Tracheitis pathophysiology: Difference between revisions

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==Overview==
The exact pathogenesis of [disease name] is not fully understood.


OR
{{CMG}}; {{AE}} [[User:Dushka|Dushka Riaz, MD]]


It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
==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 [[Membrane|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> <ref name="pmid379379">{{cite journal| author=Jones R, Santos JI, Overall JC| title=Bacterial tracheitis. | journal=JAMA | year= 1979 | volume= 242 | issue= 8 | pages= 721-6 | pmid=379379 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=379379  }} </ref> <ref name="pmid11464324">{{cite journal| author=Stroud RH, Friedman NR| title=An update on inflammatory disorders of the pediatric airway: epiglottitis, croup, and tracheitis. | journal=Am J Otolaryngol | year= 2001 | volume= 22 | issue= 4 | pages= 268-75 | pmid=11464324 | doi=10.1053/ajot.2001.24825 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11464324  }} </ref>
OR
 
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
 
OR
 
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
 
OR
 
 
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
 
OR
 
The progression to [disease name] usually involves the [molecular pathway].
 
OR
 
The pathophysiology of [disease/malignancy] depends on the histological subtype.


==Pathophysiology==
==Pathophysiology==
===Physiology===
===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]].  
[[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 [[Trachea|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 [[Lumen (anatomy)|luminal]] [[diameter]] generates negative [[pressure]] which increases the propensity for [[airway collapse]].<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> 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]].
As [[tracheal]] [[inflammation]] occurs the mucosal [[edema]] significantly constricts the [[tracheal]] lumen. This increases the airflow due to [[Venturi]] effect. The decrease in [[Lumen (anatomy)|luminal]] [[diameter]] generates negative [[pressure]] which increases the propensity for [[airway collapse]].<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> 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]]. <ref name="pmid1788120">{{cite journal| author=Gallagher PG, Myer CM| title=An approach to the diagnosis and treatment of membranous laryngotracheobronchitis in infants and children. | journal=Pediatr Emerg Care | year= 1991 | volume= 7 | issue= 6 | pages= 337-42 | pmid=1788120 | doi=10.1097/00006565-199112000-00004 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1788120  }} </ref> <ref name="pmid2237109">{{cite journal| author=Donnelly BW, McMillan JA, Weiner LB| title=Bacterial tracheitis: report of eight new cases and review. | journal=Rev Infect Dis | year= 1990 | volume= 12 | issue= 5 | pages= 729-35 | pmid=2237109 | doi=10.1093/clinids/164.5.729 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2237109  }} </ref> <ref name="pmid29742211">{{cite journal| author=Alves AE, Pereira JM| title=Antibiotic therapy in ventilator-associated tracheobronchitis: a literature review. | journal=Rev Bras Ter Intensiva | year= 2018 | volume= 30 | issue= 1 | pages= 80-85 | pmid=29742211 | doi=10.5935/0103-507x.20180014 | pmc=5885235 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29742211  }} </ref>


===Pathogenesis===
===Pathogenesis===




* The tracheal [[mucosa]] serves as a protective barrier to all inhaled [[pathogens]]
*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]].
*[[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, Parainfluenza, Respiratory Syncitial Virus, Adenovirus and Echoviruses.
*Viral pathogens include [[Influenza A virus|Influenza A]] and B, [[Parainfluenza virus|Parainfluenza,]] [[RSV|Respiratory Syncytial 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>
*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]], [[Klebsiella Pneumonia]]
*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.
*[[Staphylococcal Infections|S. Aureus]] is the most common [[etiology]]. <ref name="pmid28757125">{{cite journal| author=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 | year= 2017 | volume= 47 | issue= 7 | pages= 443-452 | pmid=28757125 | doi=10.1016/j.medmal.2017.06.006 | pmc=7125831 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28757125  }} </ref> <ref name="pmid15577783">{{cite journal| author=Salamone FN, Bobbitt DB, Myer CM, Rutter MJ, Greinwald JH| title=Bacterial tracheitis reexamined: is there a less severe manifestation? | journal=Otolaryngol Head Neck Surg | year= 2004 | volume= 131 | issue= 6 | pages= 871-6 | pmid=15577783 | doi=10.1016/j.otohns.2004.06.708 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15577783  }} </ref> <ref name="pmid18039138">{{cite journal| author=Taubenberger JK, Morens DM| title=The pathology of influenza virus infections. | journal=Annu Rev Pathol | year= 2008 | volume= 3 | issue=  | pages= 499-522 | pmid=18039138 | doi=10.1146/annurev.pathmechdis.3.121806.154316 | pmc=2504709 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18039138  }} </ref>


==Genetics==
==Genetics==
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==Associated Conditions==
==Associated Conditions==
There are no known associated conditions.
There is usually a prior [[Virus|viral]] infection that causes [[airway]] mucosal damage that leads to the [[bacterial]] infection. <ref name="pmid6314288">{{cite journal| author=Edwards KM, Dundon MC, Altemeier WA| title=Bacterial tracheitis as a complication of viral croup. | journal=Pediatr Infect Dis | year= 1983 | volume= 2 | issue= 5 | pages= 390-1 | pmid=6314288 | doi=10.1097/00006454-198309000-00015 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6314288  }} </ref> <ref name="pmid6869336">{{cite journal| author=Liston SL, Gehrz RC, Siegel LG, Tilelli J| title=Bacterial tracheitis. | journal=Am J Dis Child | year= 1983 | volume= 137 | issue= 8 | pages= 764-7 | pmid=6869336 | doi=10.1001/archpedi.1983.02140340044012 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6869336  }} </ref> <ref name="pmid8071748">{{cite journal| author=Eid NS, Jones VF| title=Bacterial tracheitis as a complication of tonsillectomy and adenoidectomy. | journal=J Pediatr | year= 1994 | volume= 125 | issue= 3 | pages= 401-2 | pmid=8071748 | doi=10.1016/s0022-3476(05)83284-6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8071748  }} </ref>


==Gross Pathology==
==Gross Pathology==
On gross pathology, [[mucosal edema]], [[ulceration]], and exudates with thick membranes are characteristic findings of [[tracheitis]].
On gross [[pathology]], mucosal [[edema]], [[ulceration]], and [[Exudate|exudates]] with thick [[Membrane|membranes]] are characteristic findings of [[tracheitis]]. <ref name="pmid7271556">{{cite journal| author=Liston SL, Gehrz RC, Jarvis CW| title=Bacterial tracheitis. | journal=Arch Otolaryngol | year= 1981 | volume= 107 | issue= 9 | pages= 561-4 | pmid=7271556 | doi=10.1001/archotol.1981.00790450037012 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7271556  }} </ref>


==Microscopic Pathology==
==Microscopic Pathology==
On microscopic histopathological analysis, [[microabscesses]] and mononuclear inflammatory cells in the tracheal wall are characteristic findings of [[tracheitis]].
On [[microscopic]] [[histopathological]] analysis, [[Abscess in body|microabscesses]] and [[Mononuclear cells|mononuclear inflammatory cells]] in the tracheal wall are characteristic findings of [[tracheitis]]. [[Bacterial]] [[tracheitis]] is generally [[polymicrobial]]. <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> <ref name="pmid29262085">{{cite journal| author=| title=StatPearls | journal= | year= 2021 | volume=  | issue=  | pages=  | pmid=29262085 | doi= | pmc= | url= }} </ref>


==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
{{WH}}
{{WS}}


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[[Category:Disease]]
[[Category:Pulmonology]]
[[Category:Pulmonology]]
[[Category:Intensive care medicine]]
[[Category:Intensive care medicine]]
[[Category:Emergency medicine]]
[[Category:Emergency medicine]]
[[Category:Pediatrics]]
[[Category:Pediatrics]]
[[Category:Thorax]]
[[Category:Thorax]]
[[Category:Primary care]]
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Latest revision as of 19:57, 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] [2] [3]

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.[4] 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. [5] [6] [7]

Pathogenesis

Genetics

There is no known genetic cause.

Associated Conditions

There is usually a prior viral infection that causes airway mucosal damage that leads to the bacterial infection. [11] [12] [13]

Gross Pathology

On gross pathology, mucosal edema, ulceration, and exudates with thick membranes are characteristic findings of tracheitis. [14]

Microscopic Pathology

On microscopic histopathological analysis, microabscesses and mononuclear inflammatory cells in the tracheal wall are characteristic findings of tracheitis. Bacterial tracheitis is generally polymicrobial. [15] [1]

References

  1. ↑ 1.0 1.1 "StatPearls". 2021. PMID 29262085.
  2. ↑ Jones R, Santos JI, Overall JC (1979). "Bacterial tracheitis". JAMA. 242 (8): 721–6. PMID 379379.
  3. ↑ Stroud RH, Friedman NR (2001). "An update on inflammatory disorders of the pediatric airway: epiglottitis, croup, and tracheitis". Am J Otolaryngol. 22 (4): 268–75. doi:10.1053/ajot.2001.24825. PMID 11464324.
  4. ↑ 4.0 4.1 4.2 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.
  5. ↑ Gallagher PG, Myer CM (1991). "An approach to the diagnosis and treatment of membranous laryngotracheobronchitis in infants and children". Pediatr Emerg Care. 7 (6): 337–42. doi:10.1097/00006565-199112000-00004. PMID 1788120.
  6. ↑ Donnelly BW, McMillan JA, Weiner LB (1990). "Bacterial tracheitis: report of eight new cases and review". Rev Infect Dis. 12 (5): 729–35. doi:10.1093/clinids/164.5.729. PMID 2237109.
  7. ↑ Alves AE, Pereira JM (2018). "Antibiotic therapy in ventilator-associated tracheobronchitis: a literature review". Rev Bras Ter Intensiva. 30 (1): 80–85. doi:10.5935/0103-507x.20180014. PMC 5885235. PMID 29742211.
  8. ↑ 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.
  9. ↑ 9.0 9.1 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.
  10. ↑ Salamone FN, Bobbitt DB, Myer CM, Rutter MJ, Greinwald JH (2004). "Bacterial tracheitis reexamined: is there a less severe manifestation?". Otolaryngol Head Neck Surg. 131 (6): 871–6. doi:10.1016/j.otohns.2004.06.708. PMID 15577783.
  11. ↑ Edwards KM, Dundon MC, Altemeier WA (1983). "Bacterial tracheitis as a complication of viral croup". Pediatr Infect Dis. 2 (5): 390–1. doi:10.1097/00006454-198309000-00015. PMID 6314288.
  12. ↑ Liston SL, Gehrz RC, Siegel LG, Tilelli J (1983). "Bacterial tracheitis". Am J Dis Child. 137 (8): 764–7. doi:10.1001/archpedi.1983.02140340044012. PMID 6869336.
  13. ↑ Eid NS, Jones VF (1994). "Bacterial tracheitis as a complication of tonsillectomy and adenoidectomy". J Pediatr. 125 (3): 401–2. doi:10.1016/s0022-3476(05)83284-6. PMID 8071748.
  14. ↑ Liston SL, Gehrz RC, Jarvis CW (1981). "Bacterial tracheitis". Arch Otolaryngol. 107 (9): 561–4. doi:10.1001/archotol.1981.00790450037012. PMID 7271556.
  15. ↑ 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.

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