Peritonsillar abscess pathophysiology

Jump to: navigation, search

Abscess Main Page

Peritonsillar abscess Microchapters

Home

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Peritonsillar abscess from other Diseases

Epidemiology and Demographics

Screening

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

X Rays

ECG

CT scan

Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Case Studies

Case #1

Peritonsillar abscess pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Peritonsillar abscess pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Peritonsillar abscess pathophysiology

CDC on Peritonsillar abscess pathophysiology

Peritonsillar abscess pathophysiology in the news

Blogs on Peritonsillar abscess pathophysiology

Directions to Hospitals Treating Peritonsillar abscess

Risk calculators and risk factors for Peritonsillar abscess pathophysiology

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.

Linked-in.jpg