CONTENTS

• Basics
• Common causes: Epidemiology & clinical presentation
• Laboratory investigations
• Radiology
• Differential diagnosis
• Bronchoscopy
• Treatment
  • Antibiotics
    • Antibiotics for anaerobic abscess due to aspiration
    • Antibiotics for other types of lung abscess
  • Drainage
  • Treatment failure
• Related: Echinococcosis
• Questions & discussion

abbreviations used in the pulmonary section: 3

• ABPA: Allergic bronchopulmonary aspergillosis 📖
• AE-ILD: Acute exacerbation of ILD 📖
• AEP: Acute eosinophilic pneumonia 📖
• AFB: Acid Fast Bacilli
• AIP: Acute interstitial pneumonia (Hamman-Rich syndrome) 📖
• ANA: Antinuclear antibody 📖
• ANCA: Antineutrophil cytoplasmic antibodies 📖
• ARDS: Acute respiratory distress syndrome 📖
• ASS: Antisynthetase Syndrome 📖
• BAL: Bronchoalveolar lavage 📖
• BiPAP: Bilevel positive airway pressure 📖
• CEP: Chronic eosinophilic pneumonia 📖
• CF: Cystic fibrosis 📖
• COP: Cryptogenic organizing pneumonia 📖
• CPAP: Continuous positive airway pressure 📖
• CPFE: Combined pulmonary fibrosis and emphysema 📖
• CTD-ILD: Connective tissue disease associated interstitial lung disease 📖
• CTEPH: Chronic thromboembolic pulmonary hypertension 📖
• DAD: Diffuse alveolar damage 📖
• DAH: Diffuse alveolar hemorrhage 📖
• DIP: Desquamative interstitial pneumonia 📖
• DLCO: Diffusing capacity for carbon monoxide 📖
• DRESS: Drug reaction with eosinophilia and systemic symptoms 📖
• EGPA: Eosinophilic granulomatosis with polyangiitis 📖
• FEV1: Forced expiratory volume in 1 second 📖
• FVC: Forced vital capacity 📖
• GGO: Ground glass opacity 📖
• GLILD: Granulomatous and lymphocytic interstitial lung disease 📖
• HFNC: High flow nasal cannula 📖
• HP: Hypersensitivity pneumonitis 📖
• IPAF: Interstitial pneumonia with autoimmune features 📖
• IPF: Idiopathic pulmonary fibrosis 📖
• IVIG: Intravenous immunoglobulin 📖
• LAM: Lymphangioleiomyomatosis 📖
• LIP: Lymphocytic interstitial pneumonia 📖
• MAC: Mycobacterium Avium complex 📖
• MCTD: Mixed connective tissue disease 📖
• NIV: Noninvasive ventilation (including CPAP or BiPAP) 📖
• NSIP: Nonspecific interstitial pneumonia 📖
• NTM: Non-tuberculous mycobacteria 📖
• OP: Organizing pneumonia 📖
• PAP: Pulmonary alveolar proteinosis 📖
• PE: Pulmonary embolism 📖
• PFT: Pulmonary function test 📖
• PLCH: Pulmonary Langerhans Cell Histiocytosis 📖
• PPFE: Pleuroparenchymal fibroelastosis 📖
• PPF: Progressive pulmonary fibrosis 📖
• PVOD/PCH Pulmonary veno-occlusive disease/pulmonary capillary hemangiomatosis 📖
• RB-ILD: Respiratory bronchiolitis-associated interstitial lung disease 📖
• RP-ILD: Rapidly progressive interstitial lung disease 📖
• TNF: tumor necrosis factor
• UIP: Usual Interstitial Pneumonia 📖

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basics

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• Lung abscess is a circumscribed, purulent infection within the lung parenchyma that destroys the lung tissue and ultimately produces a new cavity.
• Despite carrying the name “abscess,” lung abscess usually doesn't require any sort of procedural drainage.

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causes of lung abscess: epidemiology & clinical presentation

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Most lung abscesses fall into one of four categories: 

[#1/4] anaerobic abscess caused by aspiration (“primary lung abscess”)

• Lung abscess usually results from aspiration, often leading to an indolent focus of infection which causes chronic symptoms. These abscesses are generally polymicrobial, involving anaerobes and oral flora (although culturing these organisms is difficult).
• Epidemiology: Risk factors include:
  • Older age.
  • Poor dentition.
  • Dysphagia.
  • Alteration of consciousness (e.g., alcoholism, sedating medications, epilepsy).
• Clinical presentation:
  • The disease course is usually chronic, with indolent symptoms that evolve over weeks to months. Since the abscess is circumscribed (surrounded by a fibrous rim), it generally doesn't cause bacteremia or septic shock.
  • Systemic features:
    • Fever (nearly all patients), night sweats.
    • Fatigue.
    • Weight loss, anorexia (may mimic cancer).
  • Chest symptoms:
    • Cough, especially productive of foul-smelling purulent sputum.
    • Hemoptysis may occur (and can be severe).
    • Pleuritic chest pain may occur.
    • Digital clubbing may evolve over weeks.

[#2/4] bronchial obstruction (~15%)

• Bronchial obstruction (e.g., due to malignancy or foreign body) may lead to a post-obstructive pneumonia. This may eventually suppurate, leading to an abscess.
• Bronchial obstruction is present in ~15% of lung abscesses. This is important for two reasons:
  • (1) An underlying neoplasm may require therapy.
  • (2) Obstruction may prevent resolution of the abscess.

[#3/4] necrotizing pneumonia

• Severe pneumonia may lead to necrosis of areas of lung tissue. Eventually, this may produce focal, circumscribed abscesses.
• Infection is usually monomicrobial. A variety of different pathogens may cause necrotizing pneumonia (e.g., Staphylococcus aureus, Klebsiella pneumoniae, Pseudomonas aeruginosa). If there is extensive destruction of the lung, the term “pulmonary gangrene” may be used.
• Clinical presentation is generally acute, with a very severe pneumonia.
• (Further discussion of necrotizing pneumonia here: 📖).

[#4/4] septic emboli

• This usually results from tricuspid valve endocarditis. Other potential sites of septic embolization may include septic thrombophlebitis (e.g., Lemierre syndrome, which is septic thrombophlebitis of the internal jugular vein) or an infected vascular catheter.
• Multifocal septic emboli often lead to areas of lung necrosis and suppuration.
• Infection is monomicrobial. Tricuspid endocarditis often is due to Staphylococcus aureus, whereas Lemierre syndrome is frequently due to Fusobacterium necrophorum.
• Clinical presentation is often more acute.

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laboratory studies

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blood culture

• Blood culture generally has poor yield.
• Abscesses are walled off from circulation, so bacteremia is uncommon.
• Blood cultures will have higher yield in abscesses due to septic emboli.

sputum culture

• Results may be misleading (due to contamination with oral bacteria).
• If fungal or mycobacterial infection are possible, sputum should be sent for appropriate analysis.

other investigations

• ANCA serology may be obtained if the clinical picture raises a possibility of ANCA-related vasculitis.

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radiology

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CT scan will initially be important to evaluate abscess anatomy and underlying pathology. Follow-up imaging to ensure adequate healing may be performed with serial chest X-rays (supplemented by CT scans as needed). 

imaging features of an isolated lung abscess

• (#1) Initially a solid-appearing lesion is seen:
  • When the abscess initially forms (prior to communication with a bronchus), there is no air-fluid level.
  • The abscess may look like a round focus of pneumonia, with a necrotic center.
• (#2) Cavitation (+/- air fluid level):
  • Eventually cavitation occurs.
    • Wall thickness is usually 5-15 mm (thickness >16 mm or prominent nodularity may suggest cavitary malignancy rather than abscess). (Murray 2022)
    • The internal wall is usually smooth (90%), or shaggy (10%). (Rosado-de-Christenson 2022)
  • ~75% of abscesses will have an air-fluid level by the time they present clinically.

other radiologic features to evaluate:

• Surrounding consolidation (~50%). If seen, this may support the diagnosis of an abscess (as opposed to a superinfected chronic lung cyst). (Rosado-de-Christenson 2022)
• Bronchial abnormality or regional lymphadenopathy may suggest the possibility of a postobstructive abscess.
• Abscess location:
  • Aspiration typically causes abscess formation in the posterior segments of the upper lobes, or the superior or lateral basal segments of the lower lobes. (Athanassiadi 2013)
  • Septic emboli may cause numerous, scattered abscesses.

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differential diagnosis

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More common differential diagnostic considerations often include: 

infectious diseases

• Mycobacterial infection (tuberculous or nontuberculous), with or without bacterial superinfection.
• Fungal infection:
  • Aspergillosis.
  • Histoplasmosis.
  • Cryptococcosis.
• Nocardiosis.
• Loculated empyema.
• Echinococcosis.

malignancy

• Lung cancer, with or without additional pathologies such as:
  • Lung cancer causing cavitation, plus bacterial superinfection.
  • Lung cancer causing bronchial obstruction, leading to secondary abscess formation.
• Metastatic malignancy.
• Lymphoma.

inflammatory diseases

• GPA (granulomatosis with polyangiitis).
• Rheumatoid nodule.

other

• Pneumatocele (may initially be very difficult to distinguish from abscess).
• Infected bullae or cyst (suggested by thin walls).

More complete differential diagnosis of cavitation here: 📖 (Rosado-de-Christenson 2022)

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bronchoscopy

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• Bronchoscopy is generally not needed.
• Potential indications for bronchoscopy:
  • Treatment failure.
  • CT scan suggests endobronchial lesion (e.g., tumor or foreign body).
  • Suspicion for unusual pathogens (e.g., fungi or mycobacteria). (ERS handbook 3rd ed.)
• Goal of bronchoscopy:
  • Sampling for microbiology.
  • Exclusion/evaluation of an endobronchial lesion or foreign body.
• Caution should be employed during bronchoscopy, especially if the abscess hasn't yet ruptured into the bronchus. Release of large volumes of purulent material during bronchoscopy may spread the infection to other parts of the lung and/or promote acute lung injury (especially if the patient is sedated and unable to properly expectorate this material).

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antibiotics for anaerobic abscess due to aspiration

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microbiology of lung abscess due to aspiration

• Abscesses are often polymicrobial, so isolation of one bacteria doesn't necessarily exclude the presence of other bacteria.
• Most often this involves:
  • (i) Microaerophilic streptococci (including Streptococcus milleri group organisms such as Streptococcus anginosus, and also Streptococcus mitis).
  • (ii) Oral anaerobes (including Fusobacterium, Prevotella, or Peptostreptococcus spp.). (ERS handbook 3rd ed.)

overall antibiotic strategy

• Therapy generally requires oral treatment for several weeks.
• Most patients may be started on oral antibiotics and treated on an outpatient basis.
• For patients who are admitted to the hospital, it's wise to design the antibiotic regimen with a transition to oral antibiotics in mind (rather than, for example, placing the patient on a regimen of vancomycin plus piperacillin-tazobactam – for which no oral equivalents exist).

potential antibiotics

• Clindamycin 💉 has traditionally been the standard, front-line therapy (either oral or IV).
  • Intravenous therapy: 600 mg IV q8hr.
  • Oral therapy: 300 mg PO four times daily.
  • Oral bioavailability is excellent, allowing for facile transitions between PO and IV administration.
  • The drawback of clindamycin is a very high risk for C. difficile.
• Beta-lactam/beta-lactamase inhibitor is also a front-line therapy.
  • Ampicillin-sulbactam 💉 may be used, if IV administration is required.
  • Amoxicillin-clavulanate is generally used for ongoing oral therapy.
• Less desirable options:
  • Moxifloxacin is effective, but it has a greater toxicity profile.
  • Metronidazole plus penicillin is an option. Metronidazole alone misses some microaerophilic streptococcal species, which may explain why metronidazole monotherapy is associated with ~50% treatment failure. (Athanassiadi 2013) However, combination therapy is undesirable because it involves a high pill burden and because extended courses of metronidazole may cause neurotoxicity.
  • Numerous other antibiotics can be used (e.g., ertapenem). However, these are limited by a lack of any facile transition to an oral equivalent.

monitoring & duration of therapy

• Some clinical improvement should be seen within 3-4 days, with defervescence within 7-10 days. (Murray 2022) If this isn't seen, consider the possibility of treatment failure: 📖.
• Treatment duration is often ~4-6 weeks. Treatment should ideally be continued until the X-ray shows a small, stable residual scar.

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antibiotics for other types of lung abscess

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Antibiotics will vary, depending on the underlying disease and culture results. For example:

• Abscess due to septic embolization is generally treated based on treatment algorithms for the underlying source of emboli (e.g., endocarditis).
• Abscess due to necrotizing pneumonia may be treated based on treatment algorithms for necrotizing pneumonia. 📖

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management – drainage

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procedural drainage is generally not needed

• Most abscesses will rupture into a bronchus and drain into the airway. Thus, the patient is draining the abscess naturally, via coughing!

indications to consider percutaneous tube drainage:

• Percutaneous tube drainage may be considered if several of the following features are present:
  • Failure of medical management.
  • Abscess fails to drain into a bronchus.
  • Abscess abuts the chest wall with a broad area of contact that causes adhesion to the chest wall (this making it more likely that tube drainage can be performed without causing pneumothorax or empyema).
  • Abscess is large (especially if the abscess is enlarging and at risk of rupture).
• Risks of tube drainage include the following, with the magnitude of risk depending on individual patient characteristics:
  • Pneumothorax with bronchopleural fistula (due to placement of a tube through the lung parenchyma).
  • Development of empyema (due to spillage of infection into the pleural space).
  • Hemothorax.
  • Hemoptysis.
• ⚠️ Percutaneous drainage of an abscess is usually not desirable, so be very thoughtful prior to pursuing this intervention.

indications to consider surgical resection

• Surgery typically involves lobectomy to completely remove the abscess. If there is a bronchial obstructive lesion (e.g., malignancy), surgery may simultaneously resect this as well.
• Potential indications for surgery:
  • Major hemoptysis.
  • Persistent bronchopleural fistula.
  • Empyema.
  • Bronchial obstruction impairs resolution.
  • Failure to respond to medical management plus poor candidacy for interventional radiology drainage.
  • Abscess in the context of necrotizing pneumonia with pulmonary gangrene.

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treatment failure

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potential causes of treatment failure or delayed recovery

• Obstruction of the bronchus prevents drainage of the abscess (e.g., foreign body or malignancy).
• Resistant organisms:
  • Bacteria (e.g., MRSA).
  • Mycobacteria.
  • Fungi.
• Associated empyema.
• Large cavity size (>6 cm).
• Incorrect diagnosis, for example:
  • Vasculitis.
  • Cavitary neoplasm.
  • Septic emboli associated with endocarditis. (Murray 2022)
• Complications of therapy, for example:
  • C. difficile diarrhea.
  • Drug fever.

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echinococcosis

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basics

• Echinococcus causes the development of cysts (hydatid cysts) that are most commonly located in the lungs and/or liver (although other locations are possible, such as the brain).
• Cysts may lie dormant for years, prior to causing clinical manifestations.

epidemiology

• Echinococcus has a broad geographic distribution. It is most often encountered in: (33160543)
  • Central and eastern Europe.
  • Central and South America.
  • Sub-Saharan Africa.
  • The Middle East.
  • China, Russia, and countries of the former Soviet Union.
  • Australia and New Zealand.
• Exposure to sheep, cattle, or dogs in an endemic area carries the highest risk. (33160543)
• Cysts may persist for years after initial contraction of the disease.
• Young adults (20-40 years old) are most often affected. (34022020)

clinical manifestations

• Asymptomatic finding on chest imaging.
• Cyst rupture into a bronchus may cause abrupt fever and cough, with expectoration of salty fluid. (34022020) 
  • Hemoptysis may be a presenting symptom. (28146378) 
  • Ruptured cysts may become superinfected. This can mimic a bacterial lung abscess or lung cancer. (37031992) 
• Cyst rupture into the pleural space may cause empyema or hypersensitivity responses (including acute fever, urticaria, wheezing, and even anaphylaxis).
• Mass effect may cause compression of adjacent structures.

radiology

• Unruptured cyst(s) are 1-20 cm in size with smooth borders.
  • If daughter cysts can be seen within the cyst, this is more specific for echinococcus.
  • ~60% of patients have only a solitary cyst, which makes diagnosis more challenging. (Fishman 2023)
  • Cyst walls may enhance with contrast.
  • Most cysts are located in the lower lobes. (Walker 2019)
• Cyst rupturing into an airway creates an air-fluid level which will resemble a lung abscess.
  • A “water lily” sign may rarely be seen (caused by parts of the inner lining of the cyst floating within the cyst).
  • Gas within the cyst implies either cyst rupture into a bronchus and/or superinfection of the cyst.
• Cyst rupture into the pleura may generate a pleural effusion.
• Cysts may occasionally be seen in other organs as well (especially the liver, but also the spleen, kidney, brain, or heart). (34022020)
  • One third of patients may also have hepatic cysts.

laboratory studies

• Eosinophilia & IgE:
  • Peripheral eosinophilia is present in only <25% of patients, but may be more frequent if the cyst ruptures. (Fishman 2023)
  • IgE levels may be elevated.
• Serologic tests:
  • Sensitivity is only ~50% sensitive for pulmonary echinococcosis (in comparison to hepatic echinococcus, which causes seropositivity in >90% of patients). (34022020)
  • Specificity varies among tests, with some demonstrating cross-reactivity with other pathogens (e.g., cysticercosis). (Murray 2022)
• Cytologic analysis of pleural fluid or bronchial washings may reveal protoscolices or degenerated hooklets, following cyst rupture. (33160543)

treatment

• Surgical resection is usually ideal (to avoid cyst rupture – which could cause anaphylaxis and/or parasitic dissemination). However, surgery may be unnecessary for patients with small (<7 mm), isolated cysts. (33160543)
• Albendazole with or without praziquantel may suppress the disease in patients unable to undergo surgery.
  • Albendazole is also utilized peri/postoperatively to prevent spreading the infection.

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questions & discussion

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