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==Overview==
==Overview==

Revision as of 14:20, 2 March 2017

Peritonsillar abscess
ICD-10 J36
ICD-9 475
DiseasesDB 11141
eMedicine emerg/417 


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Kiran Singh, M.D. [2] Prince Tano Djan, BSc, MBChB [3]

Synonyms and keywords: PTA, tonsillar abscess, intratonsillar abscess

Overview

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]

Historical perspective

The outline below shows the historical perspective of peritonsillar abscess.[3]

  • 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.
  • 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.

Classification

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:[4]

  • Oval type or
  • Cap type

2. Location of the abscess

On the basis of abscess location it may be differentiated into the following:[4]

3. Shape and location

On the basis of shaped and location it may be classified as:[4]

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.[5] 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.[2] There are two proposed theories believed to be involved in the pathogensis of peritonsillar abscess formation.[5][3][6][7]

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.[5] Pus accumulation within tissue behind the supratonsillar space leads to tonsillar bulging, uvula and palate deviation.

Gross pathology

On gross pathology, the tonsillar region is edematous and inflamed as shown below: [8]


200PX

Causes

Peritonsillar abscess (PTA) usually arises as a complication of an untreated or partially treated episode of acute tonsillitis. The infection, in these cases, spreads to the peritonsillar area (peritonsillitis). This region comprises of loose connective tissue and is hence susceptible to formation of abscess. Peritonsilar abscess can also occur de novo. Both aerobic and anaerobic bacteria can be causative.[9][9]

Life-threatening causes

Life-threatening conditions may result in death or permanent disability within 24 hours if left untreated. Peritonsillar abscess may become a life-threatening condition and must be treated as such irrespective of the cause.[10][9]

Most common cause

The most frequent pathogen of peritonsillar abscess is Streptococcus pyogenes.[10][9][11][12]

Common causes

Some common causes of peritonsillar abscess include:[10][9]

Less common causes

Less common causes of peritonsillar abscess include:[10][9]

Differentiating Peritonsillar abscess from Other Diseases

Variable Peritonsillar abscess Croup Epiglottitis Pharyngitis Tonsilitis Retropharyngeal abscess
Presentation Severe sore throat, otalgia fever, a "hot potato" or muffled voice, drooling, and trismus[1] Cough Sore throat, pain on swallowing, fever, headache, abdominal pain, nausea and vomiting Sore throat, pain on swallowing, fever, headache, cough Neck pain, stiff neck, torticollis

fever, malaise, stridor, and barking cough

Stridor
Drooling
Others are Hoarseness, Difficulty breathing, symptoms of the common cold, Runny nose, Fever Other symptoms include difficulty breathing, fever, chills, difficulty swallowing, hoarseness of voice
Causes Aerobic and anaerobic bacteria most common is Streptococcus pyogenes.[10][9][11][12] Parainfluenza virus H. influenza type b, beta-hemolytic streptococci, Staphylococcus aureus, fungi and viruses. Group A beta-hemolytic streptococcus. Most common cause is viral including adenovirus, rhinovirus, influenza, coronavirus, and respiratory syncytial virus. Second most common causes are bacterial; Group A streptococcal bacteria,[13]  Polymicrobial infection. Mostly; Streptococcus pyogenes, Staphylococcus aureus and respiratory anaerobes (example; Fusobacteria, Prevotella, and Veillonella species)[14][15][16][10][17][18]
Physical exams findings Contralateral deflection of the uvula,

the tonsil is displaced inferiorly and medially, tender submandibular and anterior cervical lymph nodes, tonsillar hypertrophy with likely peritonsillar edema.

Suprasternal and intercostal indrawing,[19] Inspiratory stridor[20], expiratory wheezing,[20] Sternal wall retractions[21] Cyanosis, Cervical lymphadenopathy, Inflammed epiglottis Inflammed pharynx with or without exudate Fever, especially 100°F or higher.[22][23]Erythema, edema and Exudate of the tonsils.[24] cervical lymphadenopathy, Dysphonia.[25] Child may be unable to open the mouth widely. May have enlarged

cervical lymph nodes and neck mass.

Age commonly affected The highest occurrence is in adults between 20 to 40 years of age.[1] Mainly 6 months and 3 years old

rarely, adolescents and adults[26]

Used to be mostly found in

pediatric age group between 3 to 5 years,

however, recent trend favors adults

as most commonly affected individuals[27]

with a mean age of 44.94 years.

Mostly in children and young adults,

with 50% of cases identified

between the ages of 5 to 24 years.[28]

Primarily affects children

between 5 and 15 years old.[29]

Mostly between 2-4 years, but can occur in other age groups.[30][31]
Imaging finding On ultrasound peritonsillar abscess appears as focal irregularly marginated hypoechoic area.[32][33][34][35][32][33] Steeple sign on neck X-ray Thumbprint sign on neck x-ray Intraoral or transcutaneous USG may show an abscess making CT scan unnecessary.[4][36][37] On CT scan, a mass impinging on the posterior pharyngeal wall with rim enhancement is seen[38][39]
Treatment Dexamethasone and nebulised epinephrine Airway maintenance, parenteral Cefotaxime or Ceftriaxone in combination with Vancomycin. Adjuvant therapy includes corticosteroids and racemic Epinephrine.[40][41] Antimicrobial therapy mainly penicillin-based and analgesics. Antimicrobial therapy mainly penicillin-based and analgesics with tonsilectomy in selected cases. Immediate surgical drainage and antimicrobial therapy. emperic therapy involves; ampicillin-sulbactam or clindamycin.

Other differential diagnosis not listed in the table include:

Epidemiology and Demographics

Prevalence and incidence

The incidence of peritonsillar abscess is highest between November to December and April to May. This has been associated with the highest rates of streptococcal pharyngitis and exudative tonsillitis around that these times.[42][43]

Age

Peritonsillar abscess occur in all age groups. The highest occurrence is in adults between 20 to 40 years of age.[1][44][45]

Race

There is no racial predilection to developing peritonsillar abscess.

Gender

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.[46][47][48][49][50][51][52]

Developed and developing countries

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

Risk Factors

Common risk factors in the development of peritonsillar abscess include:[53][54]

  • Smoking
  • Previous peritonsillar abscess episodes
  • History of recurrent pharyngotonsillitis
  • Poor oral hygiene

Screening

There are no screening recommendations for peritonsillar abscess.

Natural History, Complications, and Prognosis

Natural history

Peritonsillar abscess if left untreated may result in extraperitonsillar extension.[55][56]

Complications

The following are some complications that may follow peritonsillar abscess:[1][57][58][59][60]

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

Prognosis

The prognosis of peritonsillar abscess is good with early and appropriate treatment.[61][62][63][64]

Diagnosis

History and Symptoms

  • Unlike tonsillitis, which is more common in the pediatric age group, peritonsillar abscess has a more even age spread — from children to adults.
  • Symptoms start appearing 2-8 days before the formation of abscess. Common symptoms are:[1]

Physical Examination

Physical examination findings suggestive of peritonsillar abscess include the following:[1][66][3][67]

Appearance of the Patient

  • They are usually acutely-ill looking.

Vital Signs

HEENT

Neck

Lungs

  • May be in obvious respiratory distress with flaring of ala nasi, subcostal and intercostal recessions.
  • Increased respiratory rate in both children and adults
  • Decreased air-entry depending of degree of airway obstruction

Extremities

  • Cyanosis

Laboratory Findings

Although the diagnosis of peritonsillar abscess may be made without the use of laboratory findings, the following nonspecific laboratory findings may be seen:[2][5][3][6][7]

  • This usually shows leukocytosis with neutrophilic predominance
  • This is useful too in patients presenting with dehydration
  • Gram stain, culture and sensitivity for sample after abscess drainage.
  • Emperic therapy should be initiated and modified accordingly when results are ready.

Imaging Findings

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.

Ultrasound

This is helpful in differentiating peritonsillar abscess from peritonsillar cellulitis as well as a guide during abscess drainage. The approach may be intraoral or submandibular.[68][34][69][70][71]

On ultrasound the following may be found:[32][33][34][35][32][33]

  • Peritonsillar abscess appears as focal irregularly marginated hypoechoic area.
  • Irregular hypoechoic areas within the tonsil may represent pockets of developing purulence or necrosis called intratonsillar abscesses.
  • Peritonsillar cellulitis appears as enlarged tonsil (arrows) with ill-defined margins and markedly increased echogenicity of surrounding soft tissues that suggests significant inflammatory change/cellulitis.

CT scan

Coronal contrast-enhanced CT scan of the neck may identify the peritonsillar abscess.[34]

Treatment

Medical Therapy

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.[62]

Antimicrobial Regimen

Below are the antimicrobial regimen available in treating peritonsillar abscess.[8]

  • Preferred regimen in children: Ampicillin-sulbactam 50 mg/kg per dose [maximum single dose 3 g] IV 6h
  • Alternative regimen in adults: Clindamycin 600mg IV 6-8h
  • Alternative regimen in children: Clindamycin 13 mg/kg per dose [maximum single dose 900 mg] IV 8h

The above alternative therapy are employed in the following situations:

Pathogen-directed antimicrobial therapy

  • Resistant Gram-positive cocci

For resistant Gram-positive cocci infections IV Vancomycin or Linezolid is added to the above emperic therapy.

Surgery

Surgical modalities in the management of peritonsillar abscess involve the use of the following:

Indications for tonsillectomy in peritonsillar abscess

  • Severe upper respirtaory obstruction
  • Previous episodes of severe recurrent pharyngitis or peritonsillar abscess
  • Unresolving peritonsillar abscess after antibiotics incision and drainage

Prevention

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

  • Immunization with the Hib vaccine protects children.[72]
  • In the United states, vaccination against Hib in children was initiated in the 1980s. Immunity against Hib has been adequate with an increasing level of immunization among children.
  • Post-splenectomy patients are also recommended to be immunized.[72]

References

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