eMedicine Specialties > Pediatrics: General Medicine > Pulmonology

Pneumatocele

Denise Serebrisky, MD, Assistant Professor, Department of Pediatrics, Albert Einstein College of Medicine; Director, Division of Pulmonary Medicine, Lewis M Fraad Department of Pediatrics, Jacobi Medical Center; Director, Jacobi Asthma and Allergy Center for Children
Arthur B Atlas, MD, Assistant Clinical Professor, Department of Pediatrics, University of Medicine and Dentistry of New Jersey; Debra Boyer, MD, Fellow, Department of Pediatrics, Division of Pulmonary Medicine, Children's Hospital of Boston

Updated: Apr 2, 2008

Introduction

Background

Pulmonary pneumatoceles are thin-walled, air-filled cysts that develop within the lung parenchyma. They can be single emphysematous lesions but are more often multiple, thin-walled, air-filled, cystlike cavities. Most often, they occur as a sequela to acute pneumonia, commonly caused by Staphylococcus aureus. However, pneumatocele formation also occurs with other agents, including Streptococcus pneumoniae, Haemophilus influenzae, Escherichia coli, group A streptococci, Serratia marcescens, Klebsiella pneumoniae, adenovirus, and tuberculosis. Pneumatoceles are generally observed soon after the development of pneumonia but can be observed on the initial chest radiograph.

Noninfectious etiologies include hydrocarbon ingestion, trauma, and positive pressure ventilation.

In most circumstances, pneumatoceles are asymptomatic and do not require surgical intervention.¹ Treatment of the underlying pneumonia with antibiotics is the first-line therapy. Close observation in the early stages of the infection and periodic follow-up care until resolution of the pneumatocele is usually adequate treatment. The natural course of a pneumatocele is slow resolution with no further clinical sequelae. Invasive approaches should only be reserved for patients who develop complications.

Pathophysiology

Since the 1950s, multiple theories have been proposed as to the exact mechanism of pneumatocele formation; however, the exact mechanism remains controversial.

Carrey suggested that the initial event is inflammation and narrowing of the bronchus, leading to the formation of an endobronchial ball valve.² Ultimately, this bronchial obstruction leads to distal dilatation of the bronchi and alveoli. In 1951, Conway proposed that a peribronchial abscess forms and subsequently ruptures its contents into the bronchial lumen.³ This also acts similarly to a ball-valve obstruction in the bronchus and leads to distal dilatation. In 1972, Boisset concluded that pneumatoceles are caused by bronchial inflammation that ruptures the bronchiolar walls and causes the formation of "air corridors."⁴ Air dissects down these corridors to the pleura and forms pneumatoceles, a form of subpleural emphysema.

Traumatic pneumatocele has a different pathophysiology from the infectious type,⁵ developing in a 2-step process. Initially, the lung is compressed by the external force of the trauma, followed by rapid decompression from increased negative intrathoracic pressure. A "bursting lesion" of the lung occurs and leads to pneumatocele formation.

Frequency

International

Incidence of postinfectious pneumatocele formation ranges from 2-8% of all cases of pneumonia in children.⁶ However, the frequency can be as high as 85% in staphylococcal pneumonias.

Mortality/Morbidity

Although mortality from the initial pneumonia can be significant, mortality associated with pneumatoceles is quite low. Complete resolution without long-term sequelae is typical; however, rare complications can occur, including the following:

• Tension pneumatocele
• Pneumothorax
• Secondarily infected pneumatocele

Race

No specific racial predilection is observed for pneumatocele formation. Because pneumatoceles are usually a complication of pneumonia, the predilection is based on susceptibility for infection.

Sex

No sex predilection is known.

Age

Infants younger than 1 year account for three fourths of the cases of staphylococcal pneumonia. Because pneumatoceles commonly develop as a complication of staphylococcal pneumonia, pneumatoceles are found more frequently in infants and young children. One study reported that 70% of pneumatoceles occurred in children younger than 3 years.⁷

Clinical

History

Children present with typical features of pneumonia, including cough, fever, and respiratory distress. No clinical findings differentiate pneumonia with or without pneumatocele formation.

Physical

• Mild, moderate, or severe respiratory distress may be present, with tachypnea, retractions, grunting, and nasal flaring.
• Fever is almost always present and may be as high as 40-41°C.
• Lung examination findings vary depending on the stage of the pneumonia. Auscultation of the chest reveals focal or bilateral decreased breath sounds. Inspiratory crackles are frequently heard. As the pneumonia resolves and the pneumatocele persists, the lung examination findings can be normal or focal decreases in breath sounds can be present, depending on the size of the pneumatocele.
• In most children admitted to the hospital, the average time from admission to the development of the pneumatocele is 4-7 days. Occasionally, pneumatoceles are present on the initial radiograph.

Causes

• Although no particular genetic predisposition is recognized, pneumatocele formation is associated with hyperimmunoglobulin E (IgE) syndrome (Buckley-Job syndrome).⁸ Because of immunodeficiency, individuals with this syndrome are predisposed to infection with staphylococcal pneumonia, with the known complications of abscess and pneumatocele formation.
• Infectious etiologies associated with pneumatocele formation include the following:
  • S aureus
  • S pneumoniae
  • H influenzae
  • K pneumoniae
  • S marcescens
  • E coli
  • Group A streptococci
  • Mycobacterium tuberculosis
  • Pseudomonas aeruginosa
  • Adenovirus
• Noninfectious etiologies include the following:
  • Trauma
  • Hydrocarbon ingestion
  • Positive pressure ventilation (especially among premature infants)

Differential Diagnoses

Other Problems to Be Considered

Pulmonary abscess

Workup

Laboratory Studies

• Blood culture: If findings are positive, blood culture helps to guide antibiotic therapy.
• Sputum culture: If sputum is available, this is a good noninvasive method to discover potential pathogens.
• Pleural fluid culture: If effusion is present, culturing pleural fluid from thoracentesis can be a direct method to identify the causative organism.
• Bacterial antigen detection: Tests for bacterial antigen detection can be performed on blood, urine and pleural fluid.

Imaging Studies

• Chest radiography: Initial chest radiography often reveals pneumonia without evidence of a pneumatocele. Parapneumonic effusion or empyema can be present. Radiographic evidence of a pneumatocele most often occurs on day 5-7 of hospitalization. Rarely, it may be visible on the initial chest radiograph.
• Chest CT scanning with contrast: Usually, this is not necessary to diagnose a pneumatocele, but CT scanning occasionally helps to differentiate an abscess from a pneumatocele. Rarely, CT-guided needle aspiration of the pneumatocele can relieve compression from a large and/or tension pneumatocele.

Other Tests

• No other specific tests are necessary.

Procedures

• Percutaneous catheter drainage: This should only be considered for a significant tension pneumatocele or a secondarily infected pneumatocele. In these rare situations, drainage has been reported to dramatically improve the patient's cardiovascular status.⁹

Histologic Findings

• Pathology is not commonly observed because most pneumatoceles resolve without surgical resection. However, a few reports documented necrotic material around the pneumatocele.
• Cavity walls can contain organized inflammatory cells with focal collections of multinucleated giant cells.
• In 1972, Boisset reported the presence of air corridors between the bronchiolar lumen and the interstitial space.⁴

Treatment

Medical Care

Medical care for pneumatocele is treatment of the underlying condition. In most circumstances, this involves administration of broad-spectrum antibiotics to treat the pneumonia.

• Therapy should be directed against the most common bacterial organisms in children, including S aureus and S pneumoniae.
• Positive pressure ventilation can result in a sudden increase in size and tension of a pneumatocele. Therefore, careful monitoring is essential in patients receiving positive pressure ventilation when pneumatoceles have been documented.

Surgical Care

• Pneumatoceles almost never require surgical resection. As mentioned above, percutaneous catheter drainage of a pneumatocele that involves more than 50% of hemithorax with severe atelectasis, tension pneumatocele, bronchopleural fistula, or an infected pneumatocele is rarely required.
• Traumatic pneumatoceles commonly resolve with observation without additional therapy. Indications for surgical intervention with a traumatic pneumatocele are similar to those of a postinfectious pneumatocele (ie, development of tension pneumatoceles, a secondary infection of the pneumatocele, and cardiovascular compromise).

Consultations

Consider consulting a surgeon in the presence of an infected pneumatocele or a tension pneumatocele and/or in the presence of a persistent bronchopleural fistula.

Diet

No special dietary requirements are indicated.

Activity

Caution patients with pneumatocele against skydiving or exposure to very high altitudes because of an increased risk of pneumothorax. Scuba diving must be avoided until the pneumatocele completely heals.

Medication

Antimicrobials

Intravenous antibiotics should be directed against the most likely bacterial pathogens, including S aureus and S pneumoniae. Other considerations should include antibiotic coverage for K pneumoniae, E coli, and group A streptococci. Most often, an appropriate single agent can be used, but combined antibiotic therapy can be considered, especially if a specific organism is not identified. As community-associated methicillin-resistant S aureus (MRSA) has increasingly been identified, reconsideration of empiric choice of antistaph beta-lactam for seriously ill patients with suspected MRSA should be carefully considered.¹⁰ The following antimicrobials may be used to target an underlying pneumonia.

Oxacillin (Bactocill)

A very effective antibiotic for treating S aureus as well as S pneumoniae.

Dosing

Adult

1-2 g IV/IM q4-6h
500-1000 mg PO q4-6h

Pediatric

<7 days, <2000 g: 50 mg/kg/d IV divided q12h
<7 days, >2000 g: 75 mg/kg/d IV divided q8h
>7 days, <2000 g: 75 mg/kg/d IV divided q8h
>7 days, >2000 g: 100mg/kg/d IV divided q6h
Infants and children: 150-200 mg/kg/d IV divided q4-6h

Interactions

Oxacillin decreases effects of contraceptives and tetracycline; concomitant administration with disulfiram and probenecid may increase oxacillin levels; effect of anticoagulants increase when large IV doses of oxacillin

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Reported serious adverse effects include thrombocytopenia, neutropenia, hemolytic anemia, and agranulocytosis

Ampicillin and sulbactam (Unasyn)

Drug combination of beta-lactamase inhibitor with ampicillin. A very effective antibiotic for treating S aureus as well as S pneumoniae. Also effective for many anaerobic infections.

Dosing

Adult

1.5 (1 g ampicillin + 0.5 g sulbactam) to 3 g (2 g ampicillin + 1 g sulbactam) IV/IM q6h; not to exceed 8 g/d of ampicillin

Pediatric

100-200 mg (based on ampicillin component) per kg/d IV/IM divided q6h

Interactions

Probenecid and disulfiram elevate ampicillin levels; allopurinol decreases ampicillin effects and has additive effects on ampicillin rash; may decrease effects of PO contraceptives

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Reported serious reactions could include thrombocytopenia, agranulocytosis, anaphylaxis, pseudomembranous colitis, Stevens-Johnson syndrome, toxic epidermal necrolysis, leukopenia, anemia, seizures, and hepatotoxicity; decrease dose with severe renal impairment (ie, CrCl <30 mL/min)

Cefuroxime (Zinacef)

Very effective antibiotic for treating S aureus and S pneumoniae.

Dosing

Adult

2.25 g IV/IM q6-8h; not to exceed 9 g/d

Pediatric

Neonates: 20-40 mg/kg/d IV/IM divided q12h
Infants and children: 50-100 mg/kg/d IV/IM divided q6-8h

Interactions

A false-positive reaction for glucose in the urine can occur with copper reduction tests (ie, Clinitest tablets); false-negative results may occur with ferricyanide test (use glucose oxidase or hexokinase methods); disulfiramlike reactions may occur when alcohol is consumed within 72 h after taking cefuroxime; may increase hypoprothrombinemic effects of anticoagulants; may increase nephrotoxicity in patients receiving potent diuretics such as loop diuretics; coadministration with aminoglycosides increases nephrotoxic potential

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Reported serious reactions include thrombocytopenia, agranulocytosis, anaphylaxis, pseudomembranous colitis, interstitial nephritis, seizures, hemolytic anemia, and neutropenia; reduce dosage by one half if CrCl is 10-30 mL/min and by three fourths if CrCl <10 mL/min (high doses may cause CNS toxicity); bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged or repeated therapy

Vancomycin (Lyphocin, Vancocin, Vancoled)

Very effective antibiotic for treating methicillin-resistant S aureus as well as for treating penicillin-resistant S pneumoniae.
To avoid toxicity, current recommendation is to assay vancomycin trough levels before fourth dose. Use CrCl to adjust dose in patients with renal impairment.

Dosing

Adult

500 mg IV q6h

Pediatric

<7 days, <1200 g: 15 mg/kg/dose IV q24h
<7 days, 1200-2000 g: 15 mg/kg/dose IV q12-18h
<7 days, >2000 g: 30 mg/kg/d IV divided q12h
>7 days, <1200 g: 15 mg/kg/dose IV q24h
>7 days, 1200-2000 g: 15 mg/kg/dose IV q8-12h
>7 days, >2000 g: 45 mg/kg/d IV divided q8h
Infants and children: 40-60 mg/kg/d IV divided q8h

Interactions

Erythema, histaminelike flushing, and anaphylactic reactions may occur when administered with anesthetic agents; concurrent administration with aminoglycosides may increase the risk of nephrotoxicity above that with aminoglycoside monotherapy; effects in neuromuscular blockade may be enhanced when coadministered with nondepolarizing muscle relaxants

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Reported serious reactions include neutropenia, anaphylaxis, Stevens-Johnson syndrome, thrombocytopenia, toxic epidermal necrolysis, nephrotoxicity, and ototoxicity; rapid infusion has been associated with red man syndrome, which can be mistaken for acute allergic reaction

Clindamycin (Cleocin)

Very effective antibiotic for treating S aureus as well as S pneumoniae. Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Dosing

Adult

300-900 mg IV/IM q6-12h; not to exceed 600 mg/dose IM or 4800 mg/d IV
150-450 mg PO qid

Pediatric

Infants and children: 15-40 mg/kg/d IV/IM divided q6-8h
10-25 mg/kg/d PO divided q6-8h

Interactions

Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects of clindamycin; antidiarrheals may delay absorption of clindamycin

Contraindications

Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Reported serious reactions include pseudomembranous colitis, diarrhea, thrombocytopenia, anaphylaxis, Stevens-Johnson syndrome, granulocytopenia, and esophagitis

Ciprofloxacin (Cipro)

Very effective antibiotic for treating S aureus as well as S pneumoniae. A fluoroquinolone with activity against Pseudomonas, streptococci, MRSA, S epidermidis, and most gram-negative organisms but no activity against anaerobes. Inhibits bacterial DNA synthesis and consequently growth.

Dosing

Adult

250-750 mg PO q12h
200-400 mg IV q12h

Pediatric

20-30 mg/kg/d PO divided q12h; not to exceed 1.5 g/d
10-20 mg/kg/d IV divided q12h; not to exceed 800 mg/d

Interactions

Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; ciprofloxacin reduces therapeutic effects of phenytoin; probenecid may increase ciprofloxacin serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)

Contraindications

Documented hypersensitivity; not approved for use in children <18 y; pregnancy; caution with impaired renal or liver function

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Reported serious reactions include hepatotoxicity, seizures, anaphylaxis, Achilles tendon rupture, and pseudomembranous colitis

Follow-up

Further Inpatient Care

• After starting appropriate intravenous antibiotic therapy, perform chest radiography to monitor improvement of pneumonia and progression of the pneumatocele.
• If significant pleural effusion is present or develops, consider thoracentesis and/or chest tube drainage.

Further Outpatient Care

• Most pneumatoceles resolve completely in a few weeks to months. However, in some healthy children, pneumatoceles persist as long as 16 months. Therefore, intermittent outpatient monitoring of chest radiographs is appropriate until resolution. Some recommend chest CT imaging after the findings on plain radiography are clear to ensure complete resolution. However, no clearly recognized radiological or clinical signs help to predict progression of the pneumatocele.
• Findings on pulmonary function studies frequently are abnormal initially because of a restrictive defect and, at times, an obstructive defect. Over time, these abnormalities improve and, most often, return to normal predicted ranges. These should not be routinely performed during the acute stages. The increased pressures in spirometry may increase the risk of rupture.

Inpatient & Outpatient Medications

• No further medications are required.

Transfer

• Consider transfer to an intensive care unit when a large tension pneumatocele is causing cardiovascular compromise or significant airway obstruction.
• Similarly, consider transfer to an intensive care unit if a rupture of the pneumatocele causes a pneumothorax.

Deterrence/Prevention

• No preventative therapy is available.

Complications

• Tension pneumatocele: A tension pneumatocele can develop if airtrapping continues and the pneumatocele expands. This complication occurs most frequently with positive pressure ventilation. If severe, the lesion can cause compression of adjacent structures, with hemodynamic instability and severe airway obstruction. If unrecognized and untreated, this can result in respiratory failure and death.
• Pneumothorax: Pneumothorax can occur from a pneumatocele rupturing into the pleural space. This can lead to collapse of the lung, requiring evacuation of the pleural air to reexpand the lung. A bronchopleural fistula can result as a complication of the pneumothorax.
• Infected pneumatoceles: A pneumatocele can become secondarily infected, usually by a different bacterium from the one that caused the primary pneumonia. Some advocate percutaneous drainage of infected pneumatoceles, especially if fluid- or pus-filled to prevent the development of severe lung abscess that may require surgical excision. Drainage can be both diagnostic and therapeutic. If drained, the fluid should be cultured for bacteria and fungus.

Prognosis

• In general, an uncomplicated pneumatocele carries an excellent prognosis. As discussed, complete resolution of the pneumatocele is the most common outcome.
• Rare complications, including tension pneumatocele, can lead to death from respiratory or cardiovascular collapse from progressive enlargement of the pneumatocele. However, this is rare and, if detected promptly, can be properly treated.

Patient Education

• No specific educational requirements are indicated.

Miscellaneous

Medicolegal Pitfalls

Although most pneumatoceles resolve without sequelae, recognition of the following potential complications may prevent an unexpected poor outcome:

• Cardiovascular or respiratory collapse secondary to a tension pneumatocele
• Pneumothorax secondary to a ruptured pneumatocele

Multimedia

Media file 1: Pneumonia with multiple pneumatoceles.

Media file 2: Pneumonia with pneumatocele (lateral).

Media file 3: Resolving pneumatocele.

Media file 4: Chest CT scan of pneumonia with pneumatocele.

References

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Keywords

pneumatocele, infectious pneumatocele, traumatic pneumatocele, lung cysts, bullae, subpleural emphysema, postinfectious pulmonary cysts, Staphylococcus aureus, pneumonia, Streptococcus pneumoniae, Haemophilus influenzae, Escherichia coli, group A streptococci, Serratia marcescens, Klebsiella pneumoniae, adenovirus, tuberculosis, hydrocarbon ingestion, positive pressure ventilation, ball-valve obstruction, tension pneumatocele, pneumothorax, secondarily infected pneumatocele, hyperimmunoglobulin E syndrome, hyper-IgE syndrome, Buckley-Job syndrome

Contributor Information and Disclosures

Author

Denise Serebrisky, MD, Assistant Professor, Department of Pediatrics, Albert Einstein College of Medicine; Director, Division of Pulmonary Medicine, Lewis M Fraad Department of Pediatrics, Jacobi Medical Center; Director, Jacobi Asthma and Allergy Center for Children
Denise Serebrisky, MD is a member of the following medical societies: American Thoracic Society
Disclosure: Nothing to disclose.

Coauthor(s)

Arthur B Atlas, MD, Assistant Clinical Professor, Department of Pediatrics, University of Medicine and Dentistry of New Jersey
Arthur B Atlas, MD is a member of the following medical societies: American Academy of Pediatrics, American Academy of Sleep Medicine, American College of Chest Physicians, American Lung Association, American Thoracic Society, and Medical Society of New Jersey
Disclosure: Nothing to disclose.

Debra Boyer, MD, Fellow, Department of Pediatrics, Division of Pulmonary Medicine, Children's Hospital of Boston
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

Charles Callahan, DO, Professor, Deputy Chief of Clinical Services, Walter Reed 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, and Christian Medical & Dental Society
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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