Peritonsillar Abscess

Peritonsillar Abscess

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Peritonsillar abscess (PTA) was first described as early as the 14th century; however, it is only since the advent of antibiotics in the 20th century that the condition has been described more extensively. A PTA is a localized accumulation of pus in the peritonsillar tissues that forms as a result of suppurative tonsillitis. An alternative explanation is that a PTA is an abscess formed in a group of salivary glands in the supratonsillar fossa, known as Weber glands.

The nidus of accumulation is located between the capsule of the palatine tonsils and the constrictor muscles of the pharynx. The anterior and posterior pillars, torus tubarius (superior), and pyriform sinus (inferior) form the boundaries of this potential peritonsillar space. Because this area is composed of loose connective tissue, severe infection may rapidly lead to formation of purulent material. Progressive inflammation and suppuration may extend to directly involve the soft palate, the lateral wall of the pharynx, and, occasionally, the base of the tongue.

PTA is usually a complication of an acute tonsillitis. Inflammatory edema may lead to significant difficulty in swallowing. Dehydration frequently occurs secondary to the patient’s avoidance of painful ingestion of food and liquids. Expansion of the abscess may lead to extension of the inflammation into adjacent fascial compartments of the head and neck, potentially resulting in airway obstruction.

For patient education resources, see the Ear, Nose, and Throat Center, as well as Peritonsillar Abscess, Tonsillitis, and Antibiotics.

The palatine tonsils are paired lymphoid organs found between the palatoglossal and palatopharyngeal folds of the oropharynx. They are surrounded by a thin capsule that separates the tonsil from the superior and middle constrictor muscles.

The anterior and posterior pillars form the front and back limits of the peritonsillar space. Superiorly, this potential space is related to the torus tubarius, while inferiorly it is bounded by the pyriform sinus. Composed solely of loose connective tissue, a severe infection may rapidly result in pus formation. The inflammation and suppurative process may extend to involve the soft palate, the lateral wall of the pharynx, and, occasionally, the base of the tongue.

The tonsillar fossa has a rich network of lymphatic vessels leading to the parapharyngeal space and the upper cervical lymph nodes, which explains the pattern of adenopathy observed clinically. Ipsilateral upper cervical lymphadenopathy is the result of the spread of infection to the regional lymphatics. Occasionally, the severity of the suppurative process may lead to a cervical abscess, especially in very fulminant or rapidly progressive cases.

The pathophysiology of PTA is unknown. The most widely accepted theory involves the progression of an episode of exudative tonsillitis first into peritonsillitis and then into frank abscess formation. Extension of the inflammatory process may occur in both treated and untreated populations. PTA also has been documented to arise de novo without any prior history of recurrent or chronic tonsillitis. A PTA also can be the presentation of an Epstein-Barr virus (ie, mononucleosis) infection.

Another theory proposes the origin of PTA in Weber glands. These minor salivary glands are found in the peritonsillar space and are thought to help in clearing debris from the tonsils. Should obstruction as a result of scarring from infection occur, tissue necrosis and abscess formation result, leading to PTA.

Any of the microorganisms that cause acute or chronic tonsillitis may be the cause of a PTA. Most commonly, aerobic and anaerobic gram-positive organisms are identified by means of culture.

Cultures of affected patients reveal group A beta-hemolytic streptococci as most prevalent. Next most commonly, staphylococci, pneumococci, and Haemophilus organisms are found. Finally, other microorganisms that can be cultured include lactobacilli, filamentous forms such as Actinomyces species, micrococci, Neisseria species, diphtheroids, Bacteroides species, and nonsporulating bacteria. Some evidence indicates that anaerobic bacteria frequently cause these infections. [1]

The incidence of PTA in the United States is about 30 cases per 100,000 people per year, representing about 45,000 new cases each year. No accurate data are available internationally.

Although tonsillitis is a disease of childhood, only one third of PTA cases are found in this age group. The age of patients with the condition is variable, ranging from 1 to 76 years, with the highest incidence in persons aged 15-35 years. No sexual or racial predilection has been established.

In a retrospective cohort study of 427 patients with PTA, Marom et al investigated how the characteristics of PTA may have changed over time. [2] The results led the authors to conclude that PTA currently tends to affect an older population than it once did, that its course in older individuals has become longer and worse, and that smoking may be a predisposing factor in its development.

A study of 685 patients by Kordeluk et al looked at the relation between peritonsillar cellulitis and abscess and outbreaks of acute tonsillitis. [3] The authors found peaks with seasonal variation for presentations with acute tonsillitis but no association with PTA, which occurred at similar rates throughout the calendar year.

Most patients treated with antibiotics and adequate drainage of their abscess cavity recover within a few days. A small number present with another abscess later, requiring tonsillectomy. If patients continue to report recurring or chronic sore throats after proper incision and drainage (I&D), a tonsillectomy may be indicated.

In a nationwide retrospective cohort study from Taiwan, Wang et al found that the risk of PTA recurrence rose with higher degrees of previous tonsillitis in patients of all ages, whereas such a rise was associated with management by needle aspiration only in pediatric patients. [4] The risk of PTA recurrence was highest in patients who were younger than 30 years and had experienced more than five prior episodes of tonsillitis.

Repanos C, Mukherjee P, Alwahab Y. Role of microbiological studies in management of peritonsillar abscess. J Laryngol Otol. 2009 Aug. 123 (8):877-9. [Medline].

Marom T, Cinamon U, Itskoviz D, Roth Y. Changing trends of peritonsillar abscess. Am J Otolaryngol. 2010 May-Jun. 31 (3):162-7. [Medline].

Kordeluk S, Novack L, Puterman M, Kraus M, Joshua BZ. Relation between peritonsillar infection and acute tonsillitis: myth or reality?. Otolaryngol Head Neck Surg. 2011 Dec. 145 (6):940-5. [Medline].

Wang YP, Wang MC, Lin HC, Chou P. The impact of prior tonsillitis and treatment modality on the recurrence of peritonsillar abscess: a nationwide cohort study. PLoS One. 2014. 9 (10):e109887. [Medline]. [Full Text].

Kilty SJ, Gaboury I. Clinical predictors of peritonsillar abscess in adults. J Otolaryngol Head Neck Surg. 2008 Apr. 37 (2):165-8. [Medline].

Thapar A, Tassone P, Bhat N, Pfleiderer A. Parapharyngeal abscess: a life-threatening complication of quinsy. Clin Anat. 2008 Jan. 21 (1):23-6. [Medline].

da Silva PS, Waisberg DR. Internal carotid artery pseudoaneurysm with life-threatening epistaxis as a complication of deep neck space infection. Pediatr Emerg Care. 2011 May. 27 (5):422-4. [Medline].

Roccia F, Pecorari GC, Oliaro A, Passet E, Rossi P, Nadalin J, et al. Ten years of descending necrotizing mediastinitis: management of 23 cases. J Oral Maxillofac Surg. 2007 Sep. 65 (9):1716-24. [Medline].

Ehrenfried Berthelsen R, Hein L. [Lemierre’s syndrome following peritonsillar abscess]. Ugeskr Laeger. 2012 May 28. 174 (22):1534-5. [Medline].

Ramirez-Schrempp D, Dorfman DH, Baker WE, Liteplo AS. Ultrasound soft-tissue applications in the pediatric emergency department: to drain or not to drain?. Pediatr Emerg Care. 2009 Jan. 25 (1):44-8. [Medline].

Ozbek C, Aygenc E, Tuna EU, Selcuk A, Ozdem C. Use of steroids in the treatment of peritonsillar abscess. J Laryngol Otol. 2004 Jun. 118 (6):439-42. [Medline].

Marom T, Cinamon U, Itskoviz D, Roth Y. Changing trends of peritonsillar abscess. Am J Otolaryngol. 2010 May-Jun. 31 (3):162-7. [Medline].

Heidemann CH, Wallén M, Aakesson M, Skov P, Kjeldsen AD, Godballe C. Post-tonsillectomy hemorrhage: assessment of risk factors with special attention to introduction of coblation technique. Eur Arch Otorhinolaryngol. 2009 Jul. 266 (7):1011-5. [Medline].

Benoit J Gosselin, MD, FRCSC Associate Professor of Surgery, Dartmouth Medical School; Director, Comprehensive Head and Neck Oncology Program, Norris Cotton Cancer Center; Staff Otolaryngologist, Division of Otolaryngology-Head and Neck Surgery, Dartmouth-Hitchcock Medical Center

Benoit J Gosselin, MD, FRCSC is a member of the following medical societies: American Head and Neck Society, American Academy of Facial Plastic and Reconstructive Surgery, North American Skull Base Society, American Academy of Otolaryngology-Head and Neck Surgery, American Medical Association, American Rhinologic Society, Canadian Medical Association, Canadian Society of Otolaryngology-Head & Neck Surgery, College of Physicians and Surgeons of Ontario, New Hampshire Medical Society, Ontario Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Amy L Friedman, MD Professor of Surgery, Director of Transplantation, State University of New York Upstate Medical University College of Medicine, Syracuse

Amy L Friedman, MD is a member of the following medical societies: Association for Academic Surgery, International College of Surgeons, New York Academy of Sciences, Pennsylvania Medical Society, Philadelphia County Medical Society, Society of Critical Care Medicine, Association of Women Surgeons, International Liver Transplantation Society, Transplantation Society, American College of Surgeons, American Medical Association, American Medical Womens Association, American Society for Artificial Internal Organs, American Society of Transplant Surgeons, American Society of Transplantation

Disclosure: Nothing to disclose.

John Geibel, MD, DSc, MSc, AGAF Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, Professor, Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director of Surgical Research, Department of Surgery, Yale-New Haven Hospital; American Gastroenterological Association Fellow

John Geibel, MD, DSc, MSc, AGAF is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, Society for Surgery of the Alimentary Tract

Disclosure: Nothing to disclose.

Brian J Daley, MD, MBA, FACS, FCCP, CNSC Professor and Program Director, Department of Surgery, Chief, Division of Trauma and Critical Care, University of Tennessee Health Science Center College of Medicine

Brian J Daley, MD, MBA, FACS, FCCP, CNSC is a member of the following medical societies: American Association for the Surgery of Trauma, Eastern Association for the Surgery of Trauma, Southern Surgical Association, American College of Chest Physicians, American College of Surgeons, American Medical Association, Association for Academic Surgery, Association for Surgical Education, Shock Society, Society of Critical Care Medicine, Southeastern Surgical Congress, Tennessee Medical Association

Disclosure: Nothing to disclose.

Peritonsillar Abscess

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