Bronchopulmonary dysplasia or BPD is a form of chronic lung disease that develops in preterm neonates and is treated with oxygen and positive-pressure ventilation (PPV). In this paper I will discuss exactly what bronchopulmonary dysplasia is, its pathophysiology, the etiology, its clinical presentation, and any differential diagnosis of the disease. I will also present in my research the treatment and management for the disease, its prognosis, and the sequelae.
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Bronchopulmonary dysplasia formerly known as Chronic Lung Disease of Infancy is a chronic lung disorder that is more prevalent in children who were born prematurely with low birthweights, and whose lungs haven’t had the time to fully develop. White male infants seem to be at a greater risk for development, and genetics may contribute to some of these cases. It is also very common in those who have received prolonged mechanical ventilation to treat respiratory distress syndrome (RDS). It is ironic that the treatment for RDS is considered to be the prime cause of BPD. With the treatment of RDS the patient is treated with high pressures and high FiO2 over a period of time. It’s the high pressures of oxygen delivery that can result in necrotizing bronchiolitis and alveolar septal injury; this action further compromises the oxygenation of blood. Bronchopulmonary dysplasia is characterized by inflammation and scarring in the lungs. The signs and symptoms to watch out for are the oxygen demands of the infant not decreasing as they should, in some cases even increasing. Fast breathing, a fast heart rate, flared nostrils, retractions, poor weight gain, and coarse crackles may be heard upon auscultation.
The pathophysiology of BPD is linked to four factors. These factors are oxygen toxicity, barotrauma, the presence of a PDA (patent ductus arteriosus), and fluid overload. Exposure to high concentrations of oxygen can lead to edema and the thickening of the alveolar membrane. When you have prolonged exposure it causes the alveolar tissues to hemorrhage and become necrotic. As the disease progresses the interstitial spaces will become fibrotic. When the lung tries to heal itself, all of the new cells are damaged by the same factors as before, and it continues in a cycle. All of this can interfere with alveolarization and lead to alveolar simplification with a reduction in the surface area for gas exchange. Any damage to the lung during a critical stage of growth will result in significant pulmonary dysfunction. With patients who have left-to-right shunting through the PDA it is more likely that they develop pulmonary congestion and worsening compliance. With this problem the patient will need higher ventilatory pressures and oxygen percentages to help with ventilation and oxygenation; therefore they have a higher risk of BPD.
Bronchopulmonary dysplasia develops as a result of an infant’s lungs becoming irritated or inflamed. The lungs of premature infants are very fragile and aren’t fully developed, and therefore they can become easily irritated. Ventilators are used to help with the breathing by using pressure to blow air into the airways and lungs. However it is the pressures used that can irritate and harm a premature infant’s lungs, so they are used only when absolutely needed. Sometimes oxygen therapy is given to make sure that the infants’ brains, hearts, livers, and kidneys get enough oxygen to work properly. However in some cases high levels of oxygen can inflame the lining of the lungs and injure the airways, it can also slow lung development. Another cause is infections that can inflame the underdeveloped lungs of premature infants. With this problem it causes narrowing of the airways and makes it harder for infants to breathe. Lung infections can also increase the need for extra oxygen and breathing support which in turn leads to the ventilation and extra oxygen requirements. There are some studies also show that heredity plays a role in causing BPD.
Infants with bronchopulmonary dysplasia will have abnormal findings on physical exams, chestx-rays, pulmonary function testing, and histopathologic examinations. Initial findings observed shortly after birth are consistent with respiratory distress syndrome (RDS). Persistence of these abnormalities can be associated with an increased risk of bronchopulmonary dysplasia. Physical examination may reveal tachypnea, tachycardia, increased work of breathing, including retractions, nasal flaring, and grunting, as well as frequent desaturations and significant weight loss during the first 10 days of life. Infants with severe bronchopulmonary dysplasia are often extremely immature and had a very low birth weight. Their requirements for oxygen and ventilatory support often increase in the first 2 weeks of life. At weeks 2-4, oxygen supplementation, ventilator support, or both are often increased to maintain adequate ventilation and oxygenation.
Dif DX Atelectasis refers to collapse of part of the lung. It may include a lung subsegment or the entire lung and is almost always a secondary phenomenon, with no sex or race proclivities; however, it may occur more frequently in younger children than in older children and adolescents. The direct morbidity from atelectasis is transient hypoxemia due to blood flowing through the lung, which does not have normal air flow. The blood does not pick up oxygen from the corresponding alveoli. This shunting results in transient hypoxemia.
Hypertension
Patent ductus arteriosus (PDA) is one of the more common congenital heart defects. The presentation widely varies. Depending on the size of the patent ductus arteriosus, the gestational age of the neonate, and the pulmonary vascular resistance, a premature neonate may develop life-threatening pulmonary overcirculation in the first few days of life. Conversely, an adult with a small patent ductus arteriosus may present with a newly discovered murmur well after adolescence. During fetal life, the ductus arteriosus is a normal structure that allows most of the blood leaving the right ventricle to bypass the pulmonary circulation and pass into the descending aorta. Typically, only about 10% of the right ventricular output passes through the pulmonary vascular bed.
Pneumonia and other lower respiratory tract infections are the leading causes of death worldwide. Because pneumonia is common and is associated with significant morbidity and mortality, properly diagnosing pneumonia, correctly recognizing any complications or underlying conditions, and appropriately treating patients are important. Although in developed countries the diagnosis is usually made on the basis of radiographic findings, the World Health Organization (WHO) has defined pneumonia solely on the basis of clinical findings obtained by visual inspection and on timing of the respiratory rate. (See Clinical Presentation.) Pneumonia may originate in the lung or may be a focal complication of a contiguous or systemic inflammatory process. Abnormalities of airway patency as well as alveolar ventilation and perfusion occur frequently due to various mechanisms. These derangements often significantly alter gas exchange and dependent cellular metabolism in the many tissues and organs that determine survival and contribute to quality of life.
Subglottic stenosis (SGS) is a narrowing of the subglottic airway (see image below), which is housed in the cricoid cartilage. The subglottic airway is the narrowest area of the airway because it is a complete, nonexpandable, and nonpliable ring, unlike the trachea, which has a posterior membranous section, and the larynx, which has a posterior muscular section.
Tracheomalacia is a structural abnormality of the tracheal cartilage allowing collapse of its walls and airway obstruction. A deficiency and/or malformation of the supporting cartilage exists, with a decrease in the cartilage-to-muscle ratio.
Immaturity of the tracheobronchial cartilage is thought to be the cause in type I, whereas degeneration of previously healthy cartilage is thought to produce other types. Inflammatory processes, extrinsic compression from vascular anomalies, or neoplasms may produce degeneration.
Diffuse malacia of the airway of the congenital origin improves by age 6-12 months as the structural integrity of the trachea is restored gradually with resolution of the process.
Treatment and management Treatment in the NICU is designed to limit stress on infants and meet their basic needs of warmth, nutrition, and protection. Once doctors diagnose BPD, some or all of the treatments used for RDS will continue in the NICU. Such treatment usually includes: Using radiant warmers or incubators to keep infants warm and reduce the chances of infection. Ongoing monitoring of blood pressure, heart rate, breathing, and temperature through sensors taped to the babies’ bodies. Using sensors on fingers or toes to check the amount of oxygen in the infants’ blood. Giving fluids and nutrients through needles or tubes inserted into the infants’ veins. This helps prevent malnutrition and promotes growth. Nutrition is critical to the growth and development of the lungs. Later, babies may be given breast milk or infant formula through feeding tubes that are passed through their noses or mouths and into their throats. Checking fluid intake to make sure that fluid doesn’t build up in the babies’ lungs. As their condition improves, babies who have BPD are weaned or taken off NCPAP or ventilators slowly, until they can breathe on their own. These infants will likely need to continue getting oxygen therapy for some time. If your infant has moderate to severe BPD, echocardiography may be done every few weeks to months to check his or her pulmonary artery pressure. If your child needs long-term support from a ventilator, he or she will likely have a tracheostomy (TRA-ke-OS-to-me). A tracheostomy is a surgically made hole that goes through the front of the neck and into the trachea (TRA-ke-ah), or windpipe. Your child’s doctor will put the breathing tube from the ventilator through the hole. Using a tracheostomy instead of an endotracheal (en-do-TRA-ke-al) tube has several advantages. (An endotracheal tube is a breathing tube inserted through the nose or mouth and into the windpipe.) Long-term use of an endotracheal tube can damage the trachea. This damage may later require surgery to correct. A tracheostomy may allow your baby to interact more with you and the NICU staff, start talking, and develop other skills.While your baby is in the NICU, he or she also may need physical therapy. Physical therapy can help strengthen your child’s muscles and clear mucus out of his or her lungs.Infants who have BPD can recover, but many spend several weeks or months in the hospital. This allows them to get the care they need. Before your baby goes home, it’s important for you to learn as much as you can about your child’s condition and how it’s treated. Your baby may continue to have some breathing symptoms after he or she leaves the hospital. Your child will likely continue on all or some of the treatments that were started at the hospital, including:Medicines, such as bronchodilators, steroids, diuretics, and caffeine. Oxygen therapy and/or breathing support from NCPAP or a ventilator. Extra nutrition and calories, which may be given through a feeding tube. Preventive treatment with a medicine called palivizumab for severe respiratory syncytial virus (RSV). This common virus leads to mild, cold-like symptoms in adults and older, healthy children. However, in infants-especially those in high-risk groups-RSV can be more serious, leading to severe breathing problems. Your child also should have regular checkups with and timely vaccinations from a pediatrician. This is a doctor who specializes in treating children. If your child needs oxygen therapy or a ventilator at home, a pulmonary specialist may help with long-term medical care and make treatment recommendations. 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.
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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.
Medication Summary
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 dyspl
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