medline].

  41. Bernstein G, Mannino FL, Heldt GP, et al. Randomized multicenter trial comparing synchronized and conventional intermittent mandatory ventilation in neonates. J Pediatr. Apr 1996;128(4):453-63. [Medline].

  42. Bhandari V, Bizzarro MJ, Shetty A, et al. Familial and genetic susceptibility to major neonatal morbidities in preterm twins. Pediatrics. 117(6):1901-6. [Medline].

  43. Bhatt AJ, Pryhuber GS, Huyck H, et al. Disrupted pulmonary vasculature and decreased vascular endothelial growth factor, Flt-1, and TIE-2 in human infants dying with bronchopulmonary dysplasia. Am J Respir Crit Care Med. 164(10 Pt 1):1971-80. [Medline].

  44. Bland RD, McMillan DD, Bressack MA. Decreased pulmonary transvascular fluid filtration in awake newborn lambs after intravenous furosemide. J Clin Invest. Sep 1978;62(3):601-9. [Medline].

  45. Bose C, Corbet A, Bose G, et al. Improved outcome at 28 days of age for very low birth weight infants treated with a single dose of a synthetic surfactant. J Pediatr. Dec 1990;117(6):947-53. [Medline].

  46. Bourbia A, Cruz MA, Rozycki HJ. NF-kappaB in tracheal lavage fluid from intubated premature infants: association with inflammation, oxygen, and outcome. Arch Dis Child Fetal Neonatal Ed. Jan 2006;91(1):F36-9. [Medline].

  47. Bourbon J, Boucherat O, Chailley-Heu B, Delacourt C. Control mechanisms of lung alveolar development and their disorders in bronchopulmonary dysplasia. Pediatr Res. 57(5 Pt 2):38R-46R. [Medline].

  48. Brayer C, Bony C, Salles M, et al. Bronchopulmonary dysplasia and cytomegalovirus pneumonia [in French]. Arch Pediatr. Mar 2004;11(3):223-5. [Medline].

  49. Bruce MC, Wedig KE, Jentoft N, et al. Altered urinary excretion of elastin cross-links in premature infants who develop bronchopulmonary dysplasia. Am Rev Respir Dis. Apr 1985;131(4):568-72. [Medline].

  50. Brundage KL, Mohsini KG, Froese AB, Fisher JT. Bronchodilator response to ipratropium bromide in infants with bronchopulmonary dysplasia. Am Rev Respir Dis. Nov 1990;142(5):1137-42. [Medline].

  51. Cassell GH, Waites KB, Crouse DT, et al. Association of Ureaplasma urealyticum infection of the lower respiratory tract with chronic lung disease and death in very-low-birth-weight infants. Lancet. Jul 30 1988;2(8605):240-5. [Medline].

  52. Cherukupalli K, Larson JE, Rotschild A, Thurlbeck WM. Biochemical, clinical, and morphologic studies on lungs of infants with bronchopulmonary dysplasia. Pediatr Pulmonol. Oct 1996;22(4):215-29. [Medline].

  53. Clark DA, Pincus LG, Oliphant M, et al. HLA-A2 and chronic lung disease in neonates. JAMA. Oct 15 1982;248(15):1868-9. [Medline].

  54. Cole CH, Colton T, Shah BL, et al. Early inhaled glucocorticoid therapy to prevent bronchopulmonary dysplasia. N Engl J Med. Apr 1 1999;340(13):1005-10. [Medline].

  55. Committee on Fetus and Newborn. Postnatal corticosteroids to treat or prevent chronic lung disease in preterm infants. Pediatrics. Feb 2002;109(2):330-8. [Medline].

  56. Couroucli XI, Welty SE, Ramsay PL, et al. Detection of microorganisms in the tracheal aspirates of preterm infants by polymerase chain reaction: association of adenovirus infection with bronchopulmonary dysplasia. Pediatr Res. Feb 2000;47(2):225-32. [Medline].

  57. Courtney SE, Weber KR, Breakie LA, et al. Capillary blood gases in the neonate. A reassessment and review of the literature. Am J Dis Child. Feb 1990;144(2):168-72. [Medline].

  58. Cummings JJ, D'Eugenio DB, Gross SJ. A controlled trial of dexamethasone in preterm infants at high risk for bronchopulmonary dysplasia. N Engl J Med. Jun 8 1989;320(23):1505-10. [Medline].

  59. Darlow BA, Graham PJ. Vitamin A supplementation for preventing morbidity and mortality in very low birthweight infants. Cochrane Database Syst Rev. 2002;CD000501. [Medline].

  60. Darlow BA, Inder TE, Graham PJ, et al. The relationship of selenium status to respiratory outcome in the very low birth weight infant. Pediatrics. Aug 1995;96(2 Pt 1):314-9. [Medline].

  61. Davis JM, Bhutani VK, Stefano JL, et al. Changes in pulmonary mechanics following caffeine administration in infants with bronchopulmonary dysplasia. Pediatr Pulmonol. 1989;6(1):49-52. [Medline].

  62. Davis JM, Richter SE, Biswas S, et al. Long-term follow-up of premature infants treated with prophylactic, intratracheal recombinant human CuZn superoxide dismutase. J Perinatol. Jun 2000;20(4):213-6. [Medline].

  63. Davis JM, Richter SE, Kendig JW, Notter RH. High-frequency jet ventilation and surfactant treatment of newborns with severe respiratory failure. Pediatr Pulmonol. Jun 1992;13(2):108-12. [Medline].

  64. Davis JM, Sinkin RA, Aranda JV. Drug therapy for bronchopulmonary dysplasia. Pediatr Pulmonol. 1990;8(2):117-25. [Medline].

  65. Dimaguila MA, Di Fiore JM, Martin RJ, Miller MJ. Characteristics of hypoxemic episodes in very low birth weight infants on ventilatory support. J Pediatr. Apr 1997;130(4):577-83. [Medline].

  66. Edwards DK. Radiographic aspects of bronchopulmonary dysplasia. J Pediatr. Nov 1979;95(5 Pt 2):823-9. [Medline].

  67. Ehrenkranz RA, Dusick AM, Vohr BR, et al. Growth in the neonatal intensive care unit influences neurodevelopmental and growth outcomes of extremely low birth weight infants. Pediatrics. 117(4):1253-61. [Medline].

  68. Ehrenkranz RA, Walsh MC, Vohr BR, et al. Validation of the National Institutes of Health consensus definition of bronchopulmonary dysplasia. Pediatrics. Dec 2005;116(6):1353-60. [Medline].

  69. Engelhardt B, Blalock WA, DonLevy S, et al. Effect of spironolactone-hydrochlorothiazide on lung function in infants with chronic bronchopulmonary dysplasia. J Pediatr. Apr 1989;114(4 Pt 1):619-24. [Medline].

  70. Engelhardt B, Elliott S, Hazinski TA. Short- and long-term effects of furosemide on lung function in infants with bronchopulmonary dysplasia. J Pediatr. Dec 1986;109(6):1034-9. [Medline].

  71. Fenton AC, Annich G, Mason E, et al. Chronic lung disease following neonatal ventilation. I. incidence in two geographically defined populations. Pediatr Pulmonol. Jan 1996;21(1):20-3. [Medline].

  72. Fenton AC, Mason E, Clarke M, Field DJ. Chronic lung disease following neonatal ventilation. II. Changing incidence in a geographically defined population. Pediatr Pulmonol. Jan 1996;21(1):24-7. [Medline].

  73. Forman HJ, Rotman EI, Fisher AB. Roles of selenium and sulfur-containing amino acids in protection against oxygen toxicity. Lab Invest. Aug 1983;49(2):148-53. [Medline].

  74. Frank L, Groseclose E. Oxygen toxicity in newborn rats: the adverse effects of undernutrition. J Appl Physiol. Nov 1982;53(5):1248-55. [Medline].

  75. Gabazza EC, Taguchi O, Tamaki S, et al. Role of nitric oxide in airway remodelling. Clin Sci (Lond). Mar 2000;98(3):291-4. [Medline].

  76. Garland JS, Alex CP, Pauly TH, et al. A three-day course of dexamethasone therapy to prevent chronic lung disease in ventilated neonates: a randomized trial. Pediatrics. Jul 1999;104(1 Pt 1):91-9. [Medline].

  77. Gerhardt T, Bancalari E. Lung function in bronchopulmonary dysplasia. In: Bronchopulmonary Dysplasia. 1988:182.

  78. Gerstmann DR, Minton SD, Stoddard RA, et al. The Provo multicenter early high-frequency oscillatory ventilation trial: improved pulmonary and clinical outcome in respiratory distress syndrome. Pediatrics. Dec 1996;98(6 Pt 1):1044-57. [Medline].

  79. Gladstone IM Jr, Levine RL. Oxidation of proteins in neonatal lungs. Pediatrics. May 1994;93(5):764-8. [Medline].

  80. Goldman SL, Gerhardt T, Sonni R, et al. Early prediction of chronic lung disease by pulmonary function testing. J Pediatr. Apr 1983;102(4):613-7. [Medline].

  81. Gonzalez A, Sosenko IR, Chandar J, et al. Influence of infection on patent ductus arteriosus and chronic lung disease in premature infants weighing 1000 grams or less. J Pediatr. Apr 1996;128(4):470-8. [Medline].

  82. Groothuis JR. Role of antibody and the use of respiratory syncytial virus immunoglobulin in the prevention of respiratory syncytial virus disease in preterm infants with and without bronchopulmonary dysplasia. Pediatr Infect Dis J. May 1994;13(5):454-7; discussion 457-8. [Medline].

  83. Groothuis JR, Simoes EA, Hemming VG. Respiratory syncytial virus (RSV) infection in preterm infants and the protective effects of RSV immune globulin (RSVIG). Respiratory Syncytial Virus Immune Globulin Study Group. Pediatrics. Apr 1995;95(4):463-7. [Medline].

  84. Groothuis JR, Simoes EA, Levin MJ, et al. Prophylactic administration of respiratory syncytial virus immune globulin to high-risk infants and young children. The Respiratory Syncytial Virus Immune Globulin Study Group. N Engl J Med. Nov 18 1993;329(21):1524-30. [Medline].

  85. Hagan R, Minutillo C, French N, et al. Neonatal chronic lung disease, oxygen dependency, and a family history of asthma. Pediatr Pulmonol. Nov 1995;20(5):277-83. [Medline].

  86. Halvorsen T, Skadberg BT, Eide GE, et al. Pulmonary outcome in adolescents of extreme preterm birth: a regional cohort study. Acta Paediatr. 93(10):1294-300. [Medline].

  87. Hanrahan JP, Tager IB, Castile RG, et al. Pulmonary function measures in healthy infants. Variability and size correction. Am Rev Respir Dis. May 1990;141(5 Pt 1):1127-35. [Medline].

  88. Harrod JR, L'Heureux P, Wangensteen OD, Hunt CE. Long-term follow-up of severe respiratory distress syndrome treated with IPPB. J Pediatr. Feb 1974;84(2):277-85. [Medline].

  89. Haynes RC. Adrenocorticotropic hormone. Adrenocortical steroids and their synthetic analogs: inhibitors of adrenocortical steroid biosynthesis. In: The Pharmacologic Basis of Therapeutics. 1985. New York: McGraw-Hill; 1459.

  90. Heggie AD, Jacobs MR, Butler VT, et al. Frequency and significance of isolation of Ureaplasma urealyticum and Mycoplasma hominis from cerebrospinal fluid and tracheal aspirate specimens from low birth weight infants. J Pediatr. Jun 1994;124(6):956-61. [Medline].

  91. Hernandez-Ronquillo L, Tellez-Zenteno JF, Weder-Cisneros N, et al. Risk factors for the development of bronchopulmonary dysplasia: a case-control study. Arch Med Res. Nov-Dec 2004;35(6):549-53. [Medline].

  92. HIFI Study Group. 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. Jan 12 1989;320(2):88-93. [Medline].

  93. Higgins RD, Richter SE, Davis JM. Nasal continuous positive airway pressure facilitates extubation of very low birth weight neonates. Pediatrics. Nov 1991;88(5):999-1003. [Medline].

  94. Hittner HM, Godio LB, Rudolph AJ, et al. Retrolental fibroplasia: efficacy of vitamin E in a double-blind clinical study of preterm infants. N Engl J Med. Dec 3 1981;305(23):1365-71. [Medline].

  95. Horning N, Bloom BT, Nelson RA. High-frequency ventilation experience: a rescue protocol for neonates with airleaks. Kans Med. Sep 1989;90(9):251-3. [Medline].

  96. Hughes CA, O'Gorman LA, Shyr Y, et al. Cognitive performance at school age of very low birth weight infants with bronchopulmonary dysplasia. J Dev Behav Pediatr. Feb 1999;20(1):1-8. [Medline].

  97. Hustead VA, Gutcher GR, Anderson SA, Zachman RD. Relationship of vitamin A (retinol) status to lung disease in the preterm infant. J Pediatr. Oct 1984;105(4):610-5. [Medline].

  98. Impact-RSV Study Group. Palivizumab, a humanized respiratory syncytial virus monoclonal antibody, reduces hospitalization from respiratory syncytial virus infection in high-risk infants. The IMpact-RSV Study Group. Pediatrics. Sep 1998;102(3 Pt 1):531-7. [Medline].

  99. Janssen LJ, Premji M, Lu-Chao H, et al. NO(+) but not NO radical relaxes airway smooth muscle via cGMP-independent release of internal Ca(2+). Am J Physiol Lung Cell Mol Physiol. May 2000;278(5):L899-905. [Medline].

  100. Jobe AH. An unknown: lung growth and development after very preterm birth. Am J Respir Crit Care Med. Dec 15 2002;166(12 Pt 1):1529-30. [Medline].

  101. Jobe AH. Antenatal associations with lung maturation and infection. J Perinatol. May 2005;25 Suppl 2:S31-5. [Medline].

  102. Kakkera DK, Siddiq MM, Parton LA. Interleukin-1 balance in the lungs of preterm infants who develop bronchopulmonary dysplasia. Biol Neonate. 2005;87(2):82-90. [Medline].

  103. Kallapur SG, Jobe AH. Contribution of inflammation to lung injury and development. Arch Dis Child Fetal Neonatal Ed. Mar 2006;91(2):F132-5. [Medline].

  104. Kao LC, Durand DJ, McCrea RC, et al. Randomized trial of long-term diuretic therapy for infants with oxygen-dependent bronchopulmonary dysplasia. J Pediatr. May 1994;124(5 Pt 1):772-81. [Medline].

  105. Kao LC, Durand DJ, Phillips BL, Nickerson BG. Oral theophylline and diuretics improve pulmonary mechanics in infants with bronchopulmonary dysplasia. J Pediatr. Sep 1987;111(3):439-44. [Medline].

  106. Kao LC, Warburton D, Cheng MH, et al. Effect of oral diuretics on pulmonary mechanics in infants with chronic bronchopulmonary dysplasia: results of a double-blind crossover sequential trial. Pediatrics. Jul 1984;74(1):37-44. [Medline].

  107. Kazzi SN, Kim UO, Quasney MW, Buhimschi I. Polymorphism of tumor necrosis factor-alpha and risk and severity of bronchopulmonary dysplasia among very low birth weight infants. Pediatrics. 114(2):e243-8. [Medline].

  108. Keszler M, Modanlou HD, Brudno DS, et al. Multicenter controlled clinical trial of high-frequency jet ventilation in preterm infants with uncomplicated respiratory distress syndrome. Pediatrics. Oct 1997;100(4):593-9. [Medline].

  109. Kim EH. Successful extubation of newborn infants without preextubation trial of continuous positive airway pressure. J Perinatol. Mar 1989;9(1):72-6. [Medline].

  110. [Best Evidence] Kinsella JP, Cutter GR, Walsh WF, et al. Early inhaled nitric oxide therapy in premature newborns with respiratory failure. N Engl J Med. 355(4):354-64. [Medline].

  111. Korhonen P, Hyodynmaa E, Lautamatti V, et al. Cardiovascular findings in very low birthweight schoolchildren with and without bronchopulmonary dysplasia. Early Hum Dev. Jun 2005;81(6):497-505. [Medline].

  112. Korhonen P, Laitinen J, Hyodynmaa E, Tammela O. Respiratory outcome in school-aged, very-low-birth-weight children in the surfactant era. Acta Paediatr. Mar 2004;93(3):316-21. [Medline].

  113. Lee MK, Pryhuber GS, Schwarz MA, et al. Developmental regulation of p66Shc is altered by bronchopulmonary dysplasia in baboons and humans. Am J Respir Crit Care Med. 171(12):1384-94. [Medline].

  114. Liechty EA, Donovan E, Purohit D, et al. Reduction of neonatal mortality after multiple doses of bovine surfactant in low birth weight neonates with respiratory distress syndrome. Pediatrics. Jul 1991;88(1):19-28. [Medline].

  115. Liljedahl M, Bodin L, Schollin J. Coagulase-negative staphylococcal sepsis as a predictor of bronchopulmonary dysplasia. Acta Paediatr. Feb 2004;93(2):211-5. [Medline].

  116. Long W, Thompson T, Sundell H, et al. Effects of two rescue doses of a synthetic surfactant on mortality rate and survival without bronchopulmonary dysplasia in 700- to 1350-gram infants with respiratory distress syndrome. The American Exosurf Neonatal Study Group I. J Pediatr. Apr 1991;118(4 (Pt 1)):595-605. [Medline].

  117. Majnemer A, Riley P, Shevell M, et al. Severe bronchopulmonary dysplasia increases risk for later neurological and motor sequelae in preterm survivors. Dev Med Child Neurol. Jan 2000;42(1):53-60. [Medline].

  118. Markestad T, Fitzhardinge PM. Growth and development in children recovering from bronchopulmonary dysplasia. J Pediatr. Apr 1981;98(4):597-602. [Medline].

  119. Meert K, Heidemann S, Lieh-Lai M, Sarnaik AP. Clinical characteristics of respiratory syncytial virus infections in healthy versus previously compromised host. Pediatr Pulmonol. 1989;7(3):167-70. [Medline].

  120. Merritt TA, Cochrane CG, Holcomb K, et al. Elastase and alpha 1-proteinase inhibitor activity in tracheal aspirates during respiratory distress syndrome. Role of inflammation in the pathogenesis of bronchopulmonary dysplasia. J Clin Invest. Aug 1983;72(2):656-66. [Medline].

  121. Merritt TA, Hallman M, Berry C, et al. Randomized, placebo-controlled trial of human surfactant given at birth versus rescue administration in very low birth weight infants with lung immaturity. J Pediatr. Apr 1991;118(4 (Pt 1)):581-94. [Medline].

  122. Merritt TA, Puccia JM, Stuard ID. Cytologic evaluation of pulmonary effluent in neonates with respiratory distress syndrome and bronchopulmonary dysplasia. Acta Cytol. Nov-Dec 1981;25(6):631-9. [Medline].

  123. Miller RW, Woo P, Kellman RK, Slagle TS. Tracheobronchial abnormalities in infants with bronchopulmonary dysplasia. J Pediatr. Nov 1987;111(5):779-82. [Medline].

  124. Mittendorf R, Covert R, Montag AG, et al. Special relationships between fetal inflammatory response syndrome and bronchopulmonary dysplasia in neonates. J Perinat Med. 33(5):428-34. [Medline].

  125. Morin FC III, Davis JM. Persistent pulmonary hypertension. In: Intensive Care Medicine of the Fetus and Newborn. 1996:506.

  126. Mourani PM, Ivy DD, Gao D, Abman SH. Pulmonary vascular effects of inhaled nitric oxide and oxygen tension in bronchopulmonary dysplasia. Am J Respir Crit Care Med. Nov 1 2004;170(9):1006-13. [Medline].

  127. Nickerson BG, Durand DJ, Kao LC. Short-term variability of pulmonary function tests in infants with bronchopulmonary dysplasia. Pediatr Pulmonol. 1989;6(1):36-41. [Medline].

  128. Nickerson BG, Taussig LM. Family history of asthma in infants with bronchopulmonary dysplasia. Pediatrics. Jun 1980;65(6):1140-4. [Medline].

  129. O'Dell BL, Kilburn KH, McKenzie WN, Thurston RJ. The lung of the copper-deficient rat. A model for developmental pulmonary emphysema. Am J Pathol. Jun 1978;91(3):413-32. [Medline].

  130. O'Shea TM, Dillard RG, Gillis DC, et al. Outcome at one year in infants with chronic lung disease receiving comprehensive follow-up care. A regional experience in North Carolina, 1984-1990. N C Med J. Oct 1992;53(10):548-54. [Medline].

  131. Overstreet DW, Jackson JC, van Belle G, Truog WE. Estimation of mortality risk in chronically ventilated infants with bronchopulmonary dysplasia. Pediatrics. Dec 1991;88(6):1153-60. [Medline].

  132. Palta M, Sadek M, Barnet JH, et al. Evaluation of criteria for chronic lung disease in surviving very low birth weight infants. Newborn Lung Project. J Pediatr. Jan 1998;132(1):57-63. [Medline].

  133. Periera GR, Fox WW, Stanley CA, et al. Decreased oxygenation and hyperlipemia during intravenous fat infusions in premature infants. Pediatrics. Jul 1980;66(1):26-30. [Medline].

  134. Pierce MR, Bancalari E. The role of inflammation in the pathogenesis of bronchopulmonary dysplasia. Pediatr Pulmonol. Jun 1995;19(6):371-8. [Medline].

  135. Pitkänen OM, Hallman M, Andersson SM. Correlation of free oxygen radical-induced lipid peroxidation with outcome in very low birth weight infants. J Pediatr. May 1990;116(5):760-4. [Medline].

  136. Raghavender B, Smith JB. Eosinophil cationic protein in tracheal aspirates of preterm infants with bronchopulmonary dysplasia. J Pediatr. Jun 1997;130(6):944-7. [Medline].

  137. Ramet M, Haataja R, Marttila R, et al. Association between the surfactant protein A (SP-A) gene locus and respiratory-distress syndrome in the Finnish population. Am J Hum Genet. May 2000;66(5):1569-79. [Medline].

  138. Rinaldo JE, English D, Levine J, et al. Increased intrapulmonary retention of radiolabeled neutrophils in early oxygen toxicity. Am Rev Respir Dis. Feb 1988;137(2):345-52. [Medline].

  139. Robbins CG, Davis JM, Merritt TA, et al. Combined effects of nitric oxide and hyperoxia on surfactant function and pulmonary inflammation. Am J Physiol. Oct 1995;269(4 Pt 1):L545-50. [Medline].

  140. Robbins SG, Rajaratnam VS, Penn JS. Evidence for upregulation and redistribution of vascular endothelial growth factor (VEGF) receptors flt-1 and flk-1 in the oxygen-injured rat retina. Growth Factors. 1998;16(1):1-9. [Medline].

  141. Robin B, Kim YJ, Huth J, et al. Pulmonary function in bronchopulmonary dysplasia. Pediatr Pulmonol. Mar 2004;37(3):236-42. [Medline].

  142. Rooklin AR, Moomjian AS, Shutack JG, et al. Theophylline therapy in bronchopulmonary dysplasia. J Pediatr. Nov 1979;95(5 Pt 2):882-8. [Medline].

  143. Rosenfeld W, Concepcion L, Evans H, et al. Serial trypsin inhibitory capacity and ceruloplasmin levels in prematures at risk for bronchopulmonary dysplasia. Am Rev Respir Dis. Dec 1986;134(6):1229-32. [Medline].

  144. Rova M, Haataja R, Marttila R, et al. Data mining and multiparameter analysis of lung surfactant protein genes in bronchopulmonary dysplasia. Hum Mol Genet. Jun 1 2004;13(11):1095-104. [Medline].

  145. Rush MG, Engelhardt B, Parker RA, Hazinski TA. Double-blind, placebo-controlled trial of alternate-day furosemide therapy in infants with chronic bronchopulmonary dysplasia. J Pediatr. Jul 1990;117(1 Pt 1):112-8. [Medline].

  146. Saldanha RL, Cepeda EE, Poland RL. The effect of vitamin E prophylaxis on the incidence and severity of bronchopulmonary dysplasia. J Pediatr. Jul 1982;101(1):89-93. [Medline].

  147. Schelonka RL, Katz B, Waites KB, Benjamin DK Jr. Critical appraisal of the role of Ureaplasma in the development of bronchopulmonary dysplasia with metaanalytic techniques. Pediatr Infect Dis J. Dec 2005;24(12):1033-9. [Medline].

  148. Schmidt B, Asztalos EV, Roberts RS. Impact of bronchopulmonary dysplasia, brain injury, and severe retinopathy on the outcome of extremely low-birth-weight infants at 18 months: results from the trial of indomethacin prophylaxis in preterms. JAMA. Mar 5 2003;289(9):1124-9. [Medline].

  149. Schulz CG, Sawicki G, Lemke RP, et al. MMP-2 and MMP-9 and their tissue inhibitors in the plasma of preterm and term neonates. Pediatr Res. May 2004;55(5):794-801. [Medline].

  150. Simoes EA, Groothuis JR, Tristram DA, et al. Respiratory syncytial virus-enriched globulin for the prevention of acute otitis media in high risk children. J Pediatr. Aug 1996;129(2):214-9. [Medline].

  151. Smith VC, Zupancic JA, McCormick MC. Trends in severe bronchopulmonary dysplasia rates between 1994 and 2002. J Pediatr. 146(4):469-73. [Medline].

  152. Smith VC, Zupancic JA, McCormick MC. Trends in severe bronchopulmonary dysplasia rates between 1994 and 2002. J Pediatr. Apr 2005;146(4):469-73. [Medline].

  153. Soll RF, Hoekstra RE, Fangman JJ, et al. Multicenter trial of single-dose modified bovine surfactant extract (Survanta) for prevention of respiratory distress syndrome. Ross Collaborative Surfactant Prevention Study Group. Pediatrics. Jun 1990;85(6):1092-102. [Medline].

  154. Sosenko IR, Rodriguez-Pierce M, Bancalari E. Effect of early initiation of intravenous lipid administration on the incidence and severity of chronic lung disease in premature infants. J Pediatr. Dec 1993;123(6):975-82. [Medline].

  155. Sosulski R, Abbasi S, Bhutani VK, Fox WW. Physiologic effects of terbutaline on pulmonary function of infants with bronchopulmonary dysplasia. Pediatr Pulmonol. Sep-Oct 1986;2(5):269-73. [Medline].

  156. St John EB, Carlo WA. Respiratory distress syndrome in VLBW infants: changes in management and outcomes observed by the NICHD Neonatal Research Network. Semin Perinatol. Aug 2003;27(4):288-92. [Medline].

  157. Stefano JL, Bhutani VK, Fox WW. A randomized placebo-controlled study to evaluate the effects of oral albuterol on pulmonary mechanics in ventilator-dependent infants at risk of developing BPD. Pediatr Pulmonol. 1991;10(3):183-90. [Medline].

  158. Stevens TP, Blennow M, Soll RF. Early surfactant administration with brief ventilation vs selective surfactant and continued mechanical ventilation for preterm infants with or at risk for respiratory distress syndrome. Cochrane Database Syst Rev. 2004;CD003063. [Medline].

  159. Stiskal JA, Dunn MS, Shennan AT, et al. alpha1-Proteinase inhibitor therapy for the prevention of chronic lung disease of prematurity: a randomized, controlled trial. Pediatrics. Jan 1998;101(1 Pt 1):89-94. [Medline].

  160. Stoelhorst GMS, Rijken M, Martens S, et al. Changes in Neonatology: Comparison of two cohorts of very preterm infants (Gestational Age <32 weeks): the Project on Preterm and Small for Gestational Age Infants 1983 and the Leiden Follow-up Project on Prematurity 1996-1997. Pediatrics. 2005;115:396-405.

  161. Subramanian KN, Weisman LE, Rhodes T, et al. Safety, tolerance and pharmacokinetics of a humanized monoclonal antibody to respiratory syncytial virus in premature infants and infants with bronchopulmonary dysplasia. MEDI-493 Study Group. Pediatr Infect Dis J. Feb 1998;17(2):110-5. [Medline].

  162. Tambunting F, Beharry KD, Hartleroad J, et al. Increased lung matrix metalloproteinase-9 levels in extremely premature baboons with bronchopulmonary dysplasia. Pediatr Pulmonol. 39(1):5-14. [Medline].

  163. Tepper RS, Morgan WJ, Cota K, Taussig LM. Expiratory flow limitation in infants with bronchopulmonary dysplasia. J Pediatr. Dec 1986;109(6):1040-6. [Medline].

  164. Thome U, Kossel H, Lipowsky G, et al. Randomized comparison of high-frequency ventilation with high-rate intermittent positive pressure ventilation in preterm infants with respiratory failure. J Pediatr. Jul 1999;135(1):39-46. [Medline].

  165. Toce SS, Farrell PM, Leavitt LA, et al. Clinical and roentgenographic scoring systems for assessing bronchopulmonary dysplasia. Am J Dis Child. Jun 1984;138(6):581-5. [Medline].

  166. Tsao PN, Wei SC, Su YN, et al. Placenta growth factor elevation in the cord blood of premature neonates predicts poor pulmonary outcome. Pediatrics. 113(5):1348-51. [Medline].

  167. Tyson JE, Wright LL, Oh W, et al. Vitamin A supplementation for extremely-low-birth-weight infants. National Institute of Child Health and Human Development Neonatal Research Network. N Engl J Med. Jun 24 1999;340(25):1962-8. [Medline].

  168. Van Marter LJ, Leviton A, Allred EN, et al. Hydration during the first days of life and the risk of bronchopulmonary dysplasia in low birth weight infants. J Pediatr. Jun 1990;116(6):942-9. [Medline].

  169. Van Marter LJ, Leviton A, Kuban KC, et al. Maternal glucocorticoid therapy and reduced risk of bronchopulmonary dysplasia. Pediatrics. Sep 1990;86(3):331-6. [Medline].

  170. Viscardi RM, Hasday JD, Gumpper KF, et al. Cromolyn sodium prophylaxis inhibits pulmonary proinflammatory cytokines in infants at high risk for bronchopulmonary dysplasia. Am J Respir Crit Care Med. Nov 1997;156(5):1523-9. [Medline].

  171. Vohr BR, Coll CG, Lobato D, et al. Neurodevelopmental and medical status of low-birthweight survivors of bronchopulmonary dysplasia at 10 to 12 years of age. Dev Med Child Neurol. Aug 1991;33(8):690-7. [Medline].

  172. Vohr BR, Garcia Coll CT. Neurodevelopmental and school performance of very low-birth-weight infants: a seven-year longitudinal study. Pediatrics. Sep 1985;76(3):345-50. [Medline].

  173. Vohr BR, Garcia-Coll C, Oh W. Language and neurodevelopmental outcome of low-birthweight infants at three years. Dev Med Child Neurol. Oct 1989;31(5):582-90. [Medline].

  174. Vohr BR, Wright LL, Dusick AM, et al. Neurodevelopmental and functional outcomes of extremely low birth weight infants in the National Institute of Child Health and Human Development Neonatal Research Network, 1993-1994. Pediatrics. Jun 2000;105(6):1216-26. [Medline].

  175. Watterberg KL, Demers LM, Scott SM, Murphy S. Chorioamnionitis and early lung inflammation in infants in whom bronchopulmonary dysplasia develops. Pediatrics. Feb 1996;97(2):210-5. [Medline].

  176. Watterberg KL, Murphy S. Failure of cromolyn sodium to reduce the incidence of bronchopulmonary dysplasia: a pilot study. The Neonatal Cromolyn Study Group. Pediatrics. Apr 1993;91(4):803-6. [Medline].

  177. Watterberg KL, Scott SM. Evidence of early adrenal insufficiency in babies who develop bronchopulmonary dysplasia. Pediatrics. Jan 1995;95(1):120-5. [Medline].

  178. Wilkie RA, Bryan MH. Effect of bronchodilators on airway resistance in ventilator-dependent neonates with chronic lung disease. J Pediatr. Aug 1987;111(2):278-82. [Medline].

  179. Wiswell TE, Bley JA, Turner BS, et al. Different high-frequency ventilator strategies: effect on the propagation of tracheobronchial histopathologic changes. Pediatrics. Jan 1990;85(1):70-8. [Medline].

  180. Wiswell TE, Graziani LJ, Kornhauser MS, et al. High-frequency jet ventilation in the early management of respiratory distress syndrome is associated with a greater risk for adverse outcomes. Pediatrics. Dec 1996;98(6 Pt 1):1035-43. [Medline].

  181. Yeh TF, Lin YJ, Huang CC, et al. Early dexamethasone therapy in preterm infants: a follow-up study. Pediatrics. May 1998;101(5):E7. [Medline].

  182. Yoon BH, Romero R, Yang SH, et al. Interleukin-6 concentrations in umbilical cord plasma are elevated in neonates with white matter lesions associated with periventricular leukomalacia. Am J Obstet Gynecol. May 1996;174(5):1433-40. [Medline].

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

Keywords

BPD, chronic lung disease, CLD, respiratory distress syndrome, RDS, synchronized intermittent mechanical ventilation, SIMV, intermittent mechanical ventilation, IMV, high-frequency jet ventilation, HFJV, antioxidant enzyme, AOE

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Namasivayam Ambalavanan, MD, MBBS, Associate Professor, Division of Neonatology, Departments of Pediatrics, Cell Biology, and Pathology, University of Alabama School of Medicine
Namasivayam Ambalavanan, MD, MBBS is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, Medical Association of the State of Alabama, Society for Pediatric Research, and Southern Society for Pediatric Research
Disclosure: Nothing to disclose.

Coauthor(s)

Thomas D Soltau, MD,, Assistant Professor, Department of Pediatrics, Division of Neonatology, University of Alabama School of Medicine
Disclosure: Mead Johnson Honoraria Speaking and teaching

Medical Editor

Steven M Donn, MD, Professor of Pediatrics, University of Michigan Medical School; Director, Division of Neonatal-Perinatal Medicine, Department of Pediatrics, CS Mott Children's Hospital, University of Michigan Health System
Steven M Donn, MD is a member of the following medical societies: American Pediatric Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Arun K Pramanik, MD, MBBS, Professor of Pediatrics, Director of Neonatal Fellowship, Louisiana State University Health Sciences Center
Arun K Pramanik, MD, MBBS is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, National Perinatal Association, and Southern Society for Pediatric Research
Disclosure: Nothing to disclose.

CME Editor

Carol L Wagner, MD, Professor of Pediatrics, Medical University of South Carolina
Carol L Wagner, MD is a member of the following medical societies: American Academy of Pediatrics, American Chemical Society, American Medical Women's Association, American Public Health Association, American Society for Bone and Mineral Research, American Society for Clinical Nutrition, Massachusetts Medical Society, National Perinatal Association, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Chief Editor

Ted Rosenkrantz, MD, Professor, Departments of Pediatrics and Obstetrics/Gynecology, Division of Neonatal-Perinatal Medicine, University of Connecticut School of Medicine
Ted Rosenkrantz, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Pediatric Society, Connecticut State Medical Society, Eastern Society for Pediatric Research, and Society for Pediatric Research
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.