Pediatric Empyema

Updated: Sep 30, 2016

Author: Peter H Michelson, MD; Chief Editor: Girish D Sharma, MD, FCCP, FAAP

Overview
Background
Bacterial pneumonia with associated pleural empyema is the most common cause of pleural
effusion found in the pediatric population. Parapneumonic effusions are predominately exudative
and occur in as many as 50-70% of patients admitted with a complicated pneumonia.

See the image below.

Most parapneumonic effusions

treated with the appropriate antimicrobials of sufficient duration resolve without the
development of complications or sequelae. The series of radiographs represent a patient treated
with thoracentesis alone. Figure A illustrates the patient at presentation. Note the amount of fluid
present. In Figure B, the radiograph demonstrates progression of the pleural fluid accumulation
with further airspace disease and scoliosis noted. Despite the radiographic evidence of disease
progression, the patient was clinically improving. Figure C illustrates the radiograph at follow-
up, 6 months following completion of therapy. Resolution of the parapneumonic effusion with
no evidence of pleural thickening or fibrosis occurred.

The pulmonary infections of these patients extend into the pleural space and require more
extensive therapy, with associated increased morbidity and extended hospital stay. Involvement
of the pleural space with pulmonary infections has been recognized since ancient times. Aristotle
identified the increased morbidity and mortality associated with empyema and described
drainage of empyema fluid with incision. The practice of surgical drainage as part of therapy for
empyema has continued into the era of modern medicine. In his 1901 text, The Principles and
Practice of Medicine, Sir William Osler, MD, stated that empyema should be treated as an
ordinary abscess, "with incision and drainage."[1] Of note, Osler underwent a rib resection for
his own postpneumonic empyema, from which he ultimately expired.

Complicated parapneumonic effusions are appearing more frequently by most accounts, with
reported increases in incidence rates in both in Europe and the United States. In England, the rate
of admission with a diagnosis of empyema increased over the last decade, most notably in
children aged 1-4 years. In addition, the identification of Streptococcus pneumoniae as the
primary pathogen has also been reported, both in both the United States and abroad.[2] Whereas
the overall rate of parapneumonic effusions may have stabilized over the last decade, the rate of
bacterial resistance, specifically methicillin-resistant Staphylococcus aureus, has predominated.
[3]

Pathophysiology
The definition of a parapneumonic effusion is a pleural effusion associated with either bacterial
pneumonia or lung abscess or, rarely, external introduction of organisms associated with chest
wall trauma. The development of parapneumonic effusions is gradual, with the pleural fluid
collection most commonly divided into 3 stages. The progression of pleural fluid collection
evolves from stage 1-3.

In stage 1, the exudative stage, the pleural inflammation from a contiguous infection results in
increased permeability and a small fluid collection. At this stage, the effusion is thin and
amenable to thoracentesis alone, contains neutrophils, has normal pH and glucose levels, and is
often sterile. Stage 2, the fibrinopurulent stage, is characterized by invasion of the organism into
the pleural space, progressive inflammation, and significant polymorphonuclear (PMN)
leukocyte invasion. The increase in fibrin deposition also results in partitions or loculations
within the pleural space. Inflammation is characterized by progressive decreases in the pleural
fluid glucose and pH levels and increased protein and lactate dehydrogenase (LDH) levels. The
last stage, stage 3, is the organizing stage, in which a pleural peel is created by the resorption of
fluid and is associated with fibroblast proliferation that can result in parenchymal entrapment.[4]

Empyema is defined by the presence of intrapleural pus and, for definition purposes, represents
an advanced parapneumonic effusion. Complicated parapneumonic effusions (CPE) refer to
those fluid collections that require thoracentesis, tube thoracostomy, or surgery for their
resolution.

The accumulation of pleural effusions can rapidly occur in the presence of infection. The pleural
surface is a mesothelial membrane that covers the lungs and chest wall. The resultant pleural
space is a potential space, containing only small volumes of transudative fluid, with a protein
content of less than 1.5 g/dL. This fluid is normally composed of lymphocytes, macrophages,
and mesothelial cells, with an absence of neutrophils. Interaction of the mesothelium with the
invading bacteria, PMNs, and resultant inflammatory mediators can increase pleural
permeability. Further PMN recruitment ensues, which results in the increased production of
neutrophil chemotactic mediators, ultimately leading to significant pleocytosis.

Activation of the coagulation cascade is common with pleural empyema. The pleural
inflammatory response favors increased procoagulant activity, as well as depressed fibrinolytic
activity, which favors fibrin deposition. Loculations result with these fibrin strands covered
rapidly by a meshwork of fibroblasts that both proliferate and deposit basement membrane
proteins onto the surface of the pleura. These proteins obscure the separation of the visceral and
parietal pleura and lead to the formation of the pleural peel.

Following initiation of appropriate therapy, the inflammatory cellular and cytokine production
recedes, and the PMN predominance of the parapneumonic effusion decreases. An influx of
macrophages assists in the clearance of PMNs, with resolution of the inflammatory process.
Migration of pleural mesothelial cells into areas of denuded mesothelium results in the
reepithelialization of the pleura and recovery of normal function; however, following exuberant
pleural inflammation, the potential for pleural fibrosis and restrictive lung disease is enhanced.
The mechanisms that lead to either the development of pleural fibrosis or pleural repair with
normal recovery are not well understood and need further investigation and characterization.

Epidemiology
Frequency

United States

Parapneumonic effusions are predominately exudative and occur in as many as 50-70% of

patients admitted with a complicated pneumonia. These patients have extension of their
pulmonary infection into the pleural space and require more extensive therapy, with associated
increased morbidity and extended hospital stay. Although incidence rates appear to be
increasing, they remain at approximately 10 cases per 10,000.[3]

International

With an increased incidence of pneumonia and tuberculosis worldwide, the frequency of CPE is
likely to be even higher. Literature emerging from Asia suggests empyema is a significant
concern, although these retrospective reviews cannot accurately describe the incidence, and
variable rates of identification suggest more standardized practices are needed.[5]

Mortality/Morbidity

Early recognition of pneumonia with parapneumonic effusion, effective intervention to identify

the infecting organism, and initiation of definitive therapy reduce the morbidity and
complications associated with this process.

Age

The bacteriology of the infection varies with patient age. In the pediatric population, the most
commonly implicated organisms are S pneumoniae, S aureus, and group A streptococci. The
latter may be observed as a complication of an infectious skin disorder, such as varicella,
impetigo, or infectious eczema. Haemophilus influenzae is rarely encountered since the advent of
the H influenzae B vaccine. Methicillin-resistant S Aureus is a concern in the older age group.

Presentation
History
Clinical manifestations of empyema include the following:

 Most patients with empyema present with clinical manifestations of bacterial pneumonia.
Their symptoms are characterized by an acute febrile response, pleuritic chest pain,
cough, dyspnea, and, possibly, cyanosis.
 The inflammation of the pleural space may cause abdominal pain and vomiting.
 Patients frequently exhibit characteristic splinting of the affected side.
 Symptoms may be blunted, and fever may not be present in patients who are
immunocompromised.

Physical
Physical examination findings can vary as well.

 Auscultation reveals crackles, decreased breath sounds, and, possibly, a pleural rub, if the
process is recognized before a large amount of fluid accumulates.
 Dullness to percussion and decreased breath sounds are likely but difficult to elicit in the
younger child, who, because of discomfort, may be less cooperative with the
examination.
 Physical findings and presentation may vary depending on the organism and the duration
of the illness.

Causes
See the list below:
  Increased pleural permeability associated with pneumonia or lung abscesses, as well as
contiguous infections of the esophagus, mediastinum, or subdiaphragmatic region, may
extend to involve the pleura.
 Similarly, retropharyngeal, retroperitoneal, or paravertebral processes may extend to
adjacent structures and involve the pleura, as well.
 Host factors that contribute to alterations in pleural permeability, such as noninfectious
inflammatory diseases, infection, trauma, or malignancy, may allow accumulation of
fluid in the pleural space, which becomes secondarily infected.
 The bacteriology of the pleural space varies with patient age. In the pediatric population,
the most common implicated organisms are S pneumoniae, S aureus, and group A
streptococci. H influenzae is rarely observed since the advent of the H influenzae B
vaccine.
 Because of the use of oral antibiotics before the recognition of the parapneumonic
effusion, most specimens cultured are sterile; thus, the relative incidences of the
aforementioned organisms are not known.
 Anaerobic infections secondary to aspiration and fungal or mycobacterial infections in
immunosuppressed patients are also reported.
 Mycoplasma pneumoniae, viruses, and atypical pneumonias can also present with
exudative pleural effusions, although mononuclear cells primarily characterize them.
 A study investigated the risk factors of empyema after acute viral infection and the
association between empyema and the use of nonsteroidal anti-inflammatory drugs
(NSAIDs). The study found that NSAIDs use during acute viral infection is associated
with an increased risk of empyema in children.[6]

DDx
Differential Diagnoses
 Emergent Management of Pleural Effusion
 Heart Failure, Congestive
 Hemothorax
 Pediatric Nephrotic Syndrome
 Pulmonary Infarction
 Pulmonary Sequestration Imaging and Diagnosis

Workup

Workup
Laboratory Studies
The following studies are indicated in empyema:

 CBC count
 Blood culture: Blood culture is obtained to assist in the identification of the offending
organism. In pediatric patients, in whom sputum production is uncommon, identifying the
cause of the pulmonary symptoms early in the course of a pulmonary infection is
difficult. However, with parapneumonic effusions, the patient may become bacteremic as
the organism invades into the pleural space, and a blood culture may reveal the organism.
 Serum lactate dehydrogenase (LDH) level
 Total protein level
 Glucose concentration
 Bacterial, mycobacterial, and fungal cultures
 Serologic studies of the aspirated pleural fluid
 pH level
 Amylase concentration
 Lipid stain or triglyceride level
 Cell count and differential: Although the pleural fluid obtained at thoracentesis is
typically purulent, with an elevated WBC count and a predominance of
polymorphonuclear cells (PMNs), an effusion evaluated early in the infectious process
may well be more transudative, with a less cellular WBC count and a differential that is
less PMN predominant. Regardless of the cell count and differential, the treatment should
be based on clinical course, pending the culture results. Cytokine analyses of pleural fluid
have been performed in experimental settings and may prove to add prognostic value on
the degree of inflammation present and may be beneficial in determining treatment
course in the near future.

Imaging Studies
See the list below:

 Radiologic evaluation is the primary tool for the diagnosis of a parapneumonic effusion.
Standard chest radiography is the first step to assess for pleural fluid. See the image
below.
 Radiographic imaging of a
parapneumonic effusion may be useful in assessing the stage of the effusion and the type
of drainage needed. In Figure A, the left heart border is obscured, and more than 50% of
the left hemithorax is filled with an effusion, as evidenced by a fluid meniscus. In Figure
B, the effusion is demonstrated to be fluid because it layers out on a decubitus film. In
Figure C, the lateral radiograph again demonstrates the fluid meniscus and filling of the
posterior sulcus. These findings suggest tube thoracostomy placement may be sufficient
to drain this pleural process.

 Examination should include upright views of the chest to examine the diaphragmatic
margins, which are obliterated with pleural fluid collections. Because as much as 400 mL
may be required before these costophrenic angles are obscured in older children and
adolescents, further diagnostic imaging may be needed.
 In cases in which the effusion is moderate, radiography may reveal displacement of the
mediastinum to the contralateral hemithorax, as well as scoliosis.
 Indistinct diaphragmatic contours merit lateral decubitus views of the chest.
 Free-flowing pleural effusions suggest less complicated parapneumonic processes, which
may not require extensive diagnostic and therapeutic interventions. Ultrasonography that
reveals the absence of loculations suggests that effective treatment can be achieved
without surgical intervention. The absence of free layering fluid on the decubitus films
does not exclude the possibility of a loculated pleural effusion.[7]
 Consider ultrasonography or CT imaging to identify the presence of consolidated lung or
fibrinous septations. In patients with complex fluid collections, chest CT imaging has
emerged as the study of choice. Chest CT imaging can be used to detect and define
pleural fluid and image the airways, guide interventional procedures, and discriminate
between pleural fluid and chest consolidation.

Other Tests
See the list below:

 Pleural fluid polymerase chain reaction (PCR), latex agglutination (or counter
immunoelectrophoresis [CIE] for specific bacteria) may be helpful if the cause of the
infection cannot be ascertained from stain or culture results.
Procedures
See the list below:

 Thoracentesis can provide both significant diagnostic information and therapeutic relief
for parapneumonic effusions.
 The presence of pus establishes the presence of an empyema, and the determination of
the Gram stain, cell differential, and chemistries helps to guide therapy.
 Performing thoracentesis before the initiation of antibiotics increases the diagnostic yield
of the fluid cultures and allows for more specific antimicrobial therapy.

Treatment
Medical Care
Treatment of parapneumonic effusions should address control of the infection and often involves
drainage of the pleural fluid and reexpansion of the affected lung tissue.

 Appropriate antibiotic selection should be based on the Gram stain and culture of the
pleural fluid; however, because a large number of patients may have already received
antibiotics at the time of thoracentesis, an empiric selection of the most appropriate
antibiotics is necessary.
o Base the choice on the most common pathogens that cause pneumonia within the
patient's age range and geographic location.
o When the organism is identified, change the antibiotics to most specifically cover
for the pathogen.
o Patients with empyema should receive a longer course of therapy analogous to
necrotizing pneumonia, but the response to therapy determines the duration of
treatment. The patient receives 10-14 days of intravenous antibiotics and receives
treatment until he or she is afebrile, off supplemental oxygen, and appropriately
responds to therapy.
o Continuation of oral antibiotics may be recommended for 1-3 weeks after
discharge but is not required for less complicated infections.
 The most controversial area in the management of parapneumonic effusions is the
identification of patients who would benefit from pleural drainage and the selection of the
appropriate drainage intervention.
o No clinical studies have effectively contrasted antibiotic treatment without
drainage to currently available drainage techniques. However, long-term follow-
up studies show no differences in pulmonary function or exercise capacity
between the groups. The therapeutic discussion rests on available clinical,
 radiologic, and laboratory evidence; host factors; and individualization to make
the appropriate decision.
o The pulmonologist, intensivist, interventional radiologist, or surgeon can perform
simple tube thoracostomy with an underwater seal.
o Diagnostic thoracentesis and chest tube drainage are effective therapies in more
than 50% of patients. Prompt drainage of a free-flowing effusion prevents the
development of loculations and a fibrous peel.
o Remove the tube when the lung re-expands and drainage ceases. If the fluid is not
free flowing, undertake further radiologic imaging to better define the pleural
space disorder.
 Clinical resolution is not hastened by chest physical therapy used as an adjunct to
standard treatment in children hospitalized with acute pneumonia.[8]
 In addition to the benefit of CT and ultrasonographic imaging to characterize loculated
pleural effusions, the radiologist has become significantly involved in the treatment of
complicated parapneumonic effusions (CPE).
o The ability of the interventional radiologist to assist in the placement of small-
bore catheters, specifically localized to loculated pleural fluid collections, has
helped to facilitate drainage. Furthermore, with smaller diameter tubes, patients
have tolerated tube placement better, with less associated morbidity.
o In addition, radiologists can lyse adhesions directly using imaging during the tube
placement.
o Finally, interventional radiologists, using fibrinolytics, have further improved the
care of the complicated empyema by improved management of loculations and
amelioration of fibrous peel formation and fibrin deposition.
 Numerous studies have documented the effectiveness of intrapleural fibrinolytics to treat
obstructed thoracostomy tubes, increase drainage in multiloculated effusions, and to lyse
adhesions; however, initial studies report on the use of urokinase, the fibrinolytic most
commonly described prior to 1998, evolving to the use of tissue plasminogen activator
(tPA), which has become the most frequently used treatment. Increased use of tPA has
shown it to be well tolerated, effective, and less costly than surgery.[9, 10] Randomized
trials of chest tube drainage with fibrinolytics versus simple drainage and surgical therapy
need to be undertaken to fully assess the relative clinical value of fibrinolytic therapy in
the more complicated patient.

Surgical Care
Controversy continues regarding the surgical treatment of CPE.

 For the uncomplicated free-flowing parapneumonic effusion, surgical intervention is

rarely needed; however, the multiloculated persistently symptomatic effusion, for which
initial therapy may have been delayed, is likely to require more than conservative
management.
 The surgical literature supports the use of thoracotomy to remove the pleural peel and
lyse the adhesions, if the patient does not respond promptly to treatment. Length of stay
and long-term morbidity are reduced by this more aggressive approach, but this must be
contrasted with the increased cost and short-term morbidity associated with thoracotomy
and decortication. This treatment regimen is very effective, with a reported 95% success
rate for patients with fibrinopurulent effusions. Because no prospective comparative
studies have contrasted the current techniques, decortication is likely to remain a
treatment of choice for advanced empyema.
 Video-assisted thoracoscopic surgery (VATS) has proven to be an effective and less-
invasive replacement for the limited decortication procedure.[11, 12] Thoracoscopic
debridement closely imitates open thoracotomy and drainage. Mechanical removal of
purulent material and the breakdown of adhesions can be easily accomplished via this
route. VATS results in more rapid relief of symptoms, earlier hospital discharge, and
significantly less discomfort and morbidity.
 Despite the benefits, a small percentage of patients still progress to require thoracotomy.
As with fibrinolytic therapy, those patients in which this therapy has been most effective
are those slightly less affected in whom earlier and potentially more aggressive treatment
has been initiated.
 The definitive approach is thoracotomy drainage with mechanical release of the pleural
peel and lysis of adhesions. Studies of decortication and debridement report 95%
effectiveness for empyemas in the fibrinopurulent stage. These outcomes are determined
by selected clinical outcomes, such as resolution of symptoms; however, these studies are
subject to selection bias and do not account for the morbidity associated with the
procedure, as well as increased costs associated with an operative procedure and the
associated anesthesia risk. Furthermore, most children heal well in the long run, even
without immediate surgical intervention.
 A meta-analysis reviewed the differences between primary operative treatment with
nonoperative management and revealed striking reductions in length of stay, duration of
tube thoracostomy, and duration of antibiotics.[13] However, these data are susceptible to
critics who point out the same concerns regarding selection biases that have been listed
above. An additional review of surgical options demonstrated that early VATS resulted in
shortening hospitalization times, but other outcomes such as duration of symptoms or
antibiotic use were less dramatic between surgical treatments. In conclusion, early
intervention of any sort is likely to improve outcomes, but early VATS is the surgical
approach now most preferred in managing children with empyema.
 Alternative procedures, such as rib resection and open drainage or pleural obliteration,
are rarely needed in the pediatric population.
 To most effectively determine the optimal therapeutic intervention, a carefully designed,
multicentered, randomized, clinical trial would help to develop evidence-based standards
for the treatment of complicated parapneumonic effusion in children.
 Marhuenda et al conducted a prospective, randomized, multicenter clinical trial
comparing the efficacy of drainage plus urokinase therapy with that of video-assisted
thoracoscopic surgery in the treatment of pediatric parapneumonic empyema.[14] The
study included a total of 103 patients (age, younger than 15 years); 53 patients were
randomly assigned to receive treatment with thoracoscopy, and 50 were assigned to
treatment with urokinase. There were no differences in demographic characteristics or in
 the main baseline characteristics between the 2 groups. No statistically significant
differences were found between the thoracoscopy group and the urokinase group in the
median postoperative stay (10 vs 9 days), the median hospital stay (14 vs 13 days), or the
number of days febrile after treatment (4 vs 6 days). A second intervention was required
in 15% of the children in the thoracoscopy group and in 10% in the urokinase group. The
investigators concluded that drainage plus therapy with urokinase is as effective as video-
assisted thoracoscopic surgery as first-line treatment of septated parapneumonic
empyema in children.[14]
 Proesmans et al reported on the use of a standardized medical treatment of
parapneumonic empyema as a first-step nonsurgical approach in a tertiary care center.
[15] The purpose of the study was to evaluate the need for surgery and to collect data on
disease course, outcome, and microbiology. The study cohort consisted of 132 children
treated for parapneumonic empyema between 2006 and 2013. Of the 132 children, 20%
required surgical intervention. Median duration of in-hospital fever was 5 days. The
duration of fever correlated with pleural LDH levels and pleural glucose levels and was
inversely correlated with pleural pH. On the basis of pleural polymerase chain reaction
results, 85% of the cases were caused by Streptococcus pneumoniae (40% were of
serotype 1). After introduction of a standardized primary medical approach (chest
drainage with or without fibrinolysis), the need for surgical rescue interventions remained
at 20%overall.[15]

Consultations
See the list below:

 Consultants may include pediatric surgeons (thoracic or general), interventional

radiologists, intensivists, and pulmonologists.

Activity
Patients should perform as much activity as can be tolerated.

 Encourage the facilitation of deep breathing and airway clearance.

 Use analgesics on an individual basis to facilitate airway clearance.

Medication
Medication Summary
Individualize intravenous antibiotics by both age and likelihood of the offending organism. In the
case of a possible aspiration, such as in the patient who is debilitated or neurologically impaired,
consider coverage for anaerobic infection.

Antibiotic, cephalosporin (second generation)

Class Summary
These agents are recommended for the most likely bacterial infections; the specific agent
selected should be individualized based on the offending organism. They may include, but are
not limited to, the following:

Cefuroxime (Zinacef)
A second-generation cephalosporin with good coverage for most staphylococcal and
streptococcal organisms, which are the most common community-acquired causative agents;
thus, this is the most often selected initial antibiotic.

Antibiotics, anaerobic infections

Class Summary
In situations in which an aspiration or likely anaerobic infection is the cause of the pneumonia,
coverage for anaerobes is recommended.

Clindamycin (Cleocin)
Provides coverage for gram-positive organisms and anaerobes and is a possible agent for
infections in patients at high risk for having aspirated PO contents as a cause of their infection.

Antibiotic, Miscellaneous
Class Summary
Vancomycin may be considered when methicillin-resistant S aureus is suspected or confirmed.

Vancomycin (Vancocin, Vancoled)

Classified as glycopeptide agent that has excellent gram-positive coverage, including methicillin-
resistant S aureus. To avoid toxicity, current recommendation is to assay vancomycin trough
levels after third dose drawn 0.5 h prior to next dosing. Use creatinine clearance to adjust dose in
patients diagnosed with renal impairment.

Thrombolytic agents
Class Summary
These agents convert plasminogen to plasmin, leading to clot lysis. These agents are used to lyse
adhesions in the pleural space.

Alteplase (Activase)
Tissue plasminogen activator exerts effect on fibrinolytic system to convert plasminogen to
plasmin. Binds to fibrin in a thrombus and converts the entrapped plasminogen to plasmin,
thereby initiating local fibrinolysis. Serum half-life is 4-6 min, but half-life is lengthened when
bound to fibrin in clot. Used to restore function of central venous access devices that have
become occluded due to thrombosis. Circulating plasma levels are not expected to reach
pharmacologic concentrations.

Follow-up
Further Outpatient Care
See the list below:

 Obtain follow-up radiographs and pulmonary function tests to determine prognosis of

patients with empyema and to confirm resolution of pleural and parenchymal changes.
 Consider a follow-up chest CT scan after the radiography findings clear.
Inpatient & Outpatient Medications
See the list below:

 See Medication.

Transfer
See the list below:

 Children should receive their care in hospitals equipped to deal with ill children and
staffed with the appropriate pediatric subspecialists.

Complications
See the list below:

 Fibrothorax, a complication reported in the adult literature, is rarely observed in pediatric

patients.

Prognosis
See the list below:

 The prognosis for most patients with parapneumonic effusions is quite good.
 Extended antibiotics may be needed in some patients with complicated parapneumonic
effusions (CPE).
 Despite the variability in presentation, most patients recover without sequelae.
 Numerous studies have demonstrated resolution of the radiographic abnormalities by 3-6
months following therapy, with few to no symptoms reported at follow-up examination.
 Pulmonary function testing performed following hospitalization has not shown marked
abnormalities, regardless of clinical course. The only abnormality observed may be slight
 expiratory flow limitation. Mild obstructive abnormalities were the only findings
observed in patients evaluated 12 years (±5) following recovery from empyema.
 Some increased bronchial reactivity has been reported at later follow-up examinations;
however, lung function and exercise response return to normal for most patients.
 Early recognition of pneumonia with parapneumonic effusion, effective intervention to
identify the causative organism, and initiation of definitive therapy reduce morbidity and
complications associated with this process.

Patient Education
See the list below:

 For excellent patient education resources, visit eMedicineHealth's Lung Disease and
Respiratory Health Center. Also, see eMedicineHealth's patient education article
Bacterial Pneumonia.

Contributor Information and Disclosures

Author

Peter H Michelson, MD Associate Professor of Pediatrics, Division of Pulmonary and Sleep

Medicine, Duke University School of Medicine

Peter H Michelson, MD is a member of the following medical societies: International Society for
Heart and Lung Transplantation, American Academy of Pediatrics, American Thoracic Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center
College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Charles Callahan, DO Professor, Chief, Department of Pediatrics and Pediatric Pulmonology,

Tripler Army Medical Center

Charles Callahan, DO is a member of the following medical societies: American Academy of

Pediatrics, American College of Chest Physicians, American College of Osteopathic
Pediatricians, American Thoracic Society, Association of Military Surgeons of the US, Christian
Medical and Dental Associations

Disclosure: Nothing to disclose.

Chief Editor

Girish D Sharma, MD, FCCP, FAAP Professor of Pediatrics, Rush Medical College; Director,
Section of Pediatric Pulmonology and Rush Cystic Fibrosis Center, Rush Children's Hospital,
Rush University Medical Center

Girish D Sharma, MD, FCCP, FAAP is a member of the following medical societies: American
Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society,
Royal College of Physicians of Ireland

Disclosure: Nothing to disclose.

Additional Contributors

Thomas Scanlin, MD Chief, Division of Pulmonary Medicine and Cystic Fibrosis Center,
Department of Pediatrics, Rutgers Robert Wood Johnson Medical School

Thomas Scanlin, MD is a member of the following medical societies: American Association for
the Advancement of Science, Society for Pediatric Research, American Society for Biochemistry
and Molecular Biology, American Thoracic Society, Society for Pediatric Research

Disclosure: Nothing to disclose.

References

1. Osler W. The Principles and Practice of Medicine. 4th ed. New York, NY: D Appleton;
1901. 108.
2. Krenke K, Sadowy E, Podsiadły E, Hryniewicz W, Demkow U, Kulus M. Etiology of
parapneumonic effusion and pleural empyema in children. The role of conventional and
molecular microbiological tests. Respir Med. 2016 Jul. 116:28-33. [Medline].
3. Buckingham SC, King MD, Miller ML. Incidence and etiologies of complicated
parapneumonic effusions in children, 1996 to 2001. Pediatr Infect Dis J. June 2003.
22(6):499-504.
4. Menon P, Rao KL, Singh M, Venkatesh MA, Kanojia RP, Samujh R, et al. Surgical
management and outcome analysis of stage III pediatric empyema thoracis. J Indian
Assoc Pediatr Surg. 2010 Jan. 15(1):9-14. [Medline]. [Full Text].
5. Nyambat B, Kilgore PE, Yong DE, et al. Survey of childhood empyema in Asia:
implications for detecting the unmeasured burden of culture-negative bacterial disease.
BMC Infect Dis. 2008 Jul 11. 8:90. [Medline].
6. Le Bourgeois M, Ferroni A, Leruez-Ville M, Varon E, Thumerelle C, Brémont F, et al.
Nonsteroidal Anti-Inflammatory Drug without Antibiotics for Acute Viral Infection
Increases the Empyema Risk in Children: A Matched Case-Control Study. J Pediatr. 2016
Aug. 175:47-53.e3. [Medline].
7. Ramnath RR, Heller RM, Ben-Ami T, et al. Implications of early sonographic evaluation
of parapneumonic effusions in children with pneumonia. Pediatrics. 1998 Jan. 101(1 Pt
1):68-71. [Medline].
8. Paludo C, Zhang L, Lincho CS, Lemos DV, Real GG, Bergamin JA. Chest physical
therapy for children hospitalised with acute pneumonia: a randomised controlled trial.
Thorax. 2008 Sep. 63(9):791-4. [Medline].
9. Ray TL, Berkenbosch JW, Russo P, Tobias JD. Tissue plasminogen activator as an
adjuvant therapy for pleural empyema in pediatric patients. J Intensive Care Med. 2004
Jan-Feb. 19(1):44-50. [Medline].
10. Stefanutti G, Ghirardo V, Barbato A, Gamba P. Evaluation of a pediatric protocol of
intrapleural urokinase for pleural empyema: a prospective study. Surgery. 2010 Sep.
148(3):589-94. [Medline].
11. Bishay M, Short M, Shah K, et al. Efficacy of video-assisted thoracoscopic surgery in
managing childhood empyema: a large single-centre study. J Pediatr Surg. 2009 Feb.
44(2):337-42. [Medline].
12. Schneider CR, Gauderer MW, Blackhurst D, Chandler JC, Abrams RS. Video-assisted
thoracoscopic surgery as a primary intervention in pediatric parapneumonic effusion and
empyema. Am Surg. 2010 Sep. 76(9):957-61. [Medline].
13. Avansino JR, Goldman B, Sawin RS, Flum DR. Primary operative versus nonoperative
therapy for pediatric empyema: a meta-analysis. Pediatrics. 2005 Jun. 115(6):1652-9.
[Medline].
14. Marhuenda C, Barceló C, Fuentes I, Guillén G, Cano I, López M, et al. Urokinase Versus
VATS for Treatment of Empyema: A Randomized Multicenter Clinical Trial. Pediatrics.
2014 Nov. 134(5):e1301-7. [Medline].
15. Proesmans M, Gijsens B, Van de Wijdeven P, De Caluwe H, Verhaegen J, Lagrou K, et
al. Clinical outcome of parapneumonic empyema in children treated according to a
standardized medical treatment. Eur J Pediatr. 2014 Oct. 173(10):1339-45. [Medline].
16. Alkrinawi S, Chernick V. Pleural infection in children. Semin Respir Infect. 1996 Sep.
11(3):148-54. [Medline].
17. Antony VB, Mohammed KA. Pathophysiology of pleural space infections. Semin Respir
Infect. 1999 Mar. 14(1):9-17. [Medline].
18. Bouros D, Schiza S, Siafakas N. Fibrinolytics in the treatment of parapneumonic
effusions. Monaldi Arch Chest Dis. 1999 Jun. 54(3):258-63. [Medline].
19. Bouros D, Schiza S, Tzanakis N, et al. Intrapleural urokinase versus normal saline in the
treatment of complicated parapneumonic effusions and empyema. A randomized, double-
blind study. Am J Respir Crit Care Med. 1999 Jan. 159(1):37-42. [Medline].
20. Brook I. Lung abscesses and pleural empyema in children. Adv Pediatr Infect Dis. 1993.
8:159-76. [Medline].
21. Bryant RE, Salmon CJ. Pleural empyema. Clin Infect Dis. 1996 May. 22(5):747-62; quiz
763-4. [Medline].
22. Gates RL, Caniano DA, Hayes JR, Arca MJ. Does VATS provide optimal treatment of
empyema in children? A systematic review. J Pediatr Surg. 2004 Mar. 39(3):381-6.
[Medline].
23. Givan DC, Eigen H. Common pleural effusions in children. Clin Chest Med. 1998 Jun.
19(2):363-71. [Medline].
24. Grewal H, Jackson RJ, Wagner CW, Smith SD. Early video-assisted thoracic surgery in
the management of empyema. Pediatrics. 1999 May. 103(5):e63. [Medline].
25. Hardie WD, Roberts NE, Reising SF, Christie CD. Complicated parapneumonic effusions
in children caused by penicillin-nonsusceptible Streptococcus pneumoniae. Pediatrics.
1998 Mar. 101(3 Pt 1):388-92. [Medline].
26. Heffner JE. Indications for draining a parapneumonic effusion: an evidence-based
approach. Semin Respir Infect. 1999 Mar. 14(1):48-58. [Medline].
27. Heffner JE. Infection of the pleural space. Clin Chest Med. 1999 Sep. 20(3):607-22.
[Medline].
28. Heffner JE, McDonald J, Barbieri C, Klein J. Management of parapneumonic effusions.
An analysis of physician practice patterns. Arch Surg. 1995 Apr. 130(4):433-8.
[Medline].
29. Hoff SJ, Neblett WW 3rd, Heller RM, et al. Postpneumonic empyema in childhood:
selecting appropriate therapy. J Pediatr Surg. 1989 Jul. 24(7):659-63; discussion 663-4.
[Medline].
30. Hoff SJ, Neblett WW, Edwards KM, et al. Parapneumonic empyema in children:
decortication hastens recovery in patients with severe pleural infections. Pediatr Infect
Dis J. 1991 Mar. 10(3):194-9. [Medline].
31. Kennedy AS, Agness M, Bailey L, White JJ. Decortication for childhood empyema. The
primary provider's peccadillo. Arch Surg. 1991 Oct. 126(10):1287-91. [Medline].
32. Kern JA, Rodgers BM. Thoracoscopy in the management of empyema in children. J
Pediatr Surg. 1993 Sep. 28(9):1128-32. [Medline].
33. Kosloske AM, Cartwright KC. The controversial role of decortication in the management
of pediatric empyema. J Thorac Cardiovasc Surg. 1988 Jul. 96(1):166-70. [Medline].
34. LeMense GP, Strange C, Sahn SA. Empyema thoracis. Therapeutic management and
outcome. Chest. 1995 Jun. 107(6):1532-7. [Medline].
35. Light RW. Pleural effusion. Nadel JA, ed. Textbook of Respiratory Medicine. 2nd ed.
Philadelphia, PA: WB Saunders; 1994. 1719-30.
36. McLaughlin FJ, Goldmann DA, Rosenbaum DM, et al. Empyema in children: clinical
course and long-term follow-up. Pediatrics. 1984 May. 73(5):587-93. [Medline].
37. Moulton JS, Benkert RE, Weisiger KH, Chambers JA. Treatment of complicated pleural
fluid collections with image-guided drainage and intracavitary urokinase. Chest. 1995
Nov. 108(5):1252-9. [Medline].
38. Pollak JS, Passik CS. Intrapleural urokinase in the treatment of loculated pleural
effusions. Chest. 1994 Mar. 105(3):868-73. [Medline].
39. Redding GJ, Walund L, Walund D, et al. Lung function in children following empyema.
Am J Dis Child. 1990 Dec. 144(12):1337-42. [Medline].
40. Sahn SA. Management of complicated parapneumonic effusions. Am Rev Respir Dis.
1993 Sep. 148(3):813-17. [Medline].
41. Stovroff M, Teague G, Heiss KF, et al. Thoracoscopy in the management of pediatric
empyema. J Pediatr Surg. 1995 Aug. 30(8):1211-5. [Medline].
42. Stringel G, Hartman AR. Intrapleural instillation of urokinase in the treatment of
loculated pleural effusions in children. J Pediatr Surg. 1994 Dec. 29(12):1539-40.
[Medline].
43. Wells RG, Havens PL. Intrapleural fibrinolysis for parapneumonic effusion and
empyema in children. Radiology. 2003 Aug. 228(2):370-8. [Medline]