Bronchiolitis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Alonso Alvarado, M.D. [2]
Overview
Bronchiolitis is transmitted by air droplets infected with RSV and that leads to infection of nasopharyngeal mucosa. After the infection, the virus will spread to the lower airway tracts till it reaches the bronchioles where the viral replication takes place. The viral infection induces inflammation which leads to edema and necrosis of the bronchioles epithelium. Cough reflex occurs due to exposure of the subepithelial tissue and nerve fibers. Vascular permeablity increases leading to edema and swelling. Histopathologically, bronchiolitis obliterans shows intraluminal polyps, inflammatory infiltration and macrophages. Constrictive bronchiolitis shows thickening of the airways and interluminal narrowing.
Pathophysiology
Transmission
- Bronchiolitis is transmitted between individuals by air droplets infected with RSV.
- This air droplets lead to infection of the nasopharyngeal mucosa.
Pathogenesis
Bronchiolitis is caused through viral replication process and inflammation as the following:[1]
- Starting from the nasopharyngeal mucosa the RSV will spread to the lower airway tracts. It will spread till reaching the bronchioles where viral replication takes place.
- The viral infection induces an inflammatory response which leads to infiltration of inflammatory cells (RSV-specific lymphocytes), edema and necrosis of the epithelium in the bronchioles which is then sloughed into the lumina causing proliferation of cuboidal epithelial cells without cilia.[2][3]
- Virus causes lysis to the epithelial tissue which leads to the exposure of the supepithelial tissue and nerve fibers so, cough reflex takes place.
- The vascular permeability increases which result in edema and swelling.
- This inflammation process leads to complete or partial obstruction due to reduction of the bronchiolar lumina and necrotic tissue accumulation producing a valve mechanism, leading to hyperinflation.
- By this mechanism, air can flow into the lungs by increased negative pressure during inspiration but is unable to flow out of the lung as the airway's diameter is smaller during expiration.[2] Obstructed areas can evolve to atelectasis. In children, Kohn channels are not well developed, therefore atelectasis and hyperinflation can be greater.
Histopathology
Bronchiolitis shows histopathological findings that may differ between bronchiolitis obliterans and constrictive bronchiolitis.[4]
- Bronchiolitis obliterans:
- Intraluminal polyps which are protrusions inside the bronchioles with fibroblastic proliferation within it.
- Inflammatory infiltration
- Type two pneumocytes lining the alveoli
- Macrophages
- Constrictive bronchiolitis:
- Scars leading to interluminal narrowing and obstruction
- Thickening of the airways due to submucosal collagen and fibrosis
References
- ↑ Garibaldi BT, Illei P, Danoff SK (2012). "Bronchiolitis". Immunol Allergy Clin North Am. 32 (4): 601–19. doi:10.1016/j.iac.2012.08.002. PMID 23102068.
- ↑ 2.0 2.1 Mandell, Gerald L.; Bennett, John E. (John Eugene); Dolin, Raphael. (2010). Mandell, Douglas, and Bennett's principles and practice of infectious disease. Philadelphia, PA: Churchill Livingstone/Elsevier.
- ↑ Wright M, Mullett CJ, Piedimonte G (2008). "Pharmacological management of acute bronchiolitis". Ther Clin Risk Manag. 4 (5): 895–903. PMC 2621418. PMID 19209271.
- ↑ Couture C, Colby TV (2003). "Histopathology of bronchiolar disorders". Semin Respir Crit Care Med. 24 (5): 489–98. doi:10.1055/s-2004-815600. PMID 16088569.