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Lung abscess

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Synonyms and keywords: Pulmonary abscess

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Overview

Lung abscess is necrosis of the pulmonary tissue and formation of cavities (more than 2 cm) containing necrotic debris or fluid caused by microbial infection. This pus-filled cavity is often caused by aspiration, which may occur during altered consciousness. Alcoholism is the most common condition predisposing to lung abscesses. Lung abscess is considered primary (60%) when it results from existing lung parenchymal process and is termed secondary when it is complicated by another process e.g. vascular emboli or follows rupture of extrapulmonary abscess into the lung.[1]

Historical Perspective

Lung abscess has been a disease entity since the days of Hippocrates. Postural physiotherapy had been the mainstay of treatment until Harold Neuhof described his concept of new one-stage open drainage for the acute abscess in 1930’s. With the invention of antibiotics in late 1940’s and their promising results led the change in management of lung abscess.[2]

Pathophysiology

Aspiration of bacteria is the inciting event for the development of lung abscess. Once the aspirate is localized it results in pneumonitis. Inflammatory mediators are released, resulting in the formation of colliquative necrosis. The right side lung is more commonly affected than the left. On gross morphology, the lesions are well circumscribed filled with necrotic debris and do not demonstrate well-defined borders with the surrounding lung parenchyma. Microscopic examination demonstrates neutrophils with dilated blood vessels and inflammatory edema.[3] [4]

Causes

Lung abscess is commonly caused by bacterial infections and these include bacteroides, peptostreptococcus and prevotella.[5]Lung abscess is commonly caused by bacterial infections and these include bacteroides, peptostreptococcus and prevotella. Most of the lung abscess is caused by polymicrobial organisms of which anaerobes play a crucial role . Less common include nocardia, actinomyces and fungi. If left untreated, life-threatening conditions may develop which may result in death or permanent disability within 24 hours .

Differentiating Lung Abscess from other Diseases

Lung abscess must be differentiated from other lesions that present with similar symptoms such as cough, fever with chills and rigor and chest includes malignancy, tuberculosis, Wegener’s granulomatosis, rheumatoid nodules.[6]

Epidemiology and Demographics

The incidence from lung abscess have greatly declined during the past several decades due to the widespread use of antibiotics and the availability of other treatment options. Lung abscess accounts for up to 4.0 to 5.5 per 10,000 hospital admissions each year in the US.[7]

Risk Factors

Factors resulting in the altered level of consciousness and decreased immune response play a key role in the development of lung abscess includes alcoholism, diabetes mellitus, neurological disorder and bronchial obstruction.[8]

Screening

There is no screening recommendations for lung abscess.

Natural history, Complications and Prognosis

Symptoms of lung abscess begin approximately 10 days after aspiration of infected material. Acute symptoms include a prodrome accompanied by fever, productive cough, pleuritic chest pain and occasional episodes of hemoptysis. Patients with chronic lung abscess develop weight loss and malaise.Without treatment based on the immune status of the patient, lung abscess can either resolve by forming a granulation tissue scar, or progressively worsens and can result in septicemia, hemorrhage, and death.The prognosis of lung abscess is good with appropriate antibiotic treatment with a high success rate. The outcomes depend on the other associated conditions underlying lung abscess such as size of the cavity, age of the patient and other underlying lung diseases. Complications include hemorrhage pyopneumothorax, pleural empyema and sepsis.[9][10]

Diagnosis

History and Symptoms

Patient history is important to establish a diagnosis of lung abscess. Common history findings include conditions associated with a risk of gastric content aspiration, a recent history of hospitalization or surgery. Common symptoms include high fever (>101°F [>38.5°C]), productive cough with purulent sputum, and pleuritic chest pain. Anaerobic bacteria is responsible for purulent sputum in acute lung abscess.

Physical Examination

Patients with acute lung abscess may present with fever, cough with purulent sputum, gag reflex may be absent in patients with an underlying neurological disorder such as stroke. Digital clubbing is present in patients with a chronic abscess.On examination of the chest, there will be features of consolidation. Abscess typically localizes in the upper lobes or apical segments of the lower lobes.[10]

Laboratory Findings

Diagnosis of lung abscess is made based on clinical symptoms, physical examination, radiographic studies and bacterial culture. Laboratory findings include increased acute phase reactants (ESR and CRP) levels and leukocytosis with consolidation being evident in a segmental or lobar distribution with central cavitation an air-fluid level on lung x-ray. Blood cultures should be performed in all suspected cases.

Treatment

Medical Therapy

The mainstay of management for lung abscess is hospital admission for chest drain and systemic antibiotics. Antimicrobial therapy is based on predisposing host factors and local resistance patterns.Empiric treatment should be commenced after culture samples are obtained. The regimens should penetrate the lung parenchyma and target both anaerobes, aerobic and microaerophilic streptococci. Any combination of a beta-lactam–beta-lactamase inhibitor or a carbapenem are reasonable to use. The standard duration of the treatment of lung abscess is ≥ 4–6 weeks of parenteral antibiotics. [11]

Surgical Therapy

Surgery is considered as the last resort of therapy when both medical and chest drain failed to resolve symptoms. Options for surgery includes chest tube drainage and surgical resection of the lung abscess with the surrounding lung tissue.Percutaneous and endoscopic drainage techniques are considered as a first-line management, especially for patients who are not candidates for surgery. Percutaneous drainage of lung abscesses is characterized by high therapeutic effectiveness and preservation of functional lung tissue, it is a minimally invasive method with fewer complications and lower mortality rates (approximately 4%) in comparison to surgical management. Surgical resection is considered in about 10% of the patients when the chest drain has failed to improve symptoms and patients presenting with one of the following conditions. The surgical approach is thoracotomy and the extent of surgical resection depends on the size of the underlying lesion.[12]

Reference

  1. Bartlett JG, Finegold SM (1972). “Anaerobic pleuropulmonary infections”. Medicine (Baltimore). 51 (6): 413–50. PMID 4564416.
  2. Neuhof H, Hurwitt E (1943). “ACUTE PUTRID ABSCESS OF THE LUNG : VII. RELATIONSHIP OF THE TECHNIC OF THE ONE-STAGE OPERATION TO RESULTS”. Ann. Surg. 118 (4): 656–64. PMC 1617784. PMID 17858299.
  3. “Lung abscess”. West. J. Med. 124 (6): 476–82. 1976. PMC 1130102. PMID 936601.
  4. Green LH, Green GM (1968). “Differential suppression of pulmonary antibacterial activity as the mechanism of selection of a pathogen in mixed bacterial infection of the lung”. Am. Rev. Respir. Dis. 98 (5): 819–24. doi:10.1164/arrd.1968.98.5.819. PMID 5683476.
  5. Cesar L, Gonzalez C, Calia FM (1975). “Bacteriologic flora of aspiration-induced pulmonary infections”. Arch. Intern. Med. 135 (5): 711–4. PMID 28705.
  6. Chaudhuri MR (1973). “Primary pulmonary cavitating carcinomas”. Thorax. 28 (3): 354–66. PMC 470041. PMID 4353362.
  7. Bartlett JG, Finegold SM (1974). “Anaerobic infections of the lung and pleural space”. Am. Rev. Respir. Dis. 110 (1): 56–77. doi:10.1164/arrd.1974.110.1.56. PMID 4834618.
  8. Hagan JL, Hardy JD (1983). “Lung abscess revisited. A survey of 184 cases”. Ann. Surg. 197 (6): 755–62. PMC 1352910. PMID 6859981.
  9. Adebonojo SA, Osinowo O, Adebo O (1979). “Lung abscess: a review of three years’ experience at the University College Hospital, Ibadan”. J Natl Med Assoc. 71 (1): 39–43. PMC 2537236. PMID 423274.
  10. 10.0 10.1 Hirshberg B, Sklair-Levi M, Nir-Paz R, Ben-Sira L, Krivoruk V, Kramer MR (1999). “Factors predicting mortality of patients with lung abscess”. Chest. 115 (3): 746–50. PMID 10084487.
  11. Allewelt M, Schüler P, Bölcskei PL, Mauch H, Lode H (2004). “Ampicillin + sulbactam vs clindamycin +/- cephalosporin for the treatment of aspiration pneumonia and primary lung abscess”. Clin. Microbiol. Infect. 10 (2): 163–70. PMID 14759242.
  12. Kelogrigoris, M; Tsagouli, P; Stathopoulos, K; Tsagaridou, I; Thanos, L (2011). “Ct-guided percutaneous drainage of lung abscesses: review of 40 cases”. Journal of the Belgian Society of Radiology. 94 (4): 191. doi:10.5334/jbr-btr.583. ISSN 1780-2393.


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Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Overview

Lung abscess has been a disease entity since the days of Hippocrates. Postural physiotherapy had been the mainstay of treatment until Harold Neuhof described his concept of new one-stage open drainage for the acute abscess in 1930’s. With the invention of antibiotics in late 1940’s and their promising results led the change in management of lung abscess.

Historical perspective

  • In 1904, Guillemot first put weight to the theory that aspirated oropharyngeal organisms are responsible for cause of lung abscess[1]
  • In 1920-1930, Harold Neuhof was the first thoracic surgeon to develop a valid and reliable therapeutic concept of drainage operation for acute pulmonary abscess.[2]
  • In 1938, the first percutaneous drain of lung abscess was performed.[3]
  • In 1942, Brock added evidence in stating that aspirated contents gravitated to the dependent part of the lungs.
  • In 1946, owing to the advent of antibiotics, and treatment of acute putrid lung abscess with penicillin showed good results and henceforth patients received antibiotics rather than surgical procedures.[2]

Reference

  1. Lima, Mario (01/24/2011). Pediatric thoracic surgery Softcover reprint of hardcover 1st ed. 2009. Harvard Medical School: Springer London. p. 145. ISBN 978-8847052017. Check date values in: |date= (help)
  2. 2.0 2.1 Neuhof H, Hurwitt E (1943). “ACUTE PUTRID ABSCESS OF THE LUNG : VII. RELATIONSHIP OF THE TECHNIC OF THE ONE-STAGE OPERATION TO RESULTS”. Ann. Surg. 118 (4): 656–64. PMC 1617784. PMID 17858299.
  3. Wali SO (2012). “An update on the drainage of pyogenic lung abscesses”. Ann Thorac Med. 7 (1): 3–7. doi:10.4103/1817-1737.91552. PMC 3277038. PMID 22347342.
Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Overview

Lung abscess is defined as an infection of lung resulting in necrosis of lung parenchyma. It can be classified into three categories based on the duration of symptoms, etiology, and mode of spread as acute or chronic, primary or secondary and bronchogenic or hematogenic.

Classification

Based on duration of symptoms

  • Acute: If the duration of symptoms is less than 4-6 weeks before presenting to medical care.[1]
  • Chronic: If the symptoms persist for more than 6 weeks.

Based on Etiology

Based on mode of spread

Bronchiogenic: Abscess formation is due to aspiration and inhalation.[1]

Hematogenic: Abscess formation due to dissemination of causative agents from other infected sites

Reference

  1. 1.0 1.1 Puligandla PS, Laberge JM (2008). “Respiratory infections: pneumonia, lung abscess, and empyema”. Semin. Pediatr. Surg. 17 (1): 42–52. doi:10.1053/j.sempedsurg.2007.10.007. PMID 18158141.
  2. Bennett, John (2015). Mandell, Douglas, and Bennett’s principles and practice of infectious diseases. Philadelphia, PA: Elsevier/Saunders. ISBN 978-1455748013.
Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Overview

Aspiration of anaerobic bacteria is the inciting event for the development of lung abscess. Once the aspirate is localized it results in pneumonitis. Inflammatory mediators are released, resulting in the formation of colliquative necrosis. The right side lung is more commonly affected than the left. On gross morphology, the lesions are well circumscribed filled with necrotic debris and do not demonstrate well-defined borders with the surrounding lung parenchyma. Microscopic examination demonstrates neutrophilic granulocytes with dilated blood vessels and inflammatory edema. .

Pathophysiology

Location of abscess

  • The right side lung is more commonly affected than the left because the right bronchus is more acutely angulated when compared to left bronchi.
  • The most common location is the posterior segment of the right apical lobe or apical segments of lower lobes of both the lungs.[5]
  • In alcoholics and hospitalized patients are in the supine position, right lateral part of the posterior segment of the upper lobe is more commonly involved.

Genetics

Gross Pathology

  • In acute lung abscess, the lesions are well circumscribed filled with necrotic debris and do not demonstrate well-defined borders with the surrounding lung parenchyma.[7]
  • In chronic long standing abscess, the lesions are irregular and filled with grayish thick debris.

Microscopic Findings

Reference

  1. “Lung abscess”. West. J. Med. 124 (6): 476–82. 1976. PMC 1130102. PMID 936601.
  2. Green LH, Green GM (1968). “Differential suppression of pulmonary antibacterial activity as the mechanism of selection of a pathogen in mixed bacterial infection of the lung”. Am. Rev. Respir. Dis. 98 (5): 819–24. doi:10.1164/arrd.1968.98.5.819. PMID 5683476.
  3. Brook I (2004). “Anaerobic pulmonary infections in children”. Pediatr Emerg Care. 20 (9): 636–40. PMID 15599270.
  4. Tsai YF, Ku YH (2012). “Necrotizing pneumonia: a rare complication of pneumonia requiring special consideration”. Curr Opin Pulm Med. 18 (3): 246–52. doi:10.1097/MCP.0b013e3283521022. PMID 22388585.
  5. Bartlett JG (1993). “Anaerobic bacterial infections of the lung and pleural space”. Clin. Infect. Dis. 16 Suppl 4: S248–55. PMID 8324127.
  6. Canny GJ, Marcotte JE, Levison H (1986). “Lung abscess in cystic fibrosis”. Thorax. 41 (3): 221–2. PMC 460300. PMID 3715782.
  7. 7.0 7.1 Kuhajda I, Zarogoulidis K, Tsirgogianni K, Tsavlis D, Kioumis I, Kosmidis C, Tsakiridis K, Mpakas A, Zarogoulidis P, Zissimopoulos A, Baloukas D, Kuhajda D (2015). “Lung abscess-etiology, diagnostic and treatment options”. Ann Transl Med. 3 (13): 183. doi:10.3978/j.issn.2305-5839.2015.07.08. PMC 4543327. PMID 26366400.


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Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ogheneochuko Ajari, MB.BS, MS [2] ,Aditya Ganti M.B.B.S. [3]

Overview

Lung abscess is commonly caused by bacterial infections and these include bacteroides, peptostreptococcus and prevotella. Most of the lung abscess is caused by polymicrobial organisms,of which anaerobes play a crucial role. Less common include nocardia, actinomyces and fungi.

Causes

Life-threatening causes

Microbiology

The following table elaborates the most common etiological pathogens responsible for lung abscess [5]

 
 
 
 
 
 
 
 
 
 
 
 
 
 
Polymicrobial
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Bacterial
 
 
 
 
 
 
 
Fungal
 
 
Parasites
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Anaerobic
 
 
 
 
 
 
 
 
 
Aerobic
 
Histoplasma capsulatum
Blastomyces
Coccidioides immitis
Aspergillus
Cryptococcus
 
 
Entamoeba histolytica
Paragonimus westermani
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Gram negative
 
 
 
Gram positive
 
 
 
Gram positive
 
 
 
Gram negative
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Bacteroides fragilis
Fusobacterium necrophorum
 
 
 
Peptostreptococcus
Microerophilic streptococci
Actinomyces
 
 
 
Staphylococcus aureus(including MRSA)
Streptococcus pyogenes
Streptococcus pneumoniae
Nocardia
 
 
 
Klebsiella pneumoniae
Haemophilus influenzae
Pseudomonas aeruginosa
Escherichia coli
Legionella
Acinetobacter spp

Common Causes

Less Common Causes

Causes by Organ System

Cardiovascular Infective endocarditis
Chemical/Poisoning No underlying causes
Dental No underlying causes
Dermatologic No underlying causes
Drug Side Effect Drug injection, porfimer
Ear Nose Throat No underlying causes
Endocrine Diabetes mellitus
Environmental No underlying causes
Gastroenterologic Cystic fibrosis
Genetic Cystic fibrosis
Hematologic No underlying causes
Iatrogenic Hospital-acquired pneumonia
Infectious Disease Actinomyces, actinomycosis, alveolar hydatid disease, amoebiasis, aspergilloma, aspergillus, bacteroides, blastomyces dermatitidis, bronchiectasis, burkholderia pseudomallei, candida, capnocytophaga, coccidioides immitis, community-acquired pneumonia, cryptococcus neoformans, cryptococcus, entamoeba histolytica, escherichia coli, fusobacterium, haemophilus influenzae, histoplasma capsulatum, HIV, hospital-acquired pneumonia, infective endocarditis, klebsiella pneumoniae, klebsiella, legionella, Lemierre’s syndrome, listeriosis, melioidosis, mycobacterium tuberculosis, nocardia, paragonimiasis, paragonimus westermani, paragonimus, peptostreptococcus, pneumonia, prevotella, pseudomonas aeruginosa, rhodococcus equi, staphylococcus aureus, streptococcus milleri, streptococcus pneumoniae, streptococcus pyogenes, streptococcus, yersinia
Musculoskeletal/Orthopedic No underlying causes
Neurologic No underlying causes
Nutritional/Metabolic Cystic fibrosis
Obstetric/Gynecologic No underlying causes
Oncologic Bronchogenic carcinoma
Ophthalmologic No underlying causes
Overdose/Toxicity No underlying causes
Psychiatric No underlying causes
Pulmonary Alveolar hydatid disease, aspiration, bronchiectasis, bronchogenic carcinoma, community-acquired pneumonia, cystic fibrosis, hospital-acquired pneumonia, mycobacterium tuberculosis, pneumonia, Wegener’s granulomatosis
Renal/Electrolyte Wegener’s granulomatosis
Rheumatology/Immunology/Allergy Chronic granulomatous disease, common variable immunodeficiency, Sjogren’s syndrome, vasculitis, Wegener’s granulomatosis
Sexual No underlying causes
Trauma No underlying causes
Urologic No underlying causes
Miscellaneous Foreign body

Causes in Alphabetical Order

Reference

  1. Cesar L, Gonzalez C, Calia FM (1975). “Bacteriologic flora of aspiration-induced pulmonary infections”. Arch. Intern. Med. 135 (5): 711–4. PMID 28705.
  2. Bartlett JG (2012). “Anaerobic bacterial infection of the lung”. Anaerobe. 18 (2): 235–9. doi:10.1016/j.anaerobe.2011.12.004. PMID 22209937.
  3. Wang JL, Chen KY, Fang CT, Hsueh PR, Yang PC, Chang SC (2005). “Changing bacteriology of adult community-acquired lung abscess in Taiwan: Klebsiella pneumoniae versus anaerobes”. Clin. Infect. Dis. 40 (7): 915–22. doi:10.1086/428574. PMID 15824979.
  4. “www.iosrjournals.org” (PDF).
  5. Lorber B, Swenson RM (1974). “Bacteriology of aspiration pneumonia. A prospective study of community- and hospital-acquired cases”. Ann. Intern. Med. 81 (3): 329–31. PMID 4850729.
  6. Bartlett JG (2005). “The role of anaerobic bacteria in lung abscess”. Clin. Infect. Dis. 40 (7): 923–5. doi:10.1086/428586. PMID 15824980.
  7. 7.0 7.1 7.2 Hirshberg B, Sklair-Levi M, Nir-Paz R, Ben-Sira L, Krivoruk V, Kramer MR (1999). “Factors predicting mortality of patients with lung abscess”. Chest. 115 (3): 746–50. PMID 10084487.


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Differentiating Lung abscess from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Overview

Lung abscess must be differentiated from other lesions that present with similar symptoms such as cough, fever with chills and rigor and chest includes malignancy, pulmonary tuberculosis, Wegener’s granulomatosis, rheumatoid nodules.

Differential

Disease Clinical features

Signs & symptoms

Radiological Findings Characterstic feature
Fever Cough Hemoptysis Dyspnea Chest pain Weight loss Night sweats
High-grade Low grade Productive Dry
Acute Lung abscess + + +
  • Air fluid level
Malignancy

(primary lung cancer)

+ + + + +
  • A coin-shaped lesion with thick wall(>15mm) is seen on chest x-ray with less ground glass opacities [2][3
  • Long H/o smoking
  • Elderly male or female
  • BAL positive for malignant cells
  • CT guided biopsy is required for confirmation and differnatiation
Pulmonary Tuberculosis + + + +
  • Chest x-ray and CT demonstrates cavities in the upper lobe of the lung
Necrotizing Pneumonia + + + +
  • Multiple cavitary lesions
  • Acute life threatening condition
  • Complication of pneumonia or lung abscess
  • Multiple organisms responsible
  • prompt treatment with antibiotics is required
  • CBC positive for causative organism
empyema + + + + +
  • Blood culture positive for causative agent.
Bronchiectasis + +
  • Specific findings include linear lucencies tram tracking appearance, clustered cysts.
High resolution CT helps in diagnosis .
Wegners granulomatosis + + +
  • Seen mostly in female age group of 40-55 years
  • Traid of Upper , lower respiratory tract and kidney disease
  • Biopsy of involved organ confirms granulomas
Sarcoidosis + + + + +
Rheumatoid nodule + +
  • Pulmonary nodules with cavitation are located in the upper lobe are seen on chest x-ray
Langerhans cell Histiocytosis + + +
  • Thin-walled cystic cavities on chest x-ray
  • Exclusively afflicts smokers.
  • Musculoskeletal and skin is involved
  • Biopsy of the involved organ
Bronchiolitis obliterans + + + +
  • Common appearance on CT is patchy consolidation,often accompanied by ground-glass opacities and nodules.
  • Occupational exposure of industrial toxins
  • Restrictive type of lung disease
  • Biopsy often confirms the diagnosis




Causes of

lung cavities

Differentiating Features Differentiating lab findings Diagnosis

confirmation

  • CXR and CT demonstrates cavities in the upper lobe of the lung
  • Sputum smear positive for acid-fast bacilli and nucleic acid amplification tests (NAAT) is used on sputum or any sterile fluid for rapid diagnosis and is positive for mycobacteria.
  • Any age group
  • Acute, fulminant life threating complication of prior infection
  • >100.4F fever, with hemodynamic instability
  • Worsening pneumonia-like symptoms
  • CBC is positive for causative organism
  • Children and elderly are at risk
  • Empyema appears lenticular in shape and has a thin wall with smooth luminal margins
  • Pulmonary nodules with cavities and infiltrates are a frequent manifestation on CXR
  • Elderly females of 40-50 age group
  • Manifestation of rheumatoid arthritis
  • Presents with other systemic symptoms including symmetric arthritis of the small joints of the hands and feet with morning stiffness are common manifestations.
  • Pulmonary nodules with cavitation are located in the upper lobe (Caplan syndrome) on Xray.
  • On CXR bilateral adenopathy and coarse reticular opacities are seen.
  • CT of the chest demonstrates extensive hilar and mediastinal adenopathy
  • Additional findings on CT include fibrosis (honeycomb, linear, or associated with bronchial distortion), pleural thickening, and ground-glass opacities.[7]
  • Common appearance on CT is patchy consolidation,often accompanied by ground-glass opacities and nodules.[11]
  • Exclusively afflicts smokers, with a peak age of onset of between 20 and 40 years.
  • Clinical presentation varies, but symptoms generally include months of dry cough, fever, night sweats and weight loss.
  • Skin is involved in 80% of the cases, scaly erythematous rash is typical.
  • Thin-walled cystic cavities are the usual radiographic manifestation, observed in over 50% of patients by either CXR or CT scans.[13]
  • Biopsy of the lung


Reference

  1. 1.0 1.1 Chaudhuri MR (1973). “Primary pulmonary cavitating carcinomas”. Thorax. 28 (3): 354–66. PMC 470041. PMID 4353362.
  2. Mouroux J, Padovani B, Elkaïm D, Richelme H (1996). “Should cavitated bronchopulmonary cancers be considered a separate entity?”. Ann. Thorac. Surg. 61 (2): 530–2. doi:10.1016/0003-4975(95)00973-6. PMID 8572761.
  3. Onn A, Choe DH, Herbst RS, Correa AM, Munden RF, Truong MT, Vaporciyan AA, Isobe T, Gilcrease MZ, Marom EM (2005). “Tumor cavitation in stage I non-small cell lung cancer: epidermal growth factor receptor expression and prediction of poor outcome”. Radiology. 237 (1): 342–7. doi:10.1148/radiol.2371041650. PMID 16183941.
  4. 4.0 4.1 Langford CA, Hoffman GS (1999). “Rare diseases.3: Wegener’s granulomatosis”. Thorax. 54 (7): 629–37. PMC 1745525. PMID 10377211.
  5. Lee KS, Kim TS, Fujimoto K, Moriya H, Watanabe H, Tateishi U, Ashizawa K, Johkoh T, Kim EA, Kwon OJ (2003). “Thoracic manifestation of Wegener’s granulomatosis: CT findings in 30 patients”. Eur Radiol. 13 (1): 43–51. doi:10.1007/s00330-002-1422-2. PMID 12541109.
  6. Baughman RP, Teirstein AS, Judson MA, Rossman MD, Yeager H, Bresnitz EA, DePalo L, Hunninghake G, Iannuzzi MC, Johns CJ, McLennan G, Moller DR, Newman LS, Rabin DL, Rose C, Rybicki B, Weinberger SE, Terrin ML, Knatterud GL, Cherniak R (2001). “Clinical characteristics of patients in a case control study of sarcoidosis”. Am. J. Respir. Crit. Care Med. 164 (10 Pt 1): 1885–9. doi:10.1164/ajrccm.164.10.2104046. PMID 11734441.
  7. Brauner MW, Grenier P, Mompoint D, Lenoir S, de Crémoux H (1989). “Pulmonary sarcoidosis: evaluation with high-resolution CT”. Radiology. 172 (2): 467–71. doi:10.1148/radiology.172.2.2748828. PMID 2748828.
  8. Murphy J, Schnyder P, Herold C, Flower C (1998). “Bronchiolitis obliterans organising pneumonia simulating bronchial carcinoma”. Eur Radiol. 8 (7): 1165–9. doi:10.1007/s003300050527. PMID 9724431.
  9. 9.0 9.1 Al-Ghanem S, Al-Jahdali H, Bamefleh H, Khan AN (2008). “Bronchiolitis obliterans organizing pneumonia: pathogenesis, clinical features, imaging and therapy review”. Ann Thorac Med. 3 (2): 67–75. doi:10.4103/1817-1737.39641. PMC 2700454. PMID 19561910.
  10. Cordier JF, Loire R, Brune J (1989). “Idiopathic bronchiolitis obliterans organizing pneumonia. Definition of characteristic clinical profiles in a series of 16 patients”. Chest. 96 (5): 999–1004. PMID 2805873.
  11. Lee KS, Kullnig P, Hartman TE, Müller NL (1994). “Cryptogenic organizing pneumonia: CT findings in 43 patients”. AJR Am J Roentgenol. 162 (3): 543–6. doi:10.2214/ajr.162.3.8109493. PMID 8109493.
  12. Suri HS, Yi ES, Nowakowski GS, Vassallo R (2012). “Pulmonary langerhans cell histiocytosis”. Orphanet J Rare Dis. 7: 16. doi:10.1186/1750-1172-7-16. PMC 3342091. PMID 22429393.
  13. Moore AD, Godwin JD, Müller NL, Naidich DP, Hammar SP, Buschman DL, Takasugi JE, de Carvalho CR (1989). “Pulmonary histiocytosis X: comparison of radiographic and CT findings”. Radiology. 172 (1): 249–54. doi:10.1148/radiology.172.1.2787035. PMID 2787035.
Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Overview

The incidence from lung abscess have greatly declined during the past several decades due to the widespread use of antibiotics and the availability of other treatment options.

Epidemiology and Demographics

  • Incidence has declined in the late 1940s and 1950s, after the practice of performing oral surgery and tonsillectomy in the sitting position was abandoned, as it became clear that this could result in lung abscess formation.[1]
  • Lung abscess accounts for up to 40 to 55 per 100,000 hospital admissions each year in the US.
  • It occurs at any age, but most frequently from the sixth to eighth decades, and is predominantly seen in men. [2]

Reference

  1. SCHWEPPE HI, KNOWLES JH, KANE L (1961). “Lung abscess. An analysis of the Massachusets General Hospital cases from 1943 through 1956”. N. Engl. J. Med. 265: 1039–43. doi:10.1056/NEJM196111232652104. PMID 14039097.
  2. Bartlett JG, Finegold SM (1974). “Anaerobic infections of the lung and pleural space”. Am. Rev. Respir. Dis. 110 (1): 56–77. doi:10.1164/arrd.1974.110.1.56. PMID 4834618.


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Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Overview

Factors resulting in altered level of consciousness and decreased immune response play a key role in the development of lung abscess includes alcoholism, diabetes mellitus, neurological disorder and bronchial obstruction.[1]

Risk Factors

Common Risk Factors

Less Common Risk factors

Reference

  1. Pohlson EC, McNamara JJ, Char C, Kurata L (1985). “Lung abscess: a changing pattern of the disease”. Am. J. Surg. 150 (1): 97–101. PMID 4014575.
  2. Hagan JL, Hardy JD (1983). “Lung abscess revisited. A survey of 184 cases”. Ann. Surg. 197 (6): 755–62. PMC 1352910. PMID 6859981.
  3. Bartlett JG, Finegold SM (1974). “Anaerobic infections of the lung and pleural space”. Am. Rev. Respir. Dis. 110 (1): 56–77. doi:10.1164/arrd.1974.110.1.56. PMID 4834618.
  4. 4.0 4.1 Hirshberg B, Sklair-Levi M, Nir-Paz R, Ben-Sira L, Krivoruk V, Kramer MR (1999). “Factors predicting mortality of patients with lung abscess”. Chest. 115 (3): 746–50. PMID 10084487.


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Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Overview

There is no screening recommendations for lung abscess.

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Overview

Symptoms of lung abscess begin approximately 10 days after aspiration of infected material. Symptoms lasting less than 14 days is considered acute lung abscess, while longer lasting symptoms constitute chronic lung abscess. Acute symptoms include a prodrome accompanied by fever, productive cough, pleuritic chest pain and occasional episodes of hemoptysis. Patients with chronic lung abscess develop weight loss and malaise. The prognosis of lung abscess is good with appropriate antibiotic treatment with a high success rate. Complications include hemorrhage, pyopneumothorax, pleural empyema and sepsis.

Natural History

  • The symptoms of lung abscess usually develop during the fifth decade of life with risk factors, and start with symptoms such as fever, productive cough, pleuritic chest pain and occasional episodes of hemoptysis, typically developing 8-14 days after aspiration [1]
  • Without treatment based on the immune status of the patient, lung abscess can either resolve by forming a granulation tissue scar, or progressively worsens and can result in septicemia, hemorrhage, and death.

Prognosis

The prognosis of lung abscess is good with appropriate antibiotic treatment with a high success rate. The outcomes depend on the other associated conditions underlying lung abscess. The mortality rate of lung abscess is as high as 75% in patients with underlying immunocompromised state and bronchial obstruction favoring poor prognosis. The following factors are considered to be associated with poor prognosis among patients.[2]

Complications

Without treatment, lung abscess can result in the following complications:

Reference

  1. Adebonojo SA, Osinowo O, Adebo O (1979). “Lung abscess: a review of three years’ experience at the University College Hospital, Ibadan”. J Natl Med Assoc. 71 (1): 39–43. PMC 2537236. PMID 423274.
  2. Hirshberg B, Sklair-Levi M, Nir-Paz R, Ben-Sira L, Krivoruk V, Kramer MR (1999). “Factors predicting mortality of patients with lung abscess”. Chest. 115 (3): 746–50. PMID 10084487.
  3. Philpott NJ, Woodhead MA, Wilson AG, Millard FJ (1993). “Lung abscess: a neglected cause of life threatening haemoptysis”. Thorax. 48 (6): 674–5. PMC 464615. PMID 8346503.
  4. Schattner A, Dubin I, Gelber M (2016). “Double jeopardy – concurrent lung abscess and pleural empyema”. QJM. 109 (8): 545–6. doi:10.1093/qjmed/hcw078. PMID 27208219.

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Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | Chest X Ray | CT | MRI | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1

Related Chapters

Template:Respiratory pathology nl:Longabces fi:Keuhkopaise


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