Peritonsillar abscess pathophysiology: Difference between revisions

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The [[pathogenesis]] of peritonsillar abscess is still not well-understood.<ref name="pmid23612569">{{cite journal| author=Powell EL, Powell J, Samuel JR, Wilson JA| title=A review of the pathogenesis of adult peritonsillar abscess: time for a re-evaluation. | journal=J Antimicrob Chemother | year= 2013 | volume= 68 | issue= 9 | pages= 1941-50 | pmid=23612569 | doi=10.1093/jac/dkt128 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23612569  }} </ref> Some authorities have proposed that peritonsillar abscess arises from blockage of drainage from tonsillar [[Crypt (anatomy)|crypt]] following [[acute]] [[tonsillitis]] results in spread of infection into the peritonsillar space. However, others believe [[infectious]] process involving Weber's [[gland]] located in the supratonsillar space account for the [[abscess]] formation.<ref name=abd>L. Michaels, H.B. Hellquist Ear, nose and throat histopathology (2nd ed.)Springer-Verlag, London (2001), pp. 281–286</ref><ref name="pmid8302122">{{cite journal| author=Passy V| title=Pathogenesis of peritonsillar abscess. | journal=Laryngoscope | year= 1994 | volume= 104 | issue= 2 | pages= 185-90 | pmid=8302122 | doi=10.1288/00005537-199402000-00011 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8302122  }} </ref><ref name="pmid25865201">{{cite journal| author=Blair AB, Booth R, Baugh R| title=A unifying theory of tonsillitis, intratonsillar abscess and peritonsillar abscess. | journal=Am J Otolaryngol | year= 2015 | volume= 36 | issue= 4 | pages= 517-20 | pmid=25865201 | doi=10.1016/j.amjoto.2015.03.002 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25865201  }} </ref><ref name="pmid16643771">{{cite journal| author=Herzon FS, Martin AD| title=Medical and surgical treatment of peritonsillar, retropharyngeal, and parapharyngeal abscesses. | journal=Curr Infect Dis Rep | year= 2006 | volume= 8 | issue= 3 | pages= 196-202 | pmid=16643771 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16643771  }} </ref> [[Antigenic]] response following any disturbance arising from within or around the tonsillar crypt [[Mucosal|mucosa]] allows for [[lymphocytic]] interaction. This disruption in the crypt [[epithelium]] may be preceded by [[infectious]] process. [[Invasion]] and [[proliferation]] of the tonsillar crypt by [[infectious]] [[pathogens]] results in localized [[edema]] and influx of [[neutrophils]]. This is clinically seen as [[inflamed]] [[tonsil]] with or without exudation.<ref name=abd>L. Michaels, H.B. Hellquist Ear, nose and throat histopathology (2nd ed.)Springer-Verlag, London (2001), pp. 281–286</ref> [[Pus]] accumulation within tissue behind the supratonsillar space leads to tonsillar bulging, [[uvula]] and [[palate]] deviation.
The [[pathogenesis]] of peritonsillar abscess is still not well-understood.<ref name="pmid23612569">{{cite journal| author=Powell EL, Powell J, Samuel JR, Wilson JA| title=A review of the pathogenesis of adult peritonsillar abscess: time for a re-evaluation. | journal=J Antimicrob Chemother | year= 2013 | volume= 68 | issue= 9 | pages= 1941-50 | pmid=23612569 | doi=10.1093/jac/dkt128 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23612569  }} </ref> Some authorities have proposed that peritonsillar abscess arises from blockage of drainage from tonsillar [[Crypt (anatomy)|crypt]] following [[acute]] [[tonsillitis]] resulting in spread of infection into the peritonsillar space. However, others believe [[infectious]] process involving Weber's [[gland]] located in the supratonsillar space account for the [[abscess]] formation.<ref name=abd>L. Michaels, H.B. Hellquist Ear, nose and throat histopathology (2nd ed.)Springer-Verlag, London (2001), pp. 281–286</ref><ref name="pmid8302122">{{cite journal| author=Passy V| title=Pathogenesis of peritonsillar abscess. | journal=Laryngoscope | year= 1994 | volume= 104 | issue= 2 | pages= 185-90 | pmid=8302122 | doi=10.1288/00005537-199402000-00011 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8302122  }} </ref><ref name="pmid25865201">{{cite journal| author=Blair AB, Booth R, Baugh R| title=A unifying theory of tonsillitis, intratonsillar abscess and peritonsillar abscess. | journal=Am J Otolaryngol | year= 2015 | volume= 36 | issue= 4 | pages= 517-20 | pmid=25865201 | doi=10.1016/j.amjoto.2015.03.002 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25865201  }} </ref><ref name="pmid16643771">{{cite journal| author=Herzon FS, Martin AD| title=Medical and surgical treatment of peritonsillar, retropharyngeal, and parapharyngeal abscesses. | journal=Curr Infect Dis Rep | year= 2006 | volume= 8 | issue= 3 | pages= 196-202 | pmid=16643771 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16643771  }} </ref> [[Antigenic]] response following any disturbance arising from within or around the tonsillar crypt [[Mucosal|mucosa]] allows for [[lymphocytic]] interaction. This disruption in the crypt [[epithelium]] may be preceded by [[infectious]] process. [[Invasion]] and [[proliferation]] of the tonsillar crypt by [[infectious]] [[pathogens]] results in localized [[edema]] and influx of [[neutrophils]]. This is clinically seen as [[inflamed]] [[tonsil]] with or without exudation.<ref name=abd>L. Michaels, H.B. Hellquist Ear, nose and throat histopathology (2nd ed.)Springer-Verlag, London (2001), pp. 281–286</ref> [[Pus]] accumulation within [[tissue]] behind the supratonsillar space leads to tonsillar bulging, [[uvula]] and [[palate]] deviation.


==Pathophysiology==
==Pathophysiology==
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A good understanding of the [[tonsil]] and its surrounding space is important in the [[pathogenesis]] of peritonsillar abscess.  
A good understanding of the [[tonsil]] and its surrounding space is important in the [[pathogenesis]] of peritonsillar abscess.  
The [[palatine tonsils]] are found in an anatomical structure called [[tonsillar fossa]]. This [[fossa]] is bounded anteriorly by palatoglossal muscle, posteriorly by palatopharyngeal muscle, laterally by a [[fibrous]] [[capsule]] and tonsillar crypts [[medially]]. Contents of the tonsillar crypts are expelled by [[contraction]] of the tonsillopharyngeus muscle.<ref name=abd>L. Michaels, H.B. Hellquist Ear, nose and throat histopathology (2nd ed.)Springer-Verlag, London (2001), pp. 281–286</ref> The [[tonsils]] form during the last months of [[pregnancy]] and becomes fully formed by 6 to 7 years of age. It then undergoes involution until small size remains in older population.
The [[palatine tonsils]] are found in an anatomical structure called [[tonsillar fossa]]. This [[fossa]] is bounded anteriorly by palatoglossal muscle, posteriorly by palatopharyngeal muscle, laterally by a [[fibrous]] [[capsule]] and tonsillar crypts [[medially]]. Contents of the tonsillar crypts are expelled by [[contraction]] of the tonsillopharyngeus muscle.<ref name=abd>L. Michaels, H.B. Hellquist Ear, nose and throat histopathology (2nd ed.)Springer-Verlag, London (2001), pp. 281–286</ref> The [[tonsils]] form during the last months of [[pregnancy]] and becomes fully formed by 6 to 7 years of age. It then undergoes involution until small size remains in older population.
Located within the soft palate is the supratonsillar space occupied by series of 20 to 25 [[salivary glands]] described as Weber's glands. The [[ducts]] of these [[glands]] form a common [[duct]] which opens onto the [[posterior]] surface of the [[tonsil]] after passing through the tonsillar [[capsule]]. It is proposed that the secretions from these [[glands]] play a rule in food [[digestion]].
Located within the [[soft palate]] is the supratonsillar space occupied by series of 20 to 25 [[salivary glands]] described as Weber's glands. The [[ducts]] of these [[glands]] form a common [[duct]] which opens onto the [[posterior]] surface of the [[tonsil]] after passing through the tonsillar [[capsule]]. It is proposed that the [[secretions]] from these [[glands]] play a rule in food [[digestion]].
Peritonsillar abscesses form in the area between the [[Palatine tonsils|palatine tonsil]] and its [[capsule]].
Peritonsillar abscesses form in the area between the [[Palatine tonsils|palatine tonsil]] and its [[capsule]].



Revision as of 19:34, 7 March 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

Overview

The pathogenesis of peritonsillar abscess is still not well-understood.[1] Some authorities have proposed that peritonsillar abscess arises from blockage of drainage from tonsillar crypt following acute tonsillitis resulting in spread of infection into the peritonsillar space. However, others believe infectious process involving Weber's gland located in the supratonsillar space account for the abscess formation.[2][3][4][5] Antigenic response following any disturbance arising from within or around the tonsillar crypt mucosa allows for lymphocytic interaction. This disruption in the crypt epithelium may be preceded by infectious process. Invasion and proliferation of the tonsillar crypt by infectious pathogens results in localized edema and influx of neutrophils. This is clinically seen as inflamed tonsil with or without exudation.[2] Pus accumulation within tissue behind the supratonsillar space leads to tonsillar bulging, uvula and palate deviation.

Pathophysiology

Anatomy

A good understanding of the tonsil and its surrounding space is important in the pathogenesis of peritonsillar abscess. The palatine tonsils are found in an anatomical structure called tonsillar fossa. This fossa is bounded anteriorly by palatoglossal muscle, posteriorly by palatopharyngeal muscle, laterally by a fibrous capsule and tonsillar crypts medially. Contents of the tonsillar crypts are expelled by contraction of the tonsillopharyngeus muscle.[2] The tonsils form during the last months of pregnancy and becomes fully formed by 6 to 7 years of age. It then undergoes involution until small size remains in older population. Located within the soft palate is the supratonsillar space occupied by series of 20 to 25 salivary glands described as Weber's glands. The ducts of these glands form a common duct which opens onto the posterior surface of the tonsil after passing through the tonsillar capsule. It is proposed that the secretions from these glands play a rule in food digestion. Peritonsillar abscesses form in the area between the palatine tonsil and its capsule.

Pathogenesis

The pathogenesis of peritonsillar abscess is still not well-understood.[1] There are two proposed theories believed to be involved in the pathogenesis of peritonsillar abscess formation.[2][3][4][5]

  • Some authorities believe that blockage of drainage from tonsillar crypt in acute tonsillitis results in spread of infection into the peritonsillar space.
  • 2. Involvement of Weber's gland account for the abscess formation.
  • Some believe that peritonsillar abscess arises from infectious process involving group of salivary glands called Weber's glands located in the supratonsillar space.

Antigenic response following any disturbance arising from within the tonsillar crypt mucosa allows for lymphocytic interaction. This disruption in the crypt epithelium may be preceded by infectious process. Invasion and proliferation of the tonsillar crypt by infectious pathogens results in localized edema and influx of neutrophils. This is clinically seen as inflamed tonsil with or without exudation.[2] Pus accumulation within tissue behind the supratonsillar space leads to tonsillar bulging, uvula and palate deviation.

Microscopic pathology

Microscopic pathology shows cellular swelling and invasion of inflammatory cells predominately neutrophils.

References

  1. 1.0 1.1 Powell EL, Powell J, Samuel JR, Wilson JA (2013). "A review of the pathogenesis of adult peritonsillar abscess: time for a re-evaluation". J Antimicrob Chemother. 68 (9): 1941–50. doi:10.1093/jac/dkt128. PMID 23612569.
  2. 2.0 2.1 2.2 2.3 2.4 L. Michaels, H.B. Hellquist Ear, nose and throat histopathology (2nd ed.)Springer-Verlag, London (2001), pp. 281–286
  3. 3.0 3.1 Passy V (1994). "Pathogenesis of peritonsillar abscess". Laryngoscope. 104 (2): 185–90. doi:10.1288/00005537-199402000-00011. PMID 8302122.
  4. 4.0 4.1 Blair AB, Booth R, Baugh R (2015). "A unifying theory of tonsillitis, intratonsillar abscess and peritonsillar abscess". Am J Otolaryngol. 36 (4): 517–20. doi:10.1016/j.amjoto.2015.03.002. PMID 25865201.
  5. 5.0 5.1 Herzon FS, Martin AD (2006). "Medical and surgical treatment of peritonsillar, retropharyngeal, and parapharyngeal abscesses". Curr Infect Dis Rep. 8 (3): 196–202. PMID 16643771.

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