Lung abscess pathophysiology

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Pathophysiology

  • Aspiration of anerobic bacteria from the oro-pharnynx, due to altered level of consciousness, absent gag reflex or inability to swallow is the inciting event for the development of primary lung abscess.[1]
  • In healthy individuals, defense mechanisms cope up with the small amounts of aspirates with no effects, however, in conditions like alcoholism, DM, and immunocompromised state these defense mechanisms can be compromised leading to decreased activity of alveolar macrophages and mobility of leucocytes. [2].
  • In secondary lung abscess, abscess formation depends on the underlying lung disease and predisposing factors,for example, bronchial obstruction from benign or malignant intrabronchial lesions or extrinsic compression of bronchus as in middle lobe syndrome results in distal abscess formation due to decrease oropharyngeal clearance due to decreased clearance meachanisms and favouring abscess formation.
  • Once the aspirate is localized it results in pneumonitis [3]
  • Inflammatory mediators along with various bacterial toxins and proteolytic enzymes from the neutrophils are released, leading to the disrupture of small blood vessels resulting in the formation of colliquative necrosis [4]

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 right Lateral part of the posterior segment of the upper lobe is more commonly involved.

Genetics

  • Congenital diseases such as cystic fibrosis, vasculitis, pulmonary sequestration and bronchial cysts are associated with increased the risk of lung abscess in children.[6]

Gross Morphology

  • 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

  • In acute lung abscess, neutrophilic granulocytes are demonstrated with dilated blood vessels and inflammatory edema.[7]
  • In chronic lung abscess, biopsy specimen demonstrates lymphocytes, plasma cells, and histiocytes around a layer of pyogenic membrane surrounding the abscess cavity which is filled with pus.

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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