INTRODUCTION — Although pleural effusions in neonates are rare, they can cause significant respiratory distress. In addition to acute management of infants with respiratory compromise, identifying the underlying cause guides management decisions and helps to predict the chronicity of the course and duration of care.
The approach to the care of a neonate with pleural effusions, including initial acute management and diagnostic evaluation, will be reviewed here. The management of chronic neonatal pleural effusions is discussed separately. (See "Management of chronic pleural effusions in the neonate".)
DEFINITIONS
●The pleural space is defined as the potential space bound by the visceral and parietal pleura mesothelial membranes that line the chest wall and lung surface (image 1).
●Pleural effusion is defined as an abnormal accumulation of fluid within the pleural space. It occurs when production exceeds absorption. Normally, there is a balance between the production of pleural fluid, thought to be produced by the visceral pleura, and absorption by the lymphatics of the parietal pleura. Pleural effusions occur when there is excessive pleural fluid production, reduced absorption, or a combination of the two.
The mechanisms of pleural liquid turnover under normal and abnormal (resulting in accumulation of pleural fluid) conditions are discussed separately. (See "Mechanisms of pleural liquid turnover in the normal state" and "Mechanisms of pleural liquid accumulation in disease".)
EPIDEMIOLOGY — Data are limited on the incidence of neonatal pleural effusions. The reported incidence ranges from 0.06 to 2.2 percent for neonates admitted to a neonatal intensive care unit [1,2]. The risk of pleural effusions is greater for infants who undergo surgery for congenital heart disease. (See 'Acquired' below.)
ETIOLOGY
Based on timing of presentation — The underlying etiology of neonatal pleural effusions can be separated based on timing of pleural fluid accumulation:
●Antenatal – Fetal or congenital causes
●Postnatal – Acquired causes
Case series report an antenatal condition in approximately one-third of neonatal cases [1,3]. In tertiary care centers with an active cardiovascular surgical center, up to 90 percent of cases are postnatally acquired [4].
Antenatal (fetal) — Causes of antenatal pleural effusion include congenital heart disease (CHD), infection, and chylothorax. Many of these disorders may present as hydrops fetalis or as a manifestation of chromosomal anomalies and/or cardiovascular/pulmonary anomalies.
In one case series, the following conditions were identified in the 20 cases of antenatally detected pleural effusions [1]:
●Hydrops fetalis (n = 11)
●Congenital chylothorax (n = 4)
●Chromosomal syndrome (n = 3)
●Twin-twin transfusion (n = 2)
●Lymphangiectasia (n = 2)
●Unknown (n = 2)
●One case of each of the following – CHD, infection, cervical teratoma, and meconium peritonitis
Hydrops fetalis — Hydrops fetalis is defined as abnormal fetal fluid collection in a minimum of two anatomic locations caused by dysregulation of the net fluid movement between the vascular and interstitial spaces. Many infants born with hydrops fetalis will have pleural effusions, which are usually bilateral. In some cases, the pleural effusions are large and can cause immediate respiratory distress at birth. (See "Postnatal care of hydrops fetalis" and 'Antenatal presentation' below and 'Management: Antenatal effusion' below.)
Conditions associated with hydrops fetalis include chromosomal syndromes, structural abnormalities, especially CHD, metabolic disorders, hematologic disorders resulting in severe anemia, and infection (table 1). More detailed discussions of the etiology of hydrops fetalis are found separately. (See "Postnatal care of hydrops fetalis", section on 'Epidemiology and etiology' and "Alloimmune hemolytic disease of the newborn: Postnatal diagnosis and management", section on 'Hydrops fetalis' and "Nonimmune hydrops fetalis", section on 'Etiology and prenatal management of disorders associated with hydrops'.)
Congenital chylothorax — Neonatal chylothorax results from the accumulation of chyle in the pleural space. It may be either congenital or an acquired condition [1,5,6]. Congenital chylothorax is most likely due to abnormal development or obstruction of the lymphatic system and is often associated with hydrops fetalis [1,5-7]. It can be idiopathic or may be associated with various chromosomal anomalies, including trisomy 21 (image 2) [1,6,8], Turner syndrome [9], Noonan syndrome [10-12], and other genetic abnormalities [13-16]. Congenital pulmonary lymphangiectasia and generalized lymphangiomatosis have also been reported to be associated with congenital chylothorax [17-19]. Several case reports indicate that congenital chylothorax can recur in subsequent offspring, suggesting a possible underlying genetic etiology [19-21].
Congenital chylothorax is rare, with an estimated incidence of 0.004 percent, or 1 case per 24,000 births [12]. Based on two case series, mortality ranges from 30 to 50 percent [6,22]. Most cases were diagnosed prenatally, and intrauterine interventions (eg, thoracentesis and thoracic-amniotic shunting) were performed in approximately 40 percent of cases. In both case series, preterm delivery was a risk factor for death. In one of the studies, successful reversal of hydrops due to thoracic-amniotic shunting improved survival [22]. (See "Nonimmune hydrops fetalis", section on 'Thoracic and lymphatic abnormalities'.)
It is important to identify infants with chylothorax, as there are specific issues that need to be addressed in the management of these patients. (See "Management of chronic pleural effusions in the neonate", section on 'Chylous effusions'.)
Congenital heart disease/vascular malformations — Various congenital heart disorders (ie, structural heart disease and cardiac arrhythmias), especially those that result in fetal heart failure, may be associated with pleural effusions and/or hydrops fetalis (see "Nonimmune hydrops fetalis", section on 'Cardiovascular abnormalities') [1,6,23]. Other rare vascular lesions associated with pleural effusions based on case reports include bilateral agenesis of the superior vena cava [24], glomuvenous malformations [25], and placental chorangioma [26].
Pulmonary malformations — Pulmonary malformations associated with fetal pleural effusions and hydrops fetalis include bronchopulmonary sequestration [27], pulmonary lymphangiectasia [17], pulmonary lymphatic hypoplasia [28], and congenital pulmonary airway malformation. The effusions may be transudates or chylous depending on the underlying cause (table 2). (See "Bronchopulmonary sequestration" and "Congenital pulmonary airway malformation" and "Nonimmune hydrops fetalis", section on 'Thoracic and lymphatic abnormalities'.)
Infection — Congenital herpes simplex viral (HSV) infections [29,30] and parvovirus [31] have been reported to cause congenital pleural effusions. Bacterial infections can also cause effusions, including group B streptococcal (GBS) infection [32]. (See "Group B streptococcal infection in neonates and young infants", section on 'Pneumonia'.)
Other causes — Other rare causes of congenital pleural effusions include:
●Obstructive uropathy [33,34]
●Congenital malignancies and benign tumors as noted in case reports of diaphragmatic rhabdomyosarcoma [35], Langerhans cell histiocytosis [36], monoblastic leukemia [37], thoracic hamartomas [38,39], and intrapericardial teratomas [40]
Acquired — Similar to congenital pleural effusions, there are numerous causes for acquired pleural effusions but the majority of cases are due to injury to the thoracic duct (eg, complications of thoracic surgery, central venous catheter insertions, or chest tube placement), followed by infection associated with either pneumonia or sepsis, and hemothorax [1,3,41]. Rare causes of neonatal acquired disease include superior vena cava syndrome and hypoproteinemia caused by congenital nephrotic syndrome.
Traumatic chylothorax — Injury to the thoracic duct resulting in chylothorax is the most frequent cause of acquired neonatal pleural effusions [4,42].
●Congenital heart disease – Although surgery for CHD is the most commonly reported antecedent event, the complication rate of chylothorax during CHD surgery varies based on case series from 1 to 9 percent [43-45]. Factors associated with acquired chylothorax during cardiac surgery included younger age and size at surgery, increased time of cardiopulmonary bypass and crossclamp times, and delayed chest closure.
●Congenital diaphragmatic hernia – Chylothorax is a common complication in infants who undergo repair of a congenital diaphragmatic hernia, with a reported incidence of approximately 5 to 6 percent [45,46].
●Esophageal atresia – Chylothorax has been reported following repair of esophageal atresia [47].
Catheter-related etiologies — Centrally placed catheters can result in pleural effusions by:
●Extravasation of intravenous fluids into the thoracic cavity [48-52]
●Venous hypertension from intravascular blood clots resulting in pleural effusions, which are often chylous [53,54]
●Esophageal perforation
Hemothorax — Neonatal hemothorax pleural effusions (blood in the pleural space) are associated with hemorrhagic disease of the newborn, disseminated intravascular coagulation, and vascular malformations [55]. Postoperative hemothorax can also occur, which is one reason why chest tubes are left in place following surgery involving the thoracic cavity.
Other causes — Other acquired causes for neonatal pleural effusions include postnatal infections (sepsis and pneumonia), hypoalbuminemia, which may be due to congenital nephrotic syndrome, transient tachypnea of the newborn, and initiation of peritoneal dialysis [1,2].
PRESENTATION
Antenatal presentation — Antenatal pleural effusions are usually detected by ultrasonography (image 3 and image 4) and are often a component of hydrops fetalis.
Large bilateral pleural effusions may cause immediate respiratory distress at birth in the delivery room. In addition, long-standing effusions developed prior to 20 weeks of gestation may result in pulmonary hypoplasia, which may also present as neonatal respiratory distress (image 5). Delivery room management should anticipate the needs of the most severely affected patients, which may include endotracheal intubation, positive pressure ventilation, and evacuation of the pleural effusion(s). These neonates are at risk for pneumothorax or pneumomediastinum because of pulmonary hypoplasia and poor lung compliance. (See 'Management: Antenatal effusion' below and "Postnatal care of hydrops fetalis", section on 'Initial resuscitation' and "Pulmonary air leak in the newborn".)
Postnatal presentation — Postnatal pleural effusions are typically detected by chest radiography (image 6 and image 7). Clinical findings vary depending on the size of the pleural effusions from those without symptoms to those in respiratory failure.
●If the pleural effusion is small, patients are asymptomatic and the pleural effusion may be noted as an incidental finding.
●Symptomatic infants with large bilateral effusions typically present with respiratory distress that is manifested by tachypnea, retractions, and cyanosis. Pleural effusion associated with intravenous fluid extravasation or hemothorax can be rapid and catastrophic (image 8), resulting in acute cardiovascular collapse. Physical findings, although of less value in the infant than in older individuals, include reduced breath sounds and dullness to percussion.
Chest radiography is usually limited to a frontal supine view. In this view, pleural effusions are identified as the characteristic white-out appearance of the affected side. If the status of the infant permits, frontal, lateral, oblique, and decubitus radiographic views can demonstrate the shift of pleural fluid as it layers in the most dependent part of the thoracic cavity. The use of bedside ultrasound may provide better delineation of the effusion with less radiation and avoids the need to position a severely ill neonate.
Conditions in which pleural effusions may be observed include:
●Congenital diaphragmatic hernia (see "Congenital diaphragmatic hernia in the neonate", section on 'Diagnosis')
●Transient tachypnea of the newborn (see "Transient tachypnea of the newborn", section on 'Diagnosis')
●Neonatal pneumonia (see "Neonatal pneumonia", section on 'Diagnostic imaging')
INITIAL ACUTE MANAGEMENT — The initial management and evaluation are dependent on the timing of presentation (antenatal versus postnatal) and the infant's cardiorespiratory status. For infants with respiratory compromise due to significant pleural effusions regardless of the clinical setting, needle aspiration is needed to drain fluid to achieve adequate ventilation.
Management: Antenatal effusion — Affected infants with antenatally detected large pleural effusions typically have hydrops fetalis with collection of fluid in other locations (eg, ascites, skin edema, or pericardial effusion) (see 'Hydrops fetalis' above and "Postnatal care of hydrops fetalis").
Prenatal care — In severe cases, fetal thoracentesis may have been performed in an attempt to prevent pulmonary hypoplasia during the second trimester, or in fetuses with large effusion, placement of a pleuroamniotic shunt. In fetuses with hydrops fetalis, ex utero intrapartum treatment (EXIT) has also been used to allow drainage of pleural fluid in the partially delivered and intubated fetus prior to clamping of the umbilical cord, which maintains the fetoplacental circulation [20,56,57]. (See "Nonimmune hydrops fetalis", section on 'Etiology and prenatal management of disorders associated with hydrops' and "Bronchopulmonary sequestration: Prenatal diagnosis and management", section on 'Routine obstetric management' and "Bronchopulmonary sequestration: Prenatal diagnosis and management", section on 'Delivery'.)
Delivery room — For fetuses that are diagnosed with potentially clinically significant pleural effusions, the delivery should be planned for at a tertiary center with staff capable of resuscitating and managing neonates with respiratory compromise. In the delivery room, the neonatal team should anticipate the needs of the most severely affected patient and be prepared to provide respiratory support that includes intubation, positive pressure ventilation, oxygen supplementation, and removal of fluid by needle aspiration. (See 'Needle aspiration' below and "Postnatal care of hydrops fetalis", section on 'Initial resuscitation' and "Neonatal resuscitation in the delivery room".)
Effusions resulting from hydrops fetalis often do not recur or do so slowly after needle aspiration and fluid removal, and further intervention is often not required.
Management: Postnatal effusion — The initial management of postnatal pleural effusions is dependent on whether the infant is symptomatic and requires immediate intervention.
Symptomatic infants — In infants with respiratory distress, typically due to large pleural effusions, respiratory support is provided including oxygen supplementation, and as appropriate, positive pressure ventilation and intubation. Needle aspiration and removal of fluid may be needed to restore adequate ventilation even in the case of a hemothorax. Pleural fluid is sent for analysis and culture. Empiric antibiotic therapy is started in patients for whom infection is suspected as a cause of the effusion pending culture results. (See 'Needle aspiration' below and 'Evaluation of pleural fluid' below.)
Asymptomatic infants — In asymptomatic neonates, small effusions can be detected incidentally by chest radiography. These effusions typically do not cause respiratory or circulatory compromise, and as a result, they are managed conservatively without intervention and ongoing surveillance. In cases where infection is suspected, diagnostic thoracentesis may be performed to obtain fluid for analysis and culture, followed by administration of empiric antibiotics.
Monitoring includes serial chest radiographs to follow effusion size and/or resolution, and ongoing cardiorespiratory assessment, including respiratory rate, heart rate, oxygen saturation, and periodic measurement of blood gasses to assess the stability of the infant's acid-base status. The frequency of testing is dependent on the clinical setting. If there is onset of respiratory distress or deterioration in oxygenation and/or acid-base status, then intervention, including needle aspiration or thoracostomy, may be warranted.
Needle aspiration — In infants with respiratory compromise, it may be necessary to drain the pleural effusion by needle aspiration if adequate ventilation is not achieved after intubation and the initiation of positive pressure ventilation.
Drainage should be performed under sterile conditions, with the infant in a supine position using an 18- to 20-gauge intravascular catheter. In this position, because the fluid layers in the posterior chest, the needle should be introduced into the pleural space in the midaxillary line in the 5th or 6th intercostal space and directed posteriorly. Placement of a three-way stopcock on the catheter after removal of the needle will facilitate aspiration of the effusion. If the effusions are bilateral, drainage is generally performed initially on the right side because it has a larger lung volume than the left.
The volume of fluid removed depends upon the size of the effusion and infant. It should be enough to restore ventilation and circulation, but not so much as to put the infant at risk of hypovolemia if the fluid reaccumulates rapidly.
Once the acute situation has been resolved, the catheter(s) is removed. Monitoring is performed to detect possible reaccumulation of the effusion and any negative effects on the cardiovascular system due to loss of fluid, which may occur with excessive movement of fluid from the vascular space into the pleural space. If there are signs of hypovolemia (tachycardia, poor peripheral perfusion, or hypotension), normal saline should be administered initially as a 20 mL/kg intravenous infusion to restore intravascular volume followed by close hemodynamic monitoring.
Culture and empiric antibiotics — An aliquot of the aspirated fluid should be sent for diagnostic evaluation including culture. Empiric, broad-spectrum intravenous antibiotic therapy is initiated pending culture results if the fluid appears purulent, fluid analysis is suggestive of an infectious process, and/or the infant appears to be severely-ill. In our center, we generally use a combination of ampicillin and gentamicin typically used to treat neonatal sepsis. (See 'Evaluation of pleural fluid' below and "Management and outcome of sepsis in term and late preterm neonates", section on 'Initial empiric therapy' and "Epidemiology, clinical presentation, and evaluation of parapneumonic effusion and empyema in children" and 'Initial acute management' above and "Epidemiology, clinical presentation, and evaluation of parapneumonic effusion and empyema in children", section on 'Pleural fluid analysis'.)
EVALUATION OF PLEURAL FLUID — Analysis of pleural fluid samples may be helpful in separating pleural effusions into etiologic categories based on pathogenesis (transudative versus exudative process).
Pleural fluid is generally obtained through the removal of fluid via needle aspiration performed to improve the patient's pulmonary status. Diagnostic thoracentesis is rarely performed, but is indicated if infection is suspected.
Analysis includes:
●Gross appearance – Diagnostic clues can be obtained during the gross inspection of the fluid:
•Red appearance is suggestive of active bleeding.
•Brown appearance is suggestive of old blood.
•White appearance is suggestive of chylothorax if feeding has been initiated. If the infant has had no enteral feeds, the fluid is typically straw colored.
•Pale yellow clear appearance is suggestive of transudate due to heart failure, hypoalbuminemia, or extravasation of intravenous fluid.
•Cloudy appearance and/or pus is suggestive of infection due to bacterial or fungal pneumonia/empyema.
●Biochemical analysis (electrolytes, lactate dehydrogenase [LDH], protein content, lipid level and profile) and cell count. Serum electrolytes, protein, albumin, and LDH should also be obtained simultaneously for comparison with the pleural fluid sample. This analysis is used to differentiate whether the pleural fluid is due to a transudative or exudative process. (See 'Transduate versus exudate' below.)
●In patients with a suspected underlying infection, microbiologic analysis including Gram stain and bacterial culture should be performed.
●In patients with suspected chylothorax, the analysis is dependent on whether the infant was fed. The fluid will be clear/yellow to slightly cloudy in the unfed state and will quickly become milky following feeding, as chylomicrons appear in the fluid. After fat-containing feedings have been initiated, triglyceride levels are elevated (>110 mg/dL) and chylomicrons are detected by lipoprotein electrophoresis. Lymphocytes predominate in the differential cell count of chyle [5].
Transduate versus exudate — Based on the results of the pleural fluid analysis, the effusion(s) can be classified into a transudative versus an exudative process. Differentiating between the two processes is based on adult data (ie, Light's criteria), as similar neonatal information is not available. (See "Diagnostic evaluation of a pleural effusion in adults: Initial testing", section on 'Pleural fluid analysis'.)
●Transudate – Transudates are largely due to imbalances in hydrostatic and oncotic pressures in the chest. Fluid moves through an intact vascular wall into the pleural space due to an elevated vascular hydrostatic and/or oncotic pressure. The transudative fluid has a low protein concentration (<3 g/dL) and LDH levels and few or no cellular elements. In the neonate, transudative effusions are usually the result of venous hypertension or obstruction due to congenital heart disease, or pulmonary malformations. Other less common causes of neonatal transudative pleural effusions include hypoalbuminemia (eg, congenial nephrotic syndrome), and extravasation of crystalloid fluid from venous lines. In the latter setting, the glucose and electrolyte composition in the pleural fluid is similar to that of the infused fluid.
●Exudate – An exudative effusion results primarily from pleural and lung inflammation or from impaired lymphatic drainage of the pleural space. Exudative fluid compared with transudate typically have higher protein and LDH concentration, and cellular elements. The most common cause of neonatal exudative pleural effusion is chylothorax. Other neonatal causes of exudative pleural effusions include pneumonia (empyema) and rare malignancies and autoimmune disorders.
SUBSEQUENT MANAGEMENT — Subsequent management is primarily dependent on the likelihood and rapidity of resolution and the risk of recurrence. In most causes of neonatal effusions, acute drainage and treatment of the underlying etiology result in resolution and a low probability of recurrence. In patients who continue to be symptomatic, needle aspiration is repeated two or three times until it is clear that the effusion(s) will either clear or continue. Chylothorax is typically a chronic process and further management is usually required.
Management of chronic pleural effusions, including chylothorax, is discussed separately. (See "Management of chronic pleural effusions in the neonate".)
SUMMARY AND RECOMMENDATIONS
●Pleural effusion is defined as an abnormal accumulation of fluid within the pleural space. It occurs when pleural fluid production exceeds absorption. Although pleural effusions in neonates are rare, they can cause significant respiratory distress. The initial approach of caring for a neonate with pleural effusion is to provide respiratory support as needed and to identify the underlying cause, which can guide further management decisions and predict the chronicity of the course and duration of care. (See 'Definitions' above and 'Epidemiology' above and 'Presentation' above.)
●Approximately one-third of neonatal pleural effusions are identified antenatally and the remaining two-thirds are detected after delivery (postnatally). (See 'Etiology' above.)
●Causes of antenatal pleural effusion include hydrops fetalis, obstruction or maldevelopment of the lymphatic system (ie, congenital chylothorax), congenital heart disease (CHD), pulmonary malformations, infection, and chromosomal syndromes. (See 'Antenatal (fetal)' above.)
●Postnatal pleural effusions are typically acquired and usually caused by injury to the thoracic duct due to complications of thoracic surgery, central venous catheter insertions, or chest tube placement. Other associated disorders include infection (eg, pneumonia or sepsis), hemothorax due to bleeding disorders, nephrotic syndrome (hypoalbuminemia), peritoneal dialysis, and transient tachypnea of the newborn. (See 'Acquired' above.)
●Antenatal pleural effusions are usually detected by prenatal ultrasonography (image 3 and image 4). Antenatal interventions should be considered in fetuses with large bilateral effusions with evidence of compromised pulmonary development. Antenatal pleural effusions are often a component of hydrops fetalis (abnormal fetal fluid collection in a minimum of two anatomic locations), which may be accompanied by pulmonary hypoplasia (image 5). (See 'Antenatal presentation' above and 'Prenatal care' above.)
Large bilateral pleural effusions in the fetus may cause immediate respiratory distress at birth, and delivery room management should anticipate the needs of the most severely affected neonate. This may include endotracheal intubation, positive pressure ventilation, oxygen supplementation, and evacuation of the effusion(s). (See 'Delivery room' above.)
●Postnatal pleural effusions are typically detected by chest radiography (image 6 and image 7). (See 'Postnatal presentation' above.)
•Asymptomatic infants – Pleural effusion may be an incidental finding in an asymptomatic neonate. These effusions typically do not cause respiratory or circulatory compromise. In asymptomatic neonates, we recommend conservative management without intervention (Grade 1C). Monitoring (respiratory rate, heart rate, oxygen saturation, and measurement of blood gases) is performed to detect any deterioration in cardiorespiratory status that would warrant intervention. (See 'Asymptomatic infants' above.)
•Symptomatic infants – Symptomatic infants with large bilateral effusions typically present with respiratory distress (ie, tachypnea, retractions, and cyanosis). Physical findings, although of less value in the infant than in older individuals, include reduced breath sounds and dullness to percussion. Infants with severe respiratory compromise require respiratory support, including oxygen supplementation, positive pressure ventilation, endotracheal intubation, and evacuation of the effusion(s). (See 'Symptomatic infants' above.)
●For infants with pleural fluid effusion in whom adequate ventilation is not achieved after intubation and the initiation of positive pressure ventilation, we recommend needle aspiration and removal of fluid (Grade 1C). Once the acute situation has been resolved, the catheter(s) is removed. Monitoring is performed to detect possible reaccumulation of the effusion or compromise of the cardiovascular system due to hypovolemia from removal of fluid. (See 'Needle aspiration' above.)
●For infants in whom the aspirated fluid appears purulent, fluid analysis is suggestive of an infectious process, and/or the infant appears to be severely-ill, we suggest administering empiric intravenous antibiotic therapy (Grade 2C). In our center, we generally use a combination of ampicillin and gentamicin typically used to treat neonatal sepsis. (See 'Culture and empiric antibiotics' above and "Management and outcome of sepsis in term and late preterm neonates", section on 'Initial empiric therapy' and "Epidemiology, clinical presentation, and evaluation of parapneumonic effusion and empyema in children" and 'Initial acute management' above and "Epidemiology, clinical presentation, and evaluation of parapneumonic effusion and empyema in children", section on 'Pleural fluid analysis'.)
●Further diagnostic evaluation is performed to determine the etiology of the pleural effusions in symptomatic patients with large- or moderate-size pleural effusions in whom a needle aspiration has been performed. In these patients, aspirated pleural fluid is sent for analysis that includes electrolyte levels, protein content, lactate dehydrogenase (LDH) level, lipid level and profile, and cell count with differential. In patients with a suspected underlying infection, microbiologic analysis including Gram stain and bacterial culture should be performed. (See 'Evaluation of pleural fluid' above.)
●Subsequent management is primarily dependent on the likelihood and rapidity of resolution, and the risk of recurrence. In most causes of neonatal effusions, treatment of the underlying etiology results in resolution and with low probability of recurrence. (See 'Subsequent management' above and "Management of chronic pleural effusions in the neonate".)
