Tracheitis pathophysiology: Difference between revisions
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*[[Tracheitis]] means [[inflammation]] of the [[trachea]]. The [[larynx]] and [[bronchi]] can also be involved in the inflammatory process, causing [[laryngotracheobronchitis]]. | *[[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]]. | * [[Viruses]] enter the body through [[inhalation]] and damage the [[mucosal]] lining of the [[trachea]]. | ||
* Viral pathogens include Influenza A and B, Parainfluenza, Respiratory Syncitial Virus, Adenovirus and Herpes Simplex Virus.<ref name="StroudFriedman2001">{{cite journal|last1=Stroud|first1=Robert H.|last2=Friedman|first2=Norman R.|title=An update on inflammatory disorders of the pediatric airway: Epiglottitis, croup, and tracheitis|journal=American Journal of Otolaryngology|volume=22|issue=4|year=2001|pages=268–275|issn=01960709|doi=10.1053/ajot.2001.24825}}</ref> | * Viral pathogens include [[Influenza A virus|Influenza A]] and B, [[Parainfluenza virus|Parainfluenza,]] [[RSV|Respiratory Syncitial Virus]], [[Adenovirus]] and [[Herpes Simplex Viruses|Herpes Simplex Virus]].<ref name="StroudFriedman2001">{{cite journal|last1=Stroud|first1=Robert H.|last2=Friedman|first2=Norman R.|title=An update on inflammatory disorders of the pediatric airway: Epiglottitis, croup, and tracheitis|journal=American Journal of Otolaryngology|volume=22|issue=4|year=2001|pages=268–275|issn=01960709|doi=10.1053/ajot.2001.24825}}</ref> | ||
* Viruses cause desquamation of the pseudostratified columnar epithelium. | *[[Viruses]] cause [[desquamation]] of the [[Pseudostratified columnar epithelia|pseudostratified columnar epithelium]]. | ||
* The epithelium regenerates into stratified non keratinized epithelium through metaplasia.<ref name="pmid18039138">{{cite journal |vauthors=Taubenberger JK, Morens DM |title=The pathology of influenza virus infections |journal=Annu Rev Pathol |volume=3 |issue= |pages=499–522 |date=2008 |pmid=18039138 |pmc=2504709 |doi=10.1146/annurev.pathmechdis.3.121806.154316 |url=}}</ref><ref name="pmid28757125">{{cite journal |vauthors=Blot M, Bonniaud-Blot P, Favrolt N, Bonniaud P, Chavanet P, Piroth L |title=Update on childhood and adult infectious tracheitis |journal=Med Mal Infect |volume=47 |issue=7 |pages=443–452 |date=November 2017 |pmid=28757125 |pmc=7125831 |doi=10.1016/j.medmal.2017.06.006 |url=}}</ref> | * The [[epithelium]] regenerates into [[Epithelium|stratified non keratinized epithelium]] through [[metaplasia]].<ref name="pmid18039138">{{cite journal |vauthors=Taubenberger JK, Morens DM |title=The pathology of influenza virus infections |journal=Annu Rev Pathol |volume=3 |issue= |pages=499–522 |date=2008 |pmid=18039138 |pmc=2504709 |doi=10.1146/annurev.pathmechdis.3.121806.154316 |url=}}</ref><ref name="pmid28757125">{{cite journal |vauthors=Blot M, Bonniaud-Blot P, Favrolt N, Bonniaud P, Chavanet P, Piroth L |title=Update on childhood and adult infectious tracheitis |journal=Med Mal Infect |volume=47 |issue=7 |pages=443–452 |date=November 2017 |pmid=28757125 |pmc=7125831 |doi=10.1016/j.medmal.2017.06.006 |url=}}</ref> | ||
* As host defenses become weak, bacterial invasion becomes more likely. | * As host defenses become weak, bacterial invasion becomes more likely. | ||
* Bacterial pathogens include [[Staphylococcus Aureus]], [[Hemophilus Influenza]], [[Moraxella Catarrhalis]] | * Bacterial pathogens include [[Staphylococcus aureus|Staphylococcus Aureus]], [[Hemophilus 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. | * 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. | * A [[Systemic inflammatory response syndrome|systemic inflammatory response]] develops due to [[Cytokines|cytokine]] release, causing [[septic shock]]. | ||
* The exudates adhere to the tracheal wall causing narrowing of the tracheal lumen. | * The [[Exudate|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. | * The [[Necrosis|necrotic]] debris and purulent membranes can slough off into the [[trachea]], causing acute obstruction. | ||
==Genetics== | ==Genetics== | ||
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==Gross Pathology== | ==Gross Pathology== | ||
On gross pathology, [[ | On gross [[pathology]], mucosal [[edema]], [[ulceration]], and [[Exudate|exudates]] with thick membranes are characteristic findings of [[tracheitis]]. | ||
==Microscopic Pathology== | ==Microscopic Pathology== | ||
On microscopic histopathological analysis, [[microabscesses]] and mononuclear inflammatory cells in the tracheal wall are characteristic findings of [[tracheitis]].<ref name="ListonGehrz1981">{{cite journal|last1=Liston|first1=S. L.|last2=Gehrz|first2=R. C.|last3=Jarvis|first3=C. W.|title=Bacterial Tracheitis|journal=Archives of Otolaryngology - Head and Neck Surgery|volume=107|issue=9|year=1981|pages=561–564|issn=0886-4470|doi=10.1001/archotol.1981.00790450037012}}</ref> | On [[microscopic]] [[histopathological]] analysis, [[Abscess in body|microabscesses]] and mononuclear inflammatory cells in the tracheal wall are characteristic findings of [[tracheitis]].<ref name="ListonGehrz1981">{{cite journal|last1=Liston|first1=S. L.|last2=Gehrz|first2=R. C.|last3=Jarvis|first3=C. W.|title=Bacterial Tracheitis|journal=Archives of Otolaryngology - Head and Neck Surgery|volume=107|issue=9|year=1981|pages=561–564|issn=0886-4470|doi=10.1001/archotol.1981.00790450037012}}</ref> | ||
==References== | ==References== | ||
Revision as of 16:04, 23 July 2020
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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 signficantly 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 Syncitial 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, 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.
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 signficantly 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.[1] 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 Syncitial Virus, Adenovirus and Herpes Simplex Virus.[2]
- Viruses cause desquamation of the pseudostratified columnar epithelium.
- The epithelium regenerates into stratified non keratinized epithelium through metaplasia.[3][1]
- 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.
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.[4]
References
- ↑ 1.0 1.1 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.