Peritonsillar abscess

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

Peritonsillar abscess (PTA), also commonly referred to as quinsy, is defined as a collection of pus located between the tonsillar capsule and the pharyngeal constrictor muscles. It is the most common deep tissue infection of the neck.^[1] Historically, it has been thought of as a complication of acute tonsillitis. However, recent studies have proposed additional hypothesis surrounding its pathogenesis making the understanding of the disease a medical dilemma.^[2]

In second and third century BC the treatment and pathogenesis of tonsillar pathology was first documented in literature by Celcius. In the 1930s and 1940s prior to the advent of antibiotics, surgical management was the most common treatment option for peritonsillar abscess. Interval tonsillectomy was mostly done after symptom resolution. By 1947, Chaud tonsillectomy or immediate surgical tonsillectomy became the treatment option.^[3]

Peritonsillar abscess may be classified into 3 broad categories based on computed tomographical findings. These are based on the shape of the abscess, location of the abscess and shape and location of the abscess. This may be oval or cap, superior or inferior.^[4]

The pathogenesis of peritonsillar abscess is still not well-understood.^[2] Some authorities have proposed that peritonsillar abscess arises from blockage of drainage from tonsillar 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.^[5][3][6][7] 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.^[5] Pus accumulation within tissue behind the supratonsillar space leads to tonsillar bulging, uvula and palate deviation.

The cause of peritonsillar abscess is usually polymicrobial. It is predominantly caused by aerobic and anaerobic bacteria.^[8] Streptococcus pyogenes is the most common cause of peritonsillar abscess.^{[9][8][10][11]} Other common causes include; Fusobacterium necrophorum, Streptococcus milleri, Staphylococci, Haemophilus, Fusobacterium, Prevotella, Acinetobacter, spp, Candida albicans, Peptostreptococcus spp., Pseudomonas spp., Enterobacter spp. and Klebsiella^[9][8]

Peritonsillar abscess must be differentiated from other upper respiratory diseases and conditions that may cause throat pain and airway obstruction. These include; croup(laryngotracheobronchitis), pharyngitis, tonsilitis, retropharyngeal abscess and epiglottitis.

The incidence of peritonsillar abscess is highest between November to December and April to May in the northern hemisphere. This has been associated with the highest rates of streptococcal pharyngitis and exudative tonsillitis around these times.^[12][13] Peritonsillar abscess occurs in all age groups. The highest occurrence is in adults between 20 to 40 years of age.^[1][14][15] There is no racial predilection to developing peritonsillar abscess. Males are more commonly affected with peritonsillar abscess than female with male to female ratio of approximately 1.4:1. However, equal male to female ratios have been reported as well.^{[16][17][18][19][20][21][22]}

There are no screening recommendations for peritonsillar abscess.

Common risk factors in the development of peritonsillar abscess include smoking, previous peritonsillar abscess episodes, history of recurrent pharyngotonsillitis (Inflammation of the pharynx and tonsils) and poor oral hygiene.^[23][24]

Peritonsillar abscess if left untreated may result in extraperitonsillar extension.^[25][26] Peritonsillar abscess may be complicated by airway obstruction, aspiration pneumonitis or lung abscess secondary to peritonsillar abscess rupture, hemorrhage from erosion or septic necrosis into carotid sheath, mediastinitis, poststreptococcal sequelae (e.g., glomerulonephritis, rheumatic fever) when infection is caused by Group A streptococcus, and necrotizing fasciitis^{[1][27][28][29][30]} The prognosis of peritonsillar abscess is good with early and appropriate treatment.^{[31][32][33][34]}

Patients presenting with peritonsillar abscess may have a prior history of acute tonsillitis. Symptoms start appearing 2-8 days before the formation of abscess. Common symptoms of peritonsillar abscess include drooling, dysphagia, foul smelling breath, fever, headache, hoarseness, muffled voice (also called hot potato voice), odynophagia, otalgia, sore throat and stridor.^[35][1]

On physical examination, patients are usually acutely ill-looking and may have high temperature, muffled voice (also called “hot potato voice”), contralateral deflection of the uvula, the tonsil is generally displaced inferiorly and medially, facial swelling, tonsillar hypertrophy,, trismus, drooling, tenderness of anterior neck and tender submandibular and anterior cervical lymph node.s^{[1][36][3][37]}

The diagnosis of peritonsillar abscess may be made without the use of laboratory findings however, some nonspecific laboratory findings may be helpful. Complete blood count with differential usually shows leukocytosis with neutrophilic predominance. Serum electrolytes may be useful in patients presenting with dehydration. Gram stain, culture and sensitivity for sample after abscess drainage may yield the causative organism however, emperic therapy should be initiated without delaying for culture results. A routine throat culture for group A streptococcus may be helpful as well.^{[2][5][3][6][7]}

X ray of the neck is not helpful in the diagnosis of peritonsillar abscess. The initial imaging of choice is ultrasound.^[38]

The diagnosis of peritonsillar abscess may be made without the use of imaging however, imaging options may help in differentiating peritonsillar abscess from other simialr conditions example, peritonsillar cellulitis, retropharyngeal abscess and epiglottitis. On ultrasound, peritonsillar abscess appears as focal irregularly marginated hypoechoic area.^{[39][40][41][42]}

CT scan is helpful in defining the characteristics of the abscess as well as to classify it. It also helps in guiding possible complications. Coronal contrast-enhanced CT scan of the neck may identify the peritonsillar abscess^[39] however, the use of CT scan is associated with a clinically significant delay in time to an otolaryngology consultation, time to admission, and time to bedside procedure.^[43] CT scan may show diffuse hypodense lesion with rim enhancement in the peritonsillar space.^[44]

Parenteral therapy is the preferred first line route of administration until the temperature of the patient has settled and clinically improved and then switched to oral therapy to complete a 14-day course.^[32] The preferred emperic therapy is ampicillin-sulbactam with clindamycinas alternative agent. For resistant gram-positive cocci infections intravenous vancomycin or linezolid is added to the above emperic therapy.^[45]

Incision and drainage, or Tonsillectomy are surgical modalities in the management of peritonsillar abscess. tonsillectomy is oindicated in peritonsillar abscess in severe upper airway obstruction, previous episodes of severe recurrent pharyngitis or peritonsillar abscess and in unresolving peritonsillar abscess after antibiotics and incision and drainage.^{[46][47][48][49]}

There are no definite preventive measures for peritonsillar abscess, however, immunization against certain organisms in childhood may decrease the burden of peritonsillar abscess resulting from such infections.

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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]

In second and third century BC, the treatment and pathogenesis of tonsillar pathology was first documented in literature by Celcius. In the 1930s and 1940s prior to the advent of antibiotics, surgical management was the most common treatment option for peritonsillar abscess. Interval tonsillectomy was mostly done after symptom resolution. By 1947, Chaud tonsillectomy or immediate surgical tonsillectomy became the treatment option.^[1]

The outline below shows the historical perspective of peritonsillar abscess.^[1]

• In second and third century BC, Celcius was the first to document in literature the treatment and pathogenesis of tonsillar pathology.
• In 1700s peritonsillar abscess was first described by Marcus.
• In the 1930s and 1940s prior to the advent of antibiotics, surgical management was the most common treatment option for peritonsillar abscess. Interval tonsillectomy was mostly done after symptom resolution.
• By 1947, Chaud tonsillectomy or immediate surgical tonsillectomy became the treatment option.

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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]

Peritonsillar abscess may be classified into 3 broad categories based on computed tomographical findings. These are based on the shape of the abscess, location of the abscess and shape and location of the abscess. This may be oval or cap, superior or inferior.^[1]

On the basis of computed tomographical findings, peritonsillar abscess may be classified into 3 broad categories based on the following:

1. Shape of the abscess

On the basis of shape it may be classified as:^[1]

• Oval type or
• Cap type

2. Location of the abscess

On the basis of abscess location it may be differentiated into the following:^[1]

• Superior or
• Inferior

3. Shape and location of the abscess

On the basis of shape and location it may be classified as:^[1]

• Superior oval type

• This is the most common type

• Superior cap type
• Inferior oval type and
• Inferior cap type

• Inferior cap-type abscess are at highest incidence of extraperitonsillar spread than the other categories of peritonsillar abscess.

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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]

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.

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.

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]

• 1. It is proposed to arise from an extension of exudative tonsillitis.

• 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 shows cellular swelling and invasion of inflammatory cells predominately neutrophils.

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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]

The cause of peritonsillar abscess is usually polymicrobial. It is predominantly caused by aerobic and anaerobic bacteria.^[1] Streptococcus pyogenes is the most common cause of peritonsillar abscess.^[2][1][3][4] Other common causes include; Fusobacterium necrophorum, Streptococcus milleri, Staphylococci, Haemophilus, Prevotella, Acinetobacter spp., Candida albicans, Peptostreptococcus spp., Pseudomonas spp., Enterobacter spp. and Klebsiella.^[2][1]

The cause of peritonsillar abscess is usually polymicrobial. It is predominantly caused by aerobic and anaerobic bacteria.^[1]

There as no life-threatening causes of peritonsillar abscess.^[2][1]

The most frequent pathogen of peritonsillar abscess is Streptococcus pyogenes.^[2][1][3][4]

Some common causes of peritonsillar abscess include:^[2][1]

• Fusobacterium necrophorum
• Streptococcus milleri
• Staphylococci
• Haemophilus
• Prevotella
• Acinetobacter spp.
• Candida albicans
• Peptostreptococcus spp.
• Pseudomonas spp.
• Enterobacter spp.
• Klebsiella

Less common causes of peritonsillar abscess include:^[2][1]

• Porphyromonas

• Acinetobacter spp.
• Candida albicans
• Enterobacter spp.
• Fusobacterium necrophorum
• Haemophilus
• Klebsiella
• Peptostreptococcus spp.
• Porphyromonas
• Prevotella
• Pseudomonas spp.
• Staphylococcus aureus (including methicillin-resistant staph. aureus)
• Streptococcus anginosus
• Streptococcus milleri
• Streptococcus pyogenes
• Veillonella species

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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]

Peritonsillar abscess must be differentiated from other upper respiratory diseases and conditions that may cause throat pain and airway obstruction. These include; croup(laryngotracheobronchitis), pharyngitis, tonsilitis, retropharyngeal abscess and epiglottitis.

Peritonsillar abscess must be differentiated from other upper respiratory diseases and conditions that may cause throat pain and airway obstruction as shown in the table below:

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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]

The incidence of peritonsillar abscess is highest between November to December and April to May in the northern hemisphere. This has been associated with the highest rates of streptococcal pharyngitis and exudative tonsillitis around these times.^[1][2] Peritonsillar abscess occurs in all age groups. The highest occurrence is in adults between 20 to 40 years of age.^[3][4][5] There is no racial predilection to developing peritonsillar abscess. Males are more commonly affected with peritonsillar abscess than female with male to female ratio of approximately 1.4:1. However, equal male to female ratios have been reported as well.^{[6][7][8][9][10][11][12]}

The incidence of peritonsillar abscess is highest between November to December and April to May in the northern hemisphere. This has been associated with the highest rates of streptococcal pharyngitis and exudative tonsillitis around these times.^[1][2]

Peritonsillar abscess occur in all age groups. The highest occurrence is in adults between 20 to 40 years of age.^[3][4][5]

There is no racial predilection to developing peritonsillar abscess.

Males are more commonly affected with peritonsillar abscess than female with male to female ratio of approximately 1.4:1. However, equal male to female ratios have been reported in some studies as well.^{[6][7][8][9][10][11][12]}

Peritonsillar abscess has not been found to vary significantly among countries.

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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]

There are no screening recommendations for peritonsillar abscess.

There are no screening recommendations for peritonsillar abscess.

Template:WH Template:WS

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

Common risk factors in the development of peritonsillar abscess include smoking, previous peritonsillar abscess episodes, history of recurrent Inflammation of the pharynx and tonsils.^[1][2]

Common risk factors in the development of peritonsillar abscess include:^[1][2]

• Smoking
• Previous peritonsillar abscess episodes
• History of recurrent pharyngotonsillitis (Inflammation of the pharynx and tonsils)
• Poor oral hygiene

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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]

Peritonsillar abscess if left untreated may result in extraperitonsillar extension.^[1][2] Peritonsillar abscess may be complicated by airway obstruction, aspiration pneumonitis or lung abscess secondary to peritonsillar abscess rupture, hemorrhage from erosion or septic necrosis into carotid sheath, mediastinitis, poststreptococcal sequelae (e.g., glomerulonephritis, rheumatic fever) when infection is caused by Group A streptococcus, and necrotizing fasciitis^{[3][4][5][6][7]} The prognosis of peritonsillar abscess is good with early and appropriate treatment.^{[8][9][10][11]}

Peritonsillar abscess if left untreated may result in extraperitonsillar extension.^[1][2]

The following are some complications that may follow peritonsillar abscess:^{[3][4][5][6][7]}

• Extraperitonsillar spread example parapharyngeal extension, deep neck tissues and posterior mediastinum^[1][2][12]

• Peritonsillar abscess may spread through the deep fascia of the neck with associated rapid progression to a more serious infection.

• Airway obstruction
• Aspiration pneumonitis or lung abscess secondary to peritonsillar abscess rupture
• Hemorrhage from erosion or septic necrosis into carotid sheath
• Mediastinitis
• Poststreptococcal sequelae (e.g., glomerulonephritis, rheumatic fever) when infection is caused by Group A streptococcus
• Necrotizing fasciitis

The prognosis of peritonsillar abscess is good with early and appropriate treatment.^{[8][9][10][11]}

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