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Revision as of 20:46, 2 March 2017

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


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.

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.[8][8]

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.[9][8]

Most common cause

The most frequent pathogen of peritonsillar abscess is Streptococcus pyogenes.[9][8][10][11]

Common causes

Some common causes of peritonsillar abscess include:[9][8]

Less common causes

Less common causes of peritonsillar abscess include:[9][8]

Differentiating Peritonsillar abscess from Other Diseases

Disease/Variable Presentation Causes Physical exams findings Age commonly affected Imaging finding Treatment
Peritonsillar abscess Severe sore throat, otalgia fever, a "hot potato" or muffled voice, drooling, and trismus[1] Aerobic and anaerobic

bacteria most common is

Streptococcus

pyogenes.[9][8][10][11]

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.

The highest occurrence is in adults between 20 to 40 years of age.[1] On ultrasound peritonsillar abscess appears as focal irregularly marginated hypoechoic area.[12][13][14][15][12][13] Ampicillin-sulbactam, Clindamycin, Vancomycin or Linezolid
Croup Has cough and stridor but no drooling. Others are Hoarseness, Difficulty breathing, symptoms of the common cold, Runny nose, Fever Parainfluenza virus Suprasternal and intercostal indrawing,[16] Inspiratory stridor[17], expiratory wheezing,[17] Sternal wall retractions[18] Mainly 6 months and 3 years old

rarely, adolescents and adults[19]

Steeple sign on neck X-ray Dexamethasone and nebulised epinephrine
Epiglottitis Has stridor and drooling but no cough. Other symptoms include difficulty breathing, fever, chills, difficulty swallowing, hoarseness of voice H. influenza type b,

beta-hemolytic streptococci, Staphylococcus aureus,

fungi and viruses.

Cyanosis, Cervical lymphadenopathy, Inflammed epiglottis Used to be mostly found in

pediatric age group between 3 to 5 years,

however, recent trend favors adults

as most commonly affected individuals[20]

with a mean age of 44.94 years

Thumbprint sign on neck x-ray Airway maintenance, parenteral Cefotaxime or Ceftriaxone in combination with Vancomycin. Adjuvant therapy includes corticosteroids and racemic Epinephrine.[21][22]
Pharyngitis Sore throat, pain on swallowing, fever, headache, abdominal pain, nausea and vomiting Group A beta-hemolytic

streptococcus.

Inflammed pharynx with or without exudate Mostly in children and young adults,

with 50% of cases identified

between the ages of 5 to 24 years.[23]

_ Antimicrobial therapy mainly penicillin-based and analgesics.
Tonsilitis Sore throat, pain on swallowing, fever, headache, cough Most common cause is

viral including adenovirus,

rhinovirus, influenza,

coronavirus, and

respiratory syncytial virus.

Second most common

causes are bacterial;

Group A streptococcal

bacteria,[24]

Fever, especially 100°F or higher.[25][26]Erythema, edema and Exudate of the tonsils.[27] cervical lymphadenopathy, Dysphonia.[28] Primarily affects children

between 5 and 15 years old.[29]

Intraoral or transcutaneous USG may show an abscess making CT scan unnecessary.[4][30][31] Antimicrobial therapy mainly penicillin-based and analgesics with tonsilectomy in selected cases.
Retropharyngeal abscess Neck pain, stiff neck, torticollis

fever, malaise, stridor, and barking cough

Polymicrobial infection.

Mostly; Streptococcus

pyogenes, Staphylococcus aureus and respiratory anaerobes (example; Fusobacteria, Prevotella,

and Veillonella species)[32][33][34][9][35][36]

Child may be unable to open the mouth widely. May have enlarged

cervical lymph nodes and neck mass.

Mostly between 2-4 years, but can occur in other age groups.[37][38] On CT scan, a mass impinging on the posterior pharyngeal wall with rim enhancement is seen[39][40] Immediate surgical drainage and antimicrobial therapy. emperic therapy involves; ampicillin-sulbactam or clindamycin.

Epidemiology and Demographics

Prevalence and incidence

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 that these times.[41][42]

Age

Peritonsillar abscess occur in all age groups. The highest occurrence is in adults between 20 to 40 years of age.[1][43][44]

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.[45][46][47][48][49][50][51]

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:[52][53]

  • 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.[54][55]

Complications

The following are some complications that may follow peritonsillar abscess:[1][56][57][58][59]

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.[60][61][62][63]

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][65][3][66]

Appearance of the Patient

  • They are usually acutely-ill looking.

Vital Signs

HEENT


Image below shows edematous and inflamed tonsillar with contralacteral uvula deviation:[67]


200PX

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

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][14][69][70][71]

On ultrasound the following may be found:[12][13][14][15][12][13]

  • 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.[14]

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.[61]

Antimicrobial Regimen

Below are the antimicrobial regimen available in treating peritonsillar abscess.[67]

  • 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

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Galioto NJ (2008). "Peritonsillar abscess". Am Fam Physician. 77 (2): 199–202. PMID 18246890.
  2. ↑ 2.0 2.1 2.2 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.
  3. ↑ 3.0 3.1 3.2 3.3 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 4.2 4.3 4.4 Kawabata M, Umakoshi M, Makise T, Miyashita K, Harada M, Nagano H; et al. (2016). "Clinical classification of peritonsillar abscess based on CT and indications for immediate abscess tonsillectomy". Auris Nasus Larynx. 43 (2): 182–6. doi:10.1016/j.anl.2015.09.014. PMID 26527518.
  5. ↑ 5.0 5.1 5.2 5.3 L. Michaels, H.B. Hellquist Ear, nose and throat histopathology (2nd ed.)Springer-Verlag, London (2001), pp. 281–286
  6. ↑ 6.0 6.1 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.
  7. ↑ 7.0 7.1 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.
  8. ↑ 8.0 8.1 8.2 8.3 8.4 8.5 8.6 Megalamani SB, Suria G, Manickam U, Balasubramanian D, Jothimahalingam S (2008). "Changing trends in bacteriology of peritonsillar abscess". J Laryngol Otol. 122 (9): 928–30. doi:10.1017/S0022215107001144. PMID 18039418.
  9. ↑ 9.0 9.1 9.2 9.3 9.4 9.5 Brook I (2004). "Microbiology and management of peritonsillar, retropharyngeal, and parapharyngeal abscesses". J Oral Maxillofac Surg. 62 (12): 1545–50. PMID 15573356.
  10. ↑ 10.0 10.1 Snow DG, Campbell JB, Morgan DW (1991). "The microbiology of peritonsillar sepsis". J Laryngol Otol. 105 (7): 553–5. PMID 1875138.
  11. ↑ 11.0 11.1 Matsuda A, Tanaka H, Kanaya T, Kamata K, Hasegawa M (2002). "Peritonsillar abscess: a study of 724 cases in Japan". Ear Nose Throat J. 81 (6): 384–9. PMID 12092281.
  12. ↑ 12.0 12.1 12.2 12.3 Lyon M, Blaivas M (2005). "Intraoral ultrasound in the diagnosis and treatment of suspected peritonsillar abscess in the emergency department". Acad Emerg Med. 12 (1): 85–8. doi:10.1197/j.aem.2004.08.045. PMID 15635144.
  13. ↑ 13.0 13.1 13.2 13.3 Boesen T, Jensen F (1992). "Preoperative ultrasonographic verification of peritonsillar abscesses in patients with severe tonsillitis". Eur Arch Otorhinolaryngol. 249 (3): 131–3. PMID 1642863.
  14. ↑ 14.0 14.1 14.2 14.3 Bandarkar AN, Adeyiga AO, Fordham MT, Preciado D, Reilly BK (2016). "Tonsil ultrasound: technical approach and spectrum of pediatric peritonsillar infections". Pediatr Radiol. 46 (7): 1059–67. doi:10.1007/s00247-015-3505-7. PMID 26637999.
  15. ↑ 15.0 15.1 Scott PM, Loftus WK, Kew J, Ahuja A, Yue V, van Hasselt CA (1999). "Diagnosis of peritonsillar infections: a prospective study of ultrasound, computerized tomography and clinical diagnosis". J Laryngol Otol. 113 (3): 229–32. PMID 10435129.
  16. ↑
  17. ↑ 17.0 17.1
  18. ↑
  19. ↑
  20. ↑
  21. ↑
  22. ↑
  23. ↑
  24. ↑
  25. ↑
  26. ↑
  27. ↑
  28. ↑
  29. ↑
  30. ↑
  31. ↑
  32. ↑
  33. ↑
  34. ↑
  35. ↑
  36. ↑
  37. ↑
  38. ↑
  39. ↑
  40. ↑
  41. ↑ Belleza WG, Kalman S (2006). "Otolaryngologic emergencies in the outpatient setting". Med Clin North Am. 90 (2): 329–53. doi:10.1016/j.mcna.2005.12.001. PMID 16448878.
  42. ↑ Bisno AL, Gerber MA, Gwaltney JM, Kaplan EL, Schwartz RH, Infectious Diseases Society of America (2002). "Practice guidelines for the diagnosis and management of group A streptococcal pharyngitis. Infectious Diseases Society of America". Clin Infect Dis. 35 (2): 113–25. doi:10.1086/340949. PMID 12087516.
  43. ↑ Steyer TE (2002). "Peritonsillar abscess: diagnosis and treatment". Am Fam Physician. 65 (1): 93–6. PMID 11804446.
  44. ↑ Khayr W, Taepke J (2005). "Management of peritonsillar abscess: needle aspiration versus incision and drainage versus tonsillectomy". Am J Ther. 12 (4): 344–50. PMID 16041198.
  45. ↑ Ong YK, Goh YH, Lee YL (2004). "Peritonsillar infections: local experience". Singapore Med J. 45 (3): 105–9. PMID 15029410.
  46. ↑ Marom T, Cinamon U, Itskoviz D, Roth Y (2010). "Changing trends of peritonsillar abscess". Am J Otolaryngol. 31 (3): 162–7. doi:10.1016/j.amjoto.2008.12.003. PMID 20015734.
  47. ↑ Klug TE (2014). "Incidence and microbiology of peritonsillar abscess: the influence of season, age, and gender". Eur J Clin Microbiol Infect Dis. 33 (7): 1163–7. doi:10.1007/s10096-014-2052-8. PMID 24474247.
  48. ↑ Gavriel H, Lazarovitch T, Pomortsev A, Eviatar E (2009). "Variations in the microbiology of peritonsillar abscess". Eur J Clin Microbiol Infect Dis. 28 (1): 27–31. doi:10.1007/s10096-008-0583-6. PMID 18612664.
  49. ↑ Sunnergren O, Swanberg J, Mölstad S (2008). "Incidence, microbiology and clinical history of peritonsillar abscesses". Scand J Infect Dis. 40 (9): 752–5. doi:10.1080/00365540802040562. PMID 19086341.
  50. ↑ Hidaka H, Kuriyama S, Yano H, Tsuji I, Kobayashi T (2011). "Precipitating factors in the pathogenesis of peritonsillar abscess and bacteriological significance of the Streptococcus milleri group". Eur J Clin Microbiol Infect Dis. 30 (4): 527–32. doi:10.1007/s10096-010-1114-9. PMID 21086007.
  51. ↑ Costales-Marcos M, López-Álvarez F, Núñez-Batalla F, Moreno-Galindo C, Alvarez Marcos C, Llorente-Pendás JL (2012). "[Peritonsillar infections: prospective study of 100 consecutive cases]". Acta Otorrinolaringol Esp. 63 (3): 212–7. doi:10.1016/j.otorri.2012.01.001. PMID 22425204.
  52. ↑ Lehnerdt G, Senska K, Fischer M, Jahnke K (2005). "[Smoking promotes the formation of peritonsillar abscesses]". Laryngorhinootologie. 84 (9): 676–9. doi:10.1055/s-2005-870289. PMID 16142623.
  53. ↑ Dilkes MG, Dilkes JE, Ghufoor K (1992). "Smoking and quinsy". Lancet. 339 (8808): 1552. PMID 1351238.
  54. ↑ 54.0 54.1 Coughlin AM, Baugh RF, Pine HS (2014). "Lingual tonsil abscess with parapharyngeal extension: a case report". Ear Nose Throat J. 93 (9): E7–8. PMID 25255362.
  55. ↑ 55.0 55.1 Deeva YV (2015). "[SURGICAL TREATMENT OF TONSILLAR NECK PHLEGMON]". Klin Khir (7): 47–8. PMID 26591220.
  56. ↑ Goldenberg D, Golz A, Joachims HZ (1997). "Retropharyngeal abscess: a clinical review". J Laryngol Otol. 111 (6): 546–50. PMID 9231089.
  57. ↑ Stevens HE (1990). "Vascular complication of neck space infection: case report and literature review". J Otolaryngol. 19 (3): 206–10. PMID 2355414.
  58. ↑ Greinwald JH, Wilson JF, Haggerty PG (1995). "Peritonsillar abscess: an unlikely cause of necrotizing fasciitis". Ann Otol Rhinol Laryngol. 104 (2): 133–7. doi:10.1177/000348949510400209. PMID 7857015.
  59. ↑ Wenig BL, Shikowitz MJ, Abramson AL (1984). "Necrotizing fasciitis as a lethal complication of peritonsillar abscess". Laryngoscope. 94 (12 Pt 1): 1576–9. PMID 6594557.
  60. ↑ Powell J, Wilson JA (2012). "An evidence-based review of peritonsillar abscess". Clin Otolaryngol. 37 (2): 136–45. doi:10.1111/j.1749-4486.2012.02452.x. PMID 22321140.
  61. ↑ 61.0 61.1 Apostolopoulos NJ, Nikolopoulos TP, Bairamis TN (1995). "Peritonsillar abscess in children. Is incision and drainage an effective management?". Int J Pediatr Otorhinolaryngol. 31 (2–3): 129–35. PMID 7782170.
  62. ↑ Johnson RF, Stewart MG, Wright CC (2003). "An evidence-based review of the treatment of peritonsillar abscess". Otolaryngol Head Neck Surg. 128 (3): 332–43. doi:10.1067/mhn.2003.93. PMID 12646835.
  63. ↑ Herzon FS (1995). "Harris P. Mosher Award thesis. Peritonsillar abscess: incidence, current management practices, and a proposal for treatment guidelines". Laryngoscope. 105 (8 Pt 3 Suppl 74): 1–17. PMID 7630308.
  64. ↑ Ferri, Fred (2015). Ferri's clinical advisor 2015 : 5 books in 1. Philadelphia, PA: Elsevier/Mosby. ISBN 978-0323083751.
  65. ↑ Ferri, Fred (2015). Ferri's clinical advisor 2015 : 5 books in 1. Philadelphia, PA: Elsevier/Mosby. ISBN 978-0323083751.
  66. ↑ Nwe TT, Singh B (2000). "Management of pain in peritonsillar abscess". J Laryngol Otol. 114 (10): 765–7. PMID 11127146.
  67. ↑ 67.0 67.1 DescriptionEnglish: A right sided peritonsilar abscess Date 13 May 2011 Source Own work Author James Heilman,MD wikimedia commons https://commons.wikimedia.org/wiki/File:PeritonsilarAbsess.jpg
  68. ↑ Costantino TG, Satz WA, Dehnkamp W, Goett H (2012). "Randomized trial comparing intraoral ultrasound to landmark-based needle aspiration in patients with suspected peritonsillar abscess". Acad Emerg Med. 19 (6): 626–31. doi:10.1111/j.1553-2712.2012.01380.x. PMID 22687177.
  69. ↑ Buckley AR, Moss EH, Blokmanis A (1994). "Diagnosis of peritonsillar abscess: value of intraoral sonography". AJR Am J Roentgenol. 162 (4): 961–4. doi:10.2214/ajr.162.4.8141026. PMID 8141026.
  70. ↑ Strong EB, Woodward PJ, Johnson LP (1995). "Intraoral ultrasound evaluation of peritonsillar abscess". Laryngoscope. 105 (8 Pt 1): 779–82. doi:10.1288/00005537-199508000-00002. PMID 7630286.
  71. ↑ Blaivas M, Theodoro D, Duggal S (2003). "Ultrasound-guided drainage of peritonsillar abscess by the emergency physician". Am J Emerg Med. 21 (2): 155–8. doi:10.1053/ajem.2003.50029. PMID 12671820.
  72. ↑ 72.0 72.1 Mathoera RB, Wever PC, van Dorsten FR, Balter SG, de Jager CP (2008). "Epiglottitis in the adult patient". Neth J Med. 66 (9): 373–7. PMID 18931398.

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