eMedicine Specialties > Pediatrics: General Medicine > Pulmonology

Pleural Effusion

Author: Ibrahim Abdulhamid, MD, Assistant Professor of Pediatrics, Wayne State University; Director of Pediatric Pulmonary Medicine, Clinical Director of Pediatric Sleep Laboratory, Children's Hospital of Michigan
Coauthor(s): Debbie S Toder, MD, Director of Cystic Fibrosis Center, Department of Pediatrics, Division of Pulmonary Medicine, Assistant Professor, Wayne State University and Children's Hospital of Michigan; Vandana Batra, MD, Consulting Staff, Baybees Pediatrics
Contributor Information and Disclosures

Updated: Apr 22, 2008

Introduction

Background

Pleural effusion is defined as the collection of at least 10-20 mL of fluid in the pleural space. Pleural effusion develops because of excessive filtration or defective absorption of accumulated fluid. Pleural effusion may be a primary manifestation or a secondary complication of many disorders.

Pathophysiology

The inner surface of the chest wall and the surface of the lungs are covered by the parietal and visceral pleural, respectively, with a potential space of 10-24 µm between the 2 pleural surfaces. This space is normally filled with a small amount of fluid. However, large amounts of fluid can accumulate in the pleural space under pathologic conditions. The parietal pleura have sensory innervation and small apertures that aid in the absorption of particles and fluid.

Systemic arterial vessels supply both pleural surfaces. Lymphatic vessels from the parietal pleura drain to lymph nodes along the anterior and posterior chest wall, whereas lymphatics from the visceral surface drain to the mediastinal lymph nodes. The pleural space normally contains 0.1-0.2 mL/kg of a colorless alkaline fluid, which has less than 1.5 g/dL of protein. The venous side drains approximately 90% of accumulated fluid in the pleural space, whereas lymphatics absorb the other 10%.

A delicate balance between the oncotic and hydrostatic pressures of the pleural space and the capillary intravascular compartments regulates filtration and drainage of pleural fluid. Hydrostatic and oncotic pressures are many times higher in the plasma than in the pleural space, but the net absorption of pleural fluid is slightly higher than the net filtration forces. In addition, lymphatic drainage from the parietal pleura can surpass the rate of fluid filtration in the pleural space by several fold.

Chest-wall and diaphragmatic movements enhance absorption of pleural fluid by the vascular and lymphatic vessels. Excessive filtration of fluid can overwhelm these efficient absorptive mechanisms and lead to the formation of pleural effusion.

Pleural effusions are usually classified as transudates and exudates. Diseases that affect the filtration of pleural fluid result in transudate formation, such as in congestive heart failure and nephrosis. Transudates usually occur bilaterally because of the systemic nature of the causative disorders. Inflammation or injury increases pleural membrane permeability to proteins and various types of cells and leads to the formation of exudative effusion.

Infectious effusions are usually unilateral. However, a recent large Turkish study revealed bilateral effusion in 5% of 515 children.

Frequency

United States

American and international frequencies are similar. The prevalence of pleural infections appears to be increasing in some developed countries; this could partly be due to increased referral of patients with these conditions to tertiary-care pediatric hospitals.

Byington and colleagues reported a significant increase in the incidence of empyema in children in Utah, from 1 case per 100,000 children to 14 cases per 100,000 children between 1993 and 2003.1,2  

International

Nonbacterial infectious agents, such as viruses and Mycoplasma pneumoniae, cause more pleural effusion in children than bacterial organisms. Although bacteria are more likely than viruses to cause effusion, viral infections in children occur more frequently than bacterial infections, explaining the observation above. As many as 20% of the viral infections can cause small and transient effusions that resolve spontaneously.

Several decades ago, pleural effusion was a complication in 70% of all cases of Staphylococcus aureus pneumonia, with positive cultures in 80% of pleural fluid specimens. In the late 1970s, pleural effusion occurred in 75% of cases of pneumonia secondary to Haemophilus influenzae type b.3 In a report by Murphy et al, empyema complicated the course of pneumonia in 9 of 21 patients with Streptococcus pneumoniae pneumonia.4 Chartrand and McCracken indicated that empyema complicated the course of pneumonia in 57 of 79 patients with S aureus infections.5

Pleural effusion occurs in 6-12% of all cases of pulmonary tuberculosis (TB) in children. Of 175 Spanish children with pulmonary TB, 39 (22.1%) had pleural effusion.6

Congenital effusions, including chylothorax, occur in 1 per 10,000-15,000 live births annually. In a review of 74 patients with intrathoracic lymphomas, Chaignaud et al found pleural effusions in 10 of 14 children (71%) with lymphoblastic lymphoma and in 7 of 60 children (12%) with non-Hodgkin lymphoma.

Mortality/Morbidity

  • Most effusions caused by viral and mycoplasmal infections spontaneously resolve.
  • Empyema has a complicated course if not treated early, especially in children younger than 2 years. Thirty years ago, the mortality rate from empyema was close to 100%. At present, the mortality rate from empyema is 6-12% in infants younger than 1 year.
  • In a series of 74 children with pneumococcal empyema, 5% died, 5.5% had hemolytic uremic syndrome, 38% had bacteremia, and 51% were admitted to intensive care.7     
  • Malignant effusion worsens the patient's prognosis depending on the underlying tumor.

Sex

Pleural effusions may be more common in boys than in girls.

Clinical

History

The clinical picture and presenting symptoms depend on the underlying disease and the size of the effusion.

  • Patients with parapneumonic effusion or empyema often have a history of a recent upper respiratory tract infection, bronchitis, or pneumonia.
  • With antibiotics, most cases initially improve, then fever and chest pain recur.
  • Pleurisy causes chest pain, tightness, and shortness of breath. Pain can be referred to the shoulder.
  • Subpulmonic fluid collection can be associated with vomiting, abdominal pain, or abdominal distension caused by partial paralytic ileus.
  • Patients with parapneumonic effusion and empyema usually present with chills, fever, anorexia, tachypnea, and sweating.
  • An accumulation of a small amount of fluid may be asymptomatic.
  • A large collection of fluid leads to dyspnea, respiratory distress, dull pain, and coughing. These symptoms may vary with an alteration in body position.
  • Malignancy-related effusion often occurs after the diagnosis is established and can be associated with clinically significant and rapid weight loss.
  • Although effusion occurs in association with systemic lupus erythematosus, it is rarely the initial manifestation. Inquire about any exposure to TB, recent trauma, surgery, and central-line placement.

Physical

  • The patient may look dyspneic and anxious because of pain, discomfort, or hypoxemia.
  • A pleural rub may be the only initial manifestation during the early stage of pleurisy. The rub disappears as fluid accumulates between the pleural surfaces.
  • Dullness to percussion, decreased air entry, decreased tactile and vocal fremitus, and voice egophony over the effusion may be present but difficult to detect in younger children.
  • A large fluid collection causes fullness of the intercostal spaces and diminished chest excursion on the affected side.
  • Excessive unilateral fluid accumulation shifts the mediastinum and displaces the trachea and cardiac apex to the contralateral side.

Causes

In children, infection is the most common cause of pleural effusion. Congenital heart disease (CHD) constitutes the second most common etiology, followed by malignancy.

  • In 1968, Wolfe reported 60 cases of empyema in 98 children with pleural effusion.8 Of the remaining 38 children, 34% had nonempyemic parapneumonic effusion, 26% had malignant effusion, and 16% had effusion caused by TB.
  • In a Canadian study of 127 children with pleural effusion, Alkrinawi and Chernick reported the frequency of several types of effusions.9 About 50% of effusions were parapneumonic, 17% were caused by CHD, 10% by malignancy, 9% by renal disease, 7% by trauma, and 6% were associated with other causes.
  • In another North American report of 210 children admitted with pleural effusion, Hardie et al showed that 68% of the effusions were parapneumonic (50 of 143 associated with empyema), 11% were caused by CHD, 5% were caused by malignancy, and 3% were associated with other causes.10
  • The types of bacteria causing pleural effusions and their sensitivities to different antibiotics have changed over the years.
    • In the 1984 review by Freij et al of 227 cases of pediatric parapneumonic effusion and empyema, 76% had positive cultures.11 S aureus accounted for 29% of cases, S pneumoniae accounted for 22% of cases, and Haemophilus species accounted for 18% of cases. Most of the cases due to H influenzae were due to type B.
    • In Brook's 1990 series of 72 patients with gross pus and positive cultures from empyema, careful anaerobic cultures were included.12 A total of 93 organisms were isolated: 60 aerobic and 33 anaerobic. H influenzae, S pneumoniae, and S aureus were the predominant aerobic organisms found in association with pneumonia. Anaerobes, including Bacteroides and Fusobacterium species, were frequently found, particularly in empyema associated with aspiration pneumonia. Anaerobes were also found in empyema associated with intraoral and subdiaphragmatic abscesses.
    • In a series of 64 children with complicated parapneumonic effusions, 26 had positive cultures, 88% of which were due to S pneumoniae.13 About 26% of the S pneumoniae organisms were penicillin resistant. The decrease in complicated parapneumonic effusion caused by H influenzae is attributed to immunization. The authors speculate that the availability of broad-spectrum antibiotics effective against S aureus may account for the decrease in complicated parapneumonic effusion caused by this organism.
    • S pneumoniae is the most common organism that causes empyema in the developed countries such as the United States and the United Kingdom. S aureus is becoming a major infectious agent, especially during humid and hot seasons. Schultz et al reported a decrease in the prevalence of S pneumoniae since the use of pneumococcal conjugate vaccine and reported a predominance of S aureus, especially methicillin-resistant S aureus (MRSA), as the cause of empyema in a large children's hospital in the United States.14
    • Staphylococcus pyogenes can cause secondary pleural effusion and empyema in children with varicella infections.  
  • Pleural effusion occurs in 8-22% of all cases of pulmonary TB in children. TB pleural effusion is usually unilateral and is associated with an underlying parenchymal disease in almost 60% of cases. According to Chiu, TB pleural effusion usually presents as an acute illness.15  The exudative effusion usually has a normal leukocyte count with a lymphocytic predominance. Sputum acid-fast bacillus (AFB) stain and culture seem more effective and sensitive, especially in children pulmonary involvement.
  • Malignancy-related effusion is more often associated with lymphoblastic lymphoma than with Hodgkin disease.
  • Congenital effusions, including chylothorax, occur in 1 per 10,000-15,000 births (see Media file 9).
  • Congenital effusion can be associated with Down syndrome, diaphragmatic hernia, hydrops fetalis, polyhydramnios, and/or pulmonary hypoplasia.
  • Chylothorax may be congenital or acquired.
    • Acquired chylothorax usually occurs after surgical trauma to the thoracic duct.
    • Obstruction, thrombosis, or high pressure in the superior vena cava caused by cardiac malformation or Fontan repair of various cardiac anomalies can also cause chylothorax.
  • Unusual intrapleural fluid collections include fluids given by means of a central venous catheter that was inadvertently placed or that migrated to an intrathoracic location, as well as inadequate absorption of cerebrospinal fluid from a ventriculopleural shunt.
  • Other rare causes of pediatric pleural effusion include rupture of a pulmonary hydatid cyst into the pleural space in association with Lemierre syndrome (postpharyngitis anaerobic sepsis with thrombophlebitis of the internal jugular vein).
  • Hemothorax can occur as a result of trauma, malignancy, pulmonary infarction, and postpericardiotomy syndrome. Hemothorax has been reported from puncture of the pleura by a costal exostosis. Hemothorax should be suspected if pleural fluid hematocrit is more than 50% of peripheral blood hematocrit.

More on Pleural Effusion

Overview: Pleural Effusion
Differential Diagnoses & Workup: Pleural Effusion
Treatment & Medication: Pleural Effusion
Follow-up: Pleural Effusion
Multimedia: Pleural Effusion
References

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Further Reading

Keywords

pleural effusion, fluid, pleural space, congestive heart failure, nephrosis, infectious effusion, bilateral effusion, pleural infection, empyema, Mycoplasma pneumoniae, Staphylococcus aureus pneumonia, Haemophilus influenzae type b, Streptococcus pneumoniae pneumonia, tuberculosis, TB, congenital effusion, chylothorax, intrathoracic lymphomas, lymphoblastic lymphoma, non-Hodgkin lymphoma, hemolytic uremic syndrome, pneumococcal empyema, bacteremia, malignant effusion, parapneumonic effusion, upper respiratory tract infection, bronchitis, pleurisy
 
subpulmonic fluid collection, abdominal distension, dyspnea, respiratory distress, systemic lupus erythematosus, pleural rub, congenital heart disease, CHD, methicillin-resistant Staphylococcus aureus, MRSA, varicella, Staphylococcus pyogenes, Hodgkin disease, Down syndrome, diaphragmatic hernia, hydrops fetalis, polyhydramnios, pulmonary hypoplasia, Lemierre syndrome, hemothorax, pulmonary infarction, postpericardiotomy syndrome

Contributor Information and Disclosures

Author

Ibrahim Abdulhamid, MD, Assistant Professor of Pediatrics, Wayne State University; Director of Pediatric Pulmonary Medicine, Clinical Director of Pediatric Sleep Laboratory, Children's Hospital of Michigan
Ibrahim Abdulhamid, MD is a member of the following medical societies: American Academy of Pediatrics, American Academy of Sleep Medicine, and American Thoracic Society
Disclosure: Nothing to disclose.

Coauthor(s)

Debbie S Toder, MD, Director of Cystic Fibrosis Center, Department of Pediatrics, Division of Pulmonary Medicine, Assistant Professor, Wayne State University and Children's Hospital of Michigan
Debbie S Toder, MD is a member of the following medical societies: American Academy of Pediatrics and American Thoracic Society
Disclosure: Nothing to disclose.

Vandana Batra, MD, Consulting Staff, Baybees Pediatrics
Vandana Batra, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Medical Editor

Girish D Sharma, MD, Associate Professor, Department of Pediatrics, Rush University Medical Center, Rush Children's Hospital; Director of Pediatric Pulmonary Section and Rush Cystic Fibrosis Center
Girish D Sharma, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Royal College of Physicians of Ireland
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Heidi Connolly, MD, Associate Professor of Pediatrics and Psychiatry, University of Rochester;Director, Pediatric Sleep Medicine Services, Strong Sleep Disorders Center
Heidi Connolly, MD is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

CME Editor

Mary E Cataletto, MD, Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Associate Professor, Department of Clinical Pediatrics, State University of New York at Stony Brook
Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics, American Heart Association, and American Thoracic Society
Disclosure: Nothing to disclose.

Chief Editor

Michael R Bye, MD, Attending Physician, Pediatric Pulmonary Medicine, Columbia University Medical Center; Professor of Clinical Pediatrics, Division of Pulmonary Medicine, Columbia University College of Physicians and Surgeons
Michael R Bye, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, and American Thoracic Society
Disclosure: Merck Honoraria Speaking and teaching

 
 
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