Tracheitis pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
[[Trachea]] connects [[larynx]] with the [[bronchi]] and conducts air to the [[Lungs|lungs.]] The [[mucus membrane]] of trachea is lined by [[Pseudostratified ciliated columnar epithelium|pseudostratified ciliated columnar]] [[epithelium]]. The [[goblet cells]] in the [[epithelium]] secrete [[mucus]] which captures inhaled [[pathogens]]. The [[cilia]] propagate the movement of the [[mucus]] towards the [[larynx]] and [[Pharynx|pharynx.]] Bronchial associated lymphoid tissue further augments the defensive system by providing [[Humoral immunity|humoral]] and [[cellular immunity]]. The tracheal mucosa therefore serves as a protective barrier to all inhaled [[pathogens]]. [[Tracheitis]] means [[inflammation]] of the [[Trachea|trachea.]] . As tracheal [[inflammation]] occurs the mucosal edema significantly constricts the tracheal lumen. This increases the airflow due to Venturi effect. The decrease in luminal diameter generates negative pressure which increases the propensity for airway collapse. This causes turbulent airflow which can be heard as a [[stridor]]. Tracheal [[inflammation]] further reduces the luminal diameter which causes difficulty in [[breathing]]. [[Tracheitis (patient information)|Tracheitis]] is caused by a secondary [[bacterial]] [[inflammation]] which follows a prodromal viral illness. Viral pathogens include [[Influenza A virus|Influenza A]] and B, [[Parainfluenza virus|Parainfluenza]], [[RSV|Respiratory Syncytial Virus]], [[Adenovirus]] and [[Herpes simplex virus|Herpes Simplex Virus]]. [[Virus|Viruses]] enter the body through inhalation and damage the mucosal lining of the [[trachea]]. They induce local [[inflammation]] which impairs the host defenses making [[bacterial]] [[invasion]] more likely. Bacterial pathogens include [[Staphylococcus aureus|Staphylococcus Aureus]], [[Haemophilus influenzae|Haemophilus Influenza]], [[Moraxella catarrhalis|Moraxella Catarrhalis]], [[Klebsiella pneumoniae|Klebsiella Pneumonia]]. They infiltrate the [[epithelial]] lining causing mucosal [[edema]], mucopurulent exudation and [[necrosis]] of the tracheal wall. A systemic inflammatory response develops due to [[Cytokines|cytokine]] release, causing [[septic shock]]. The [[Exudate|exudates]] adhere to the [[Trachea|tracheal]] wall causing narrowing of the tracheal lumen. The [[necrotic]] debris and purulent membranes can slough off into the [[trachea]], causing acute obstruction. | [[Trachea]] connects [[larynx]] with the [[bronchi]] and conducts air to the [[Lungs|lungs.]] The [[mucus membrane]] of trachea is lined by [[Pseudostratified ciliated columnar epithelium|pseudostratified ciliated columnar]] [[epithelium]]. The [[goblet cells]] in the [[epithelium]] secrete [[mucus]] which captures inhaled [[pathogens]]. The [[cilia]] propagate the movement of the [[mucus]] towards the [[larynx]] and [[Pharynx|pharynx.]] Bronchial associated lymphoid tissue further augments the defensive system by providing [[Humoral immunity|humoral]] and [[cellular immunity]]. The tracheal mucosa therefore serves as a protective barrier to all inhaled [[pathogens]]. [[Tracheitis]] means [[inflammation]] of the [[Trachea|trachea.]] . As tracheal [[inflammation]] occurs the mucosal edema significantly constricts the tracheal lumen. This increases the airflow due to Venturi effect. The decrease in luminal diameter generates negative pressure which increases the propensity for airway collapse. This causes turbulent airflow which can be heard as a [[stridor]]. Tracheal [[inflammation]] further reduces the luminal diameter which causes difficulty in [[breathing]]. [[Tracheitis (patient information)|Tracheitis]] is caused by a secondary [[bacterial]] [[inflammation]] which follows a prodromal viral illness. Viral pathogens include [[Influenza A virus|Influenza A]] and B, [[Parainfluenza virus|Parainfluenza]], [[RSV|Respiratory Syncytial Virus]], [[Adenovirus]] and [[Herpes simplex virus|Herpes Simplex Virus]]. [[Virus|Viruses]] enter the body through inhalation and damage the mucosal lining of the [[trachea]]. They induce local [[inflammation]] which impairs the host defenses making [[bacterial]] [[invasion]] more likely. Bacterial pathogens include [[Staphylococcus aureus|Staphylococcus Aureus]], [[Haemophilus influenzae|Haemophilus Influenza]], [[Moraxella catarrhalis|Moraxella Catarrhalis]], [[Klebsiella pneumoniae|Klebsiella Pneumonia]]. They infiltrate the [[epithelial]] lining causing mucosal [[edema]], mucopurulent exudation and [[necrosis]] of the tracheal wall. A systemic inflammatory response develops due to [[Cytokines|cytokine]] release, causing [[septic shock]]. The [[Exudate|exudates]] adhere to the [[Trachea|tracheal]] wall causing narrowing of the tracheal lumen. The [[necrotic]] debris and purulent membranes can slough off into the [[trachea]], causing acute obstruction. <ref name="pmid29262085">{{cite journal| author=| title=StatPearls | journal= | year= 2021 | volume= | issue= | pages= | pmid=29262085 | doi= | pmc= | url= }} </ref> | ||
==Pathophysiology== | ==Pathophysiology== | ||
Revision as of 19:38, 2 May 2021
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dushka Riaz, MD
Overview
Trachea connects larynx with the bronchi and conducts air to the lungs. The mucus membrane of trachea is lined by pseudostratified ciliated columnar epithelium. The goblet cells in the epithelium secrete mucus which captures inhaled pathogens. The cilia propagate the movement of the mucus towards the larynx and pharynx. Bronchial associated lymphoid tissue further augments the defensive system by providing humoral and cellular immunity. The tracheal mucosa therefore serves as a protective barrier to all inhaled pathogens. Tracheitis means inflammation of the trachea. . As tracheal inflammation occurs the mucosal edema significantly constricts the tracheal lumen. This increases the airflow due to Venturi effect. The decrease in luminal diameter generates negative pressure which increases the propensity for airway collapse. This causes turbulent airflow which can be heard as a stridor. Tracheal inflammation further reduces the luminal diameter which causes difficulty in breathing. Tracheitis is caused by a secondary bacterial inflammation which follows a prodromal viral illness. Viral pathogens include Influenza A and B, Parainfluenza, Respiratory Syncytial Virus, Adenovirus and Herpes Simplex Virus. Viruses enter the body through inhalation and damage the mucosal lining of the trachea. They induce local inflammation which impairs the host defenses making bacterial invasion more likely. Bacterial pathogens include Staphylococcus Aureus, Haemophilus Influenza, Moraxella Catarrhalis, Klebsiella Pneumonia. They infiltrate the epithelial lining causing mucosal edema, mucopurulent exudation and necrosis of the tracheal wall. A systemic inflammatory response develops due to cytokine release, causing septic shock. The exudates adhere to the tracheal wall causing narrowing of the tracheal lumen. The necrotic debris and purulent membranes can slough off into the trachea, causing acute obstruction. [1]
Pathophysiology
Physiology
Trachea connects larynx with the bronchi and conducts air to the lungs. It is made of C shaped rings of cartilage. Muscles and fibers connect the tracheal rings together. This structural strength enables the trachea to withstand the variations in air pressure during each breathing cycle. The mucus membrane of trachea is lined by pseudostratified ciliated columnar epithelium. The goblet cells in the epithelium secrete mucus which captures inhaled pathogens. The cilia propagate the movement of the mucus towards the larynx and pharynx. It is either swallowed or expectorated as phlegm out of the body. Bronchial Associated Lymphoid tissue further augments the defensive system by providing humoral and cellular immunity. As tracheal inflammation occurs the mucosal edema significantly constricts the tracheal lumen. This increases the airflow due to Venturi effect. The decrease in luminal diameter generates negative pressure which increases the propensity for airway collapse.[2] This causes turbulent airflow which can be heard as a stridor. Children have a narrower subglottic region compared to adults. Tracheal inflammation further reduces the luminal diameter which causes difficulty in breathing. Therefore, patients with tracheitis present with tachypnea, tachycardia, respiratory fatigue and stridor.
Pathogenesis
- The tracheal mucosa serves as a protective barrier to all inhaled pathogens
- Tracheitis means inflammation of the trachea. The larynx and bronchi can also be involved in the inflammatory process, causing laryngotracheobronchitis.
- Viruses enter the body through inhalation and damage the mucosal lining of the trachea.
- Viral pathogens include Influenza A and B, Parainfluenza, Respiratory Syncytial Virus, Adenovirus and Herpes Simplex Virus.[3]
- Viruses cause desquamation of the pseudostratified columnar epithelium.
- The epithelium regenerates into stratified non keratinized epithelium through metaplasia.[4][2]
- As host defenses become weak, bacterial invasion becomes more likely.
- Bacterial pathogens include Staphylococcus Aureus, Hemophilus Influenza, Moraxella Catarrhalis, Klebsiella Pneumonia
- They infiltrate the epithelial lining causing mucosal edema, mucopurulent exudation and necrosis of the tracheal wall.
- A systemic inflammatory response develops due to cytokine release, causing septic shock.
- The exudates adhere to the tracheal wall causing narrowing of the tracheal lumen.
- The necrotic debris and purulent membranes can slough off into the trachea, causing acute obstruction.
- S. Aureus is the most common etiology.
Genetics
There is no known genetic cause.
Associated Conditions
There are no known associated conditions.
Gross Pathology
On gross pathology, mucosal edema, ulceration, and exudates with thick membranes are characteristic findings of tracheitis.
Microscopic Pathology
On microscopic histopathological analysis, microabscesses and mononuclear inflammatory cells in the tracheal wall are characteristic findings of tracheitis.[5]
References
- ↑ "StatPearls". 2021. PMID 29262085.
- ↑ 2.0 2.1 Blot M, Bonniaud-Blot P, Favrolt N, Bonniaud P, Chavanet P, Piroth L (November 2017). "Update on childhood and adult infectious tracheitis". Med Mal Infect. 47 (7): 443–452. doi:10.1016/j.medmal.2017.06.006. PMC 7125831 Check
|pmc=value (help). PMID 28757125. - ↑ Stroud, Robert H.; Friedman, Norman R. (2001). "An update on inflammatory disorders of the pediatric airway: Epiglottitis, croup, and tracheitis". American Journal of Otolaryngology. 22 (4): 268–275. doi:10.1053/ajot.2001.24825. ISSN 0196-0709.
- ↑ Taubenberger JK, Morens DM (2008). "The pathology of influenza virus infections". Annu Rev Pathol. 3: 499–522. doi:10.1146/annurev.pathmechdis.3.121806.154316. PMC 2504709. PMID 18039138.
- ↑ Liston, S. L.; Gehrz, R. C.; Jarvis, C. W. (1981). "Bacterial Tracheitis". Archives of Otolaryngology - Head and Neck Surgery. 107 (9): 561–564. doi:10.1001/archotol.1981.00790450037012. ISSN 0886-4470.