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Adenoiditis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahshid Mir, M.D. [2]

Synonyms and keywords: Inflamed adenoids; Adenotonstilis; Adenoid Hypertrophy; Swollen adenoids; Chronic adenoiditis; Acute adenoiditis.

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Mahshid Mir, M.D. [2]

Overview

Adenoid is a lymphoid tissue that forms the Waldeyer ring. Adenoiditis is the inflammation of adenoid tissue. Adenoid infection is mostly due to viral infections. Some bacterial pathogens including H. influenzae, group A β-hemolytic streptococcus, and S. aureus can cause the disease as well. Adenoids can cause recurrent sinusitis and chronic persistent or recurrent otitis if left untreated and can lead to chronic adenoiditis. Medications (antibiotics or steroids) or surgical approach may be required for the management of adenoiditis, depending on the causative agent.

Historical perspective

Adenoid was thought to be a part of tonsils and responsible for the symptoms of nasal congestion and obstruction. As a result adenotonsilectomy was performed for at least 2000 years. In the early beginning of 19th century, adenoid and tonsil tissue were known as remnants of an unknown infectious disease, and so they were removed with adenotonsilectomy. Willhelm Meyer of Copenhagen, Denmark in 1800 firstly describe adenoiditis due to adenoid vegetations responsible for nasal symptoms and impaired hearing. He probably was the first one who performed an adenoidectomy separately.

Classification

Adenoiditis can be classified into the following types including acute adenoiditis, recurrent acute adenoiditis, and chronic/persistant adenoiditis.[1]

Pathophysiology

Adenoids are involved in the production of mostly secretory IgA. IgA is transported to the surface providing local immune protection. Studies suggest that a reduction in IgA will occur after an adenoidectomy.[2] bacteria in the normal flora of the oral cavity, are found in adenoid tissue as well. These include alpha-hemolytic streptococci, enterococci, Corynebacterium species, Coagulase-negative staphylococci, Neisseria species, haemophilus species, micrococcus species, stomatococcus species. Adenoiditis can occur as a result of infection. They can harbor pathogenic bacteria, which may lead to the development of disease of the ears, nose, and sinuses. Adenoiditis can progress to chronic disease if it remains untreated for a long period of time.

Causes

Acute adenoiditis is mainly due to viral infection but bacterial infections can cause the disease as well. Bacterial infections have a more important role in recurrent and chronic adenoiditis. The most important viral causes of adenoiditis include EBV, CMV and RSV. The most important bacterial causes adenoiditis include Haemophilus influenzae, group A β-hemolytic streptococcus, and staphylococcus aureus.[3]

Differentiating tonsillitis from other diseases

Diagnosis of adenoiditis can be challenging as majority of upper respiratory tract infections present in the same pattern. The most important differential diagnosis of adenoiditis includes tonsilitis, viral upper respiratory tract infection, sinusitis and pharyngitis.

Epidemiology and Demographics

The prevalence of adenoiditis is not completely known. Research indicates that 15-30% of sore throats in children and 5-10% sore throats in adults are due to bacterial adenotonsillitis. The prevalence of adenoiditis decreases with age. Adenoid tissue undergoes atrophy after 10 years of age, so adenoiditis is rarely seen after 15 years.[4][5][6][7][8]

Risk Factors

The most potent risk factor in the development of adenoiditis is being a young child. Other risk factors include immunodeficiencies, living in an urban environment with more exposure to viruses or bacteria and usage of immunosuppressant drugs.

Screening

There is insufficient evidence to recommend routine screening for adenoiditis.

Natural history, complications and prognosis

Natural History

Acute adenoiditis will usually present with erythema and edema of the adenoids. This occurs rapidly upon infiltration of the adenoids by the pathogen.[9] Symptoms including fever and sore throat will usually manifest within 24 hours of infection. Adenoiditis is usually combined with tonsillitis due to close anatomical location.

Complications

Complications of adenoiditis are caused by persistence and/or spread of the responsible pathogen – usually bacterial. The complications of adenoiditis include speech abnormalities, otitis media, acute sinusitis, pneumonia, adenoid hyperplasia, peritonsillar abscess, and sleep apnea.

Prognosis

The prognosis for acute adenoiditis without treatment is usually good. Adenoiditis is usually a self-limiting disease and resolves by itself within 3-4 days.[10]

Diagnosis

Diagnostic criteria

There is no criteria for the diagnosis of adenoiditis. However, seeing inflamed and hypertrophied adenoid tissue with flexible or rigid nasopharyngoscopy can be used as a criteria for adenoidectomy in patients suspected of chronic adenoiditis.

History and Symptoms

A positive history of fever, nasal obstruction, and snoring is suggestive of adenoiditis. The most common symptoms of adenoiditis include purulent nasal discharge, mouth breathing, nasal pain and sore throat.[11][12][13]

Physical Examination

Patients with adenoiditis are usually well-appearing. Physical examination of patients with adenoiditis is usually remarkable for fever, and purulent nasal discharge.[14][15][16]

Laboratory Findings

Laboratory findings consistent with the diagnosis of adenoiditis include neutrophilia, positive culture for organism from throat exam sampling, and positive blood culture for the organism in severe cases.[17]

Imaging Findings

On lateral neck x-ray, adenoiditis is characterized by enlargement of adenoids and narrowing of airways. Adenoiditis diagnosis can be confirmed if during flexible or rigid nasopharyngoscopy inflamed adenoid tissue is seen. Flexible or rigid nasopharyngoscopy can provide a direct visualization of nasopharynx and Waldeyer ring so that the inflamed adenoid tissue can be seen too.[18]

Treatment

Medical Therapy

The mainstay of therapy for adenoiditis is symptomatic therapy. Medical therapy is recommended among patients with recurrent and chronic adenoiditis. The best antibiotic therapy regimen include amoxicillinclavulanic acid or cephalosporin.

Surgery

Surgery is not the first-line treatment option for patients with adenoiditis. Adenoidectomy is usually reserved for patients with chronic persistent adenoiditis who developed adenoid hypertrophy. Adenoidectomy has shown to be effective independent of the size of the adenoids.[19]

Prevention

Primary Prevention

Primary prevention strategies to prevent adenoiditis include hygienic practices.

Secondary Prevention

Secondary prevention involves usage of antibiotics to prevent recurrence of adenoiditis. It can be helpful in certain circumstances like history of rheumatic fever, to prevent pharyngitis cause by group A beta-hemolytic streptococci.[20]

References

  1. “Head & Neck Surgery–otolaryngology – Google Books”.
  2. Havas T, Lowinger D (2002). “Obstructive adenoid tissue: an indication for powered-shaver adenoidectomy”. Arch. Otolaryngol. Head Neck Surg. 128 (7): 789–91. PMID 12117336.
  3. Havas T, Lowinger D (2002). “Obstructive adenoid tissue: an indication for powered-shaver adenoidectomy”. Arch. Otolaryngol. Head Neck Surg. 128 (7): 789–91. PMID 12117336.
  4. Komaroff AL, Pass TM, Aronson MD, Ervin CT, Cretin S, Winickoff RN, Branch WT (1986). “The prediction of streptococcal pharyngitis in adults”. J Gen Intern Med. 1 (1): 1–7. PMID 3534166.
  5. Kaplan EL, Top FH, Dudding BA, Wannamaker LW (1971). “Diagnosis of streptococcal pharyngitis: differentiation of active infection from the carrier state in the symptomatic child”. J. Infect. Dis. 123 (5): 490–501. PMID 5115179.
  6. Schroeder BM (2003). “Diagnosis and management of group A streptococcal pharyngitis”. Am Fam Physician. 67 (4): 880, 883–4. PMID 12613739.
  7. Sharav, Yair; Benoliel, Rafael (2008). Orofacial Pain and Headache. Elsevier. ISBN 0723434123.
  8. Pagella F, De Amici M, Pusateri A, Tinelli G, Matti E, Benazzo M, Licari A, Nigrisoli S, Quaglini S, Ciprandi G, Marseglia GL (2015). “Adenoids and clinical symptoms: Epidemiology of a cohort of 795 pediatric patients”. Int. J. Pediatr. Otorhinolaryngol. 79 (12): 2137–41. doi:10.1016/j.ijporl.2015.09.035. PMID 26478108.
  9. “Tonsillitis – NHS Choices”.
  10. “Tonsillitis – NHS Choices”.
  11. Kosikowska U, Korona-Głowniak I, Niedzielski A, Malm A (2015). “Nasopharyngeal and Adenoid Colonization by Haemophilus influenzae and Haemophilus parainfluenzae in Children Undergoing Adenoidectomy and the Ability of Bacterial Isolates to Biofilm Production”. Medicine (Baltimore). 94 (18): e799. doi:10.1097/MD.0000000000000799. PMC 4602522. PMID 25950686.
  12. Kajan ZD, Sigaroudi AK, Mohebbi M (2016). “Prevalence and patterns of palatine and adenoid tonsilloliths in cone-beam computed tomography images of an Iranian population”. Dent Res J (Isfahan). 13 (4): 315–21. PMC 4993058. PMID 27605988.
  13. Galli J, Calò L, Ardito F, Imperiali M, Bassotti E, Fadda G, Paludetti G (2007). “Biofilm formation by Haemophilus influenzae isolated from adeno-tonsil tissue samples, and its role in recurrent adenotonsillitis”. Acta Otorhinolaryngol Ital. 27 (3): 134–8. PMC 2640046. PMID 17883191.
  14. Kosikowska U, Korona-Głowniak I, Niedzielski A, Malm A (2015). “Nasopharyngeal and Adenoid Colonization by Haemophilus influenzae and Haemophilus parainfluenzae in Children Undergoing Adenoidectomy and the Ability of Bacterial Isolates to Biofilm Production”. Medicine (Baltimore). 94 (18): e799. doi:10.1097/MD.0000000000000799. PMC 4602522. PMID 25950686.
  15. Kajan ZD, Sigaroudi AK, Mohebbi M (2016). “Prevalence and patterns of palatine and adenoid tonsilloliths in cone-beam computed tomography images of an Iranian population”. Dent Res J (Isfahan). 13 (4): 315–21. PMC 4993058. PMID 27605988.
  16. Galli J, Calò L, Ardito F, Imperiali M, Bassotti E, Fadda G, Paludetti G (2007). “Biofilm formation by Haemophilus influenzae isolated from adeno-tonsil tissue samples, and its role in recurrent adenotonsillitis”. Acta Otorhinolaryngol Ital. 27 (3): 134–8. PMC 2640046. PMID 17883191.
  17. Galli J, Calò L, Ardito F, Imperiali M, Bassotti E, Fadda G, Paludetti G (2007). “Biofilm formation by Haemophilus influenzae isolated from adeno-tonsil tissue samples, and its role in recurrent adenotonsillitis”. Acta Otorhinolaryngol Ital. 27 (3): 134–8. PMC 2640046. PMID 17883191.
  18. Ramji M, Biron VL, Jeffery CC, Côté DW, El-Hakim H (2014). “Validation of pharyngeal findings on sleep nasopharyngoscopy in children with snoring/sleep disordered breathing”. J Otolaryngol Head Neck Surg. 43: 13. doi:10.1186/1916-0216-43-13. PMC 4092353. PMID 24919758.
  19. El-Badrawy A, Abdel-Aziz M (2009). “Transoral endoscopic adenoidectomy”. Int J Otolaryngol. 2009: 949315. doi:10.1155/2009/949315. PMC 2809357. PMID 20111586.
  20. Dagnelie CF, Bartelink ML, van der Graaf Y, Goessens W, de Melker RA (1998). “Towards a better diagnosis of throat infections (with group A beta-haemolytic streptococcus) in general practice”. Br J Gen Pract. 48 (427): 959–62. PMC 1409991. PMID 9624764.

adenoids can contribute to recurrent sinusitis and chronic persistent or recurrent ear disease because they can harbor a chronic infection.adenoids can contribute to recurrent sinusitis and chronic persistent or recurrent ear disease because they can harbor a chronic infection.

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Mahshid Mir, M.D. [2]

Overview

Adenoiditis was first discovered by Willhelm Meyer in 1800. Adenoids were thought to be a part of tonsills and adenotonsillectomy has been performed for at least 2000 years.

Historical Perspective

  • Cornelius Caesus in A.D 30. explained that tonsils are covered by a membrane and require to be separated and extracted by a process called tonsillectomy. This encyclopedia was recovered in 1478 in Papal library, after being lost for 1400 years.[1]
  • Adenoids were thought to be a part of tonsills and responsible for the symptoms of nasal congestion and obstruction. As a result adenotonsillectomy has been performed for at least 2000 years.[1]
  • In the sixth and seventh centuries Aetius and Paul described surgical treatment of adenotonsillitis, as one of the most ancient surgical procedures.
  • In the early beginning of 19th century, adenoid and tonsill tissue were known as remnants of an unknown infectious disease, and so they were removed with adenotonsillectomy.[1]
  • Willhelm Meyer of Copenhagen, Denmark in 1800 first described adenoiditis due to adenoid vegetations responsible for nasal symptoms and impaired hearing. It is believed that Meyer was the first one who performed an adenoidectomy separately.[2]

References

  1. 1.0 1.1 1.2 Kamel RH, Ishak EA (1990). “Enlarged adenoid and adenoidectomy in adults: endoscopic approach and histopathological study”. J Laryngol Otol. 104 (12): 965–7. PMID 2280151.
  2. Semon F (1997). “Speech made at the unveiling of the Wilhelm Meyer monument, at Copenhagen”. Laryngoscope. 107 (3): 307–9. PMID 9121303.
Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Mahshid Mir, M.D. [2]

Overview

Adenoiditis may be classified according to duration of symptoms into 3 subtypes: acute adenoiditis, recurrent acute adenoiditis, and chronic/persistant adenoiditis.[1] Adenoiditis may also be classified according to the responsible pathogen/mechanism of disease into 4 subtypes: viral adenoiditis, bacterial adenoiditis, parasitic adenoiditis, and non-infectious adenoiditis.

Classification

Adenoiditis may be classified according to duration of symptoms into 3 subtypes: acute adenoiditis, recurrent acute adenoiditis, and chronic/persistant adenoiditis.[1] Adenoiditis may also be classified according to the responsible pathogen/mechanism of disease into 4 subtypes: viral adenoiditis, bacterial adenoiditis, parasitic adenoiditis, and non-infectious adenoiditis.

Adenoiditis classification based on durtion of symptoms
Subtypes Duration of symptoms
Acute adenoiditis Acute onset of symptoms[2]
Recurrent acute adenoiditis At least 4 or more episodes of acute adenoiditis within a 6 months period[3]
Chronic/persistent adenoiditis Persistent adenoiditis for more than 6 months

Presence of complications

Adenoiditis classification based on the responsible pathogen and coexisting conditions
Pathogen Clinical features

(other than adenoiditis)

Treatment
Viral adenoiditis[4][5][6] Epstein-barr virus (EBV)
  • Asymptomatic
    • In small children, the course of the disease is frequently asymptomatic. Majority of adults infected with mono also remain asymptomatic with serological evidence of past infection.
  • Treating symptoms and complications of the infection
Human adenovirus
  • Treating symptoms and complications of the infection
Enterovirus
  • Treating symptoms and complications of the infection
Rhinovirus
Respiratory syncytial virus
  • Treating symptoms and complications of the infection
  • Ribavirin
Cytomegalovirus
Herpes virus
  • Acyclovir
  • Valacyclovir
  • Famcyclovir
Bacterial adenoiditis Acute [7][8][9][10] Haemophilus influenzae
  • Beta lactamase inhibitor antibiotics
Group A β-hemolytic streptococcus
Staphylococcus aureus
Moraxella catarrhalis
Streptococcus pneumoniae
Recurrent[4][9] Usually due to normal flora pathogens:
Chronic [11][9]
Parasitic adenoiditis Toxoplasma gondii
  • Cervical lymphadenopathy, sore throat, muscle aches and pains that last for a month or more, fever, malaise, night sweats
Non-infectious adenoiditis[4][11][5] Allergies
Asthma
GERD

References

  1. 1.0 1.1 “Head & Neck Surgery–otolaryngology – Google Books”.
  2. Havas T, Lowinger D (2002). “Obstructive adenoid tissue: an indication for powered-shaver adenoidectomy”. Arch. Otolaryngol. Head Neck Surg. 128 (7): 789–91. PMID 12117336.
  3. Mohseni S, Shojaiefard A, Khorgami Z, Alinejad S, Ghorbani A, Ghafouri A (2014). “Peripheral lymphadenopathy: approach and diagnostic tools”. Iran J Med Sci. 39 (2 Suppl): 158–70. PMC 3993046. PMID 24753638.
  4. 4.0 4.1 4.2 Sadeghi-Shabestari M, Jabbari Moghaddam Y, Ghaharri H (2011). “Is there any correlation between allergy and adenotonsillar tissue hypertrophy?”. Int J Pediatr Otorhinolaryngol. 75 (4): 589–91. doi:10.1016/j.ijporl.2011.01.026. PMID 21377220.
  5. 5.0 5.1 Proenca-Modena JL, Pereira Valera FC, Jacob MG, Buzatto GP, Saturno TH, Lopes L; et al. (2012). “High rates of detection of respiratory viruses in tonsillar tissues from children with chronic adenotonsillar disease”. PLoS One. 7 (8): e42136. doi:10.1371/journal.pone.0042136. PMC 3411673. PMID 22870291.
  6. Endo LH, Ferreira D, Montenegro MC, Pinto GA, Altemani A, Bortoleto AE, Vassallo J (2001). “Detection of Epstein-Barr virus in tonsillar tissue of children and the relationship with recurrent tonsillitis”. Int. J. Pediatr. Otorhinolaryngol. 58 (1): 9–15. PMID 11249975.
  7. Lilja M, Räisänen S, Stenfors LE (1998). “Initial events in the pathogenesis of acute tonsillitis caused by Streptococcus pyogenes”. Int. J. Pediatr. Otorhinolaryngol. 45 (1): 15–20. PMID 9804015.
  8. Wessels MR, Bronze MS (1994). “Critical role of the group A streptococcal capsule in pharyngeal colonization and infection in mice”. Proc. Natl. Acad. Sci. U.S.A. 91 (25): 12238–42. PMC 45412. PMID 7991612.
  9. 9.0 9.1 9.2 Cunningham, M. W. (2000). “Pathogenesis of Group A Streptococcal Infections”. Clinical Microbiology Reviews. 13 (3): 470–511. doi:10.1128/CMR.13.3.470-511.2000. ISSN 0893-8512.
  10. Ellen RP, Gibbons RJ (1972). “M protein-associated adherence of Streptococcus pyogenes to epithelial surfaces: prerequisite for virulence”. Infect. Immun. 5 (5): 826–30. PMC 422446. PMID 4564883.
  11. 11.0 11.1 Akcay A, Tamay Z, Dağdeviren E, Guler N, Ones U, Kara CO; et al. (2006). “Childhood asthma and its relationship with tonsillar tissue”. Asian Pac J Allergy Immunol. 24 (2–3): 129–34. PMID 17136878.
Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Mahshid Mir, M.D. [2]

Overview

The pathogenesis of adenoiditis is characterized by its inflammation. This process is primarily due to an elevated rate of trafficking of lymphocytes into adenoid from the blood, exceeding the rate of outflow from the adenoid.[1] Adenoids are involved in the production of mostly secretory IgA, which is transported to the surface where it provides local immune protection. Adenoids can be infected by either bacterial and viral pathogens leading to adenoiditis.[2]

Pathophysiology

  • Adenoids are on the posterior nasopharynx, posterior to the nasal cavity. They are a component of the Waldeyer’s ring of lymphoid tissue, which is a ring of lymphoid tissue and includes adenoids and tonsils.
  • Adenoids are developed from lymphocytes infiltration in subendothelium of nasopharynx during the 16th week of gestation.
  • Adenoids start to shrink by the age 6-7.
  • By the time children reach 10-12, the adenoids are usually small enough for the child to become asymptomatic.

Pathogenesis

  • Adenoids are involved in the production of mostly secretory IgA, which is transported to the surface providing local immune protection. Studies suggest that a reduction in IgA will happen postoperative of adenoidectomy.[2]
  • Adenoiditis can happen as a result of infection and harbor pathogenic bacterial activity, which may lead to the development of disease of the ears, nose, and sinuses. Adenoiditis can progress to chronic disease if remain untreated for a long term.
  • Parental history of tonsillectomy and atopy hold significant predictive power in pediatric adenoiditis.[3][4]
  • The pathogenesis of adenoiditis is characterized by its inflammation. This process is primarily due to an elevated rate of trafficking of lymphocytes into adenoid from the blood, exceeding the rate of outflow from the adenoid.[1]
  • The persistence of tonsillitis beyond 3 months is known as chronic tonsillitis. In case of chronic bacterial tonsillitis the bacteria persist in the tonsils and lead to chronic inflammation. This persistent infection and inflammation leads to chronic tonsillitis. Manifestations appear whenever the patient has decline in immunity.
  • The immune response between the antigen and lymphocyte that leads to cellular proliferation and enlargement of the adeoid especially in paracortex area which lead to excess enlargement of the adenoids.
  • Bacterial adenoiditis is primarily caused by group A β-hemolytic streptococcus (GABHS) Streptococcus pyogenes infection.[5]
  • Adenoid paracortex may also be enlarged secondarily as a result of the activation and proliferation of antigen-specific T and B cells (clonal expansion).

Gross pathology

  • On gross pathology, characteristic findings of adenoiditis, include:
  • Enlarged adenoids
  • Soft greasy yellow areas within capsule

Microscopic Pathology

References

  1. 1.0 1.1 Mohseni S, Shojaiefard A, Khorgami Z, Alinejad S, Ghorbani A, Ghafouri A (2014). “Peripheral lymphadenopathy: approach and diagnostic tools”. Iran J Med Sci. 39 (2 Suppl): 158–70. PMC 3993046. PMID 24753638.
  2. 2.0 2.1 Havas T, Lowinger D (2002). “Obstructive adenoid tissue: an indication for powered-shaver adenoidectomy”. Arch. Otolaryngol. Head Neck Surg. 128 (7): 789–91. PMID 12117336.
  3. Capper R, Canter RJ (2001). “Is the incidence of tonsillectomy influenced by the family medical or social history?”. Clin Otolaryngol Allied Sci. 26 (6): 484–7. PMID 11843928.
  4. Kvestad, Ellen; Kværner, Kari Jorunn; Røysamb, Espen; Tambs, Kristian; Harris, Jennifer Ruth; Magnus, Per (2005). “Heritability of Recurrent Tonsillitis”. Archives of Otolaryngology–Head & Neck Surgery. 131 (5): 383. doi:10.1001/archotol.131.5.383. ISSN 0886-4470.
  5. Lilja M, Räisänen S, Stenfors LE (1998). “Initial events in the pathogenesis of acute tonsillitis caused by Streptococcus pyogenes”. Int. J. Pediatr. Otorhinolaryngol. 45 (1): 15–20. PMID 9804015.
  6. 6.0 6.1 Beachey EH, Courtney HS (1987). “Bacterial adherence: the attachment of group A streptococci to mucosal surfaces”. Rev. Infect. Dis. 9 Suppl 5: S475–81. PMID 3317744.
  7. Gibbons RJ (1989). “Bacterial adhesion to oral tissues: a model for infectious diseases”. J. Dent. Res. 68 (5): 750–60. PMID 2654229.
  8. Zhang JM, An J (2007). “Cytokines, inflammation, and pain”. Int Anesthesiol Clin. 45 (2): 27–37. doi:10.1097/AIA.0b013e318034194e. PMC 2785020. PMID 17426506.
  9. 9.0 9.1 Zautner AE, Krause M, Stropahl G, Holtfreter S, Frickmann H, Maletzki C, Kreikemeyer B, Pau HW, Podbielski A (2010). “Intracellular persisting Staphylococcus aureus is the major pathogen in recurrent tonsillitis”. PLoS ONE. 5 (3): e9452. doi:10.1371/journal.pone.0009452. PMC 2830486. PMID 20209109.
  10. Alexander EH, Hudson MC (2001). “Factors influencing the internalization of Staphylococcus aureus and impacts on the course of infections in humans”. Appl. Microbiol. Biotechnol. 56 (3–4): 361–6. PMID 11549002.
Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Mahshid Mir, M.D. [2]

Overview

Acute adenoiditis is mainly due to viral infection but bacterial infections can cause the disease as well. Bacterial infections have a more important role in recurrent and chronic adenoiditis. The most important viral causes include EBV, CMV and RSV. The most important bacterial causes include Haemophilus influenzae, group A β-hemolytic streptococcus, and staphylococcus aureus.[1]

Casuses

Acute adenoiditis is mainly due to viral infection but bacterial infections can cause the disease as well. Bacterial infections have a more important role in recurrent and chronic adenoiditis[2][3]:

Viral Causes

Bacterial Causes

Other causes[4]

References

  1. Havas T, Lowinger D (2002). “Obstructive adenoid tissue: an indication for powered-shaver adenoidectomy”. Arch. Otolaryngol. Head Neck Surg. 128 (7): 789–91. PMID 12117336.
  2. Karlıdağ T, Bulut Y, Keleş E, Alpay HC, Seyrek A, Orhan İ, Karlıdağ GE, Kaygusuz İ (2012). “Presence of herpesviruses in adenoid tissues of children with adenoid hypertrophy and chronic adenoiditis”. Kulak Burun Bogaz Ihtis Derg. 22 (1): 32–7. PMID 22339566.
  3. Havas T, Lowinger D (2002). “Obstructive adenoid tissue: an indication for powered-shaver adenoidectomy”. Arch. Otolaryngol. Head Neck Surg. 128 (7): 789–91. PMID 12117336.
  4. Huang SW, Giannoni C (2001). “The risk of adenoid hypertrophy in children with allergic rhinitis”. Ann. Allergy Asthma Immunol. 87 (4): 350–5. doi:10.1016/S1081-1206(10)62251-X. PMID 11686429.
Differentiating adenoiditis from other diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Mahshid Mir, M.D. [2]

Overview

Diagnosis of adenoiditis can be challenging as majority of upper respiratory tract infections show the same pattern. The most important differential diagnosis include tonsilitis, viral upper respiratory tract infection, sinusitis and pharyngitis.

Differential diagnosis

Adenoiditis must be differentiated from other diseases that cause fever, nasal airway obstruction and snoring, and sore throat.

The table below outlines the differences between adenoiditis and other respiratory tract infections.

Differential diagnosis based on fever and sore throat
Disease/Variable Presentation Causes Imaging finding Treatment
Upper respiratory tract infection[1][2][3] _ Symptomatic therapy:
Peritonsillar abscess[4][5] On ultrasound peritonsillar abscess appears as focal irregularly marginated hypoechoic area
Croup[6][7][8] Steeple sign on neck X-ray
Epiglottitis[9][10] Thumbprint sign on neck x-ray
Pharyngitis[11][12] _
Tonsilitis [13][14] Intraoral or transcutaneous USG may show an abscess making CT scan unnecessary
Sinusitis[15][16] On CT scan, a mass impinging on the posterior pharyngeal wall with rim enhancement is seen
  • Supportive therapy is the mainstay of treatment for both cases of acute and chronic rhinosinusitis
  • Antibiotics (macrolides, penicillins, clavulonic acid- amoxicillin) an be added in select cases of acute, as well as chronic rhinosinusitis

References

  1. “Antibiotics for adults with acute laryngitis | Cochrane Summaries”.
  2. http://www.cochrane.org/reviews/en/ab004403.html Antibiotics for exacerbations of chronic obstructive pulmonary disease
  3. http://www.cochrane.org/reviews/en/ab000980.html Vitamin C for preventing and treating the common cold
  4. 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.
  5. 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.
  6. Cherry, James D. (2008). “Croup”. New England Journal of Medicine. 358 (4): 384–391. doi:10.1056/NEJMcp072022. ISSN 0028-4793.
  7. Henrickson, K. J. (2003). “Parainfluenza Viruses”. Clinical Microbiology Reviews. 16 (2): 242–264. doi:10.1128/CMR.16.2.242-264.2003. ISSN 0893-8512.
  8. Schomacker, Henrick; Schaap-Nutt, Anne; Collins, Peter L; Schmidt, Alexander C (2012). “Pathogenesis of acute respiratory illness caused by human parainfluenza viruses”. Current Opinion in Virology. 2 (3): 294–299. doi:10.1016/j.coviro.2012.02.001. ISSN 1879-6257.
  9. Wick F, Ballmer PE, Haller A (2002). “Acute epiglottis in adults”. Swiss Med Wkly. 132 (37–38): 541–7. PMID 12557859.
  10. Nickas BJ (2005). “A 60-year-old man with stridor, drooling, and “tripoding” following a nasal polypectomy”. J Emerg Nurs. 31 (3): 234–5, quiz 321. doi:10.1016/j.jen.2004.10.015. PMID 15983574.
  11. Ferri, Fred (2005). Md consult/first consult 14-month subscription : combo retail pack. Place of publication not identified: Elsevier Saunders. ISBN 9781416026075.
  12. Kline JA, Runge JW (1994) Streptococcal pharyngitis: a review of pathophysiology, diagnosis, and management. J Emerg Med 12 (5):665-80. PMID: 7989695
  13. Nogan S, Jandali D, Cipolla M, DeSilva B (2015). “The use of ultrasound imaging in evaluation of peritonsillar infections”. Laryngoscope. 125 (11): 2604–7. doi:10.1002/lary.25313. PMID 25946659.
  14. Putto A (1987). “Febrile exudative tonsillitis: viral or streptococcal?”. Pediatrics. 80 (1): 6–12. PMID 3601520.
  15. Vural C, Gungor A, Comerci S (2003). “Accuracy of computerized tomography in deep neck infections in the pediatric population”. Am J Otolaryngol. 24 (3): 143–8. PMID 12761699.
  16. Philpott CM, Selvadurai D, Banerjee AR (2004). “Paediatric retropharyngeal abscess”. J Laryngol Otol. 118 (12): 919–26. PMID 15667676.
Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahshid Mir, M.D. [2]

Overview

The prevalence of adenoiditis is not completely known. In 2015, the prevalence and incidence of adenoiditis was estimated to be 12000 cases per 100,000 individuals worldwide.[1] The prevalence of adenoiditis decreases with age. Adenoid tissue go through atrophy process after 10 years of age so adeoiditis is rarely seen after 15 .[2]

Epidemiology and Demographics

Prevalence

  • The prevalence of adenoiditis is not completely known.
  • In 2015, the prevalence of adenoiditis was estimated to be 12000 cases per 100,000 individuals worldwide.[1]

Incidence

  • The prevalence of adenoiditis is not completely known.
  • In 2015, the incidence of adenoiditis was estimated to be 12000 cases per 100,000 individuals worldwide.

Case Fatality Rate

  • The case fatality rate of tonsillitis is unknown.

Age

  • Adenoiditis commonly affects children.
  • The prevalence of adenoiditis decreases with age.
  • Adenoid tissue undergo atrophy after 10 years of age so adenoiditis is rarely seen after 15.
  • Adenoiditis can be seen in adults too, although it is rare in this patient population. However due to improved diagnostic modalities, adenoiditis is usually treated or removed during childhood.

Gender

  • Adenoiditis does not show predilection for any gender.

Race

  • Adenoiditis does not show predilection for any race.

Developed and Developing Countries

  • There is no geographic predisposition to tonsillitis.

References

  1. 1.0 1.1 Kara CO, Ergin H, Koçak G, Kiliç I, Yurdakul M (2002). “Prevalence of tonsillar hypertrophy and associated oropharyngeal symptoms in primary school children in Denizli, Turkey”. Int. J. Pediatr. Otorhinolaryngol. 66 (2): 175–9. PMID 12393253.
  2. Pagella F, De Amici M, Pusateri A, Tinelli G, Matti E, Benazzo M, Licari A, Nigrisoli S, Quaglini S, Ciprandi G, Marseglia GL (2015). “Adenoids and clinical symptoms: Epidemiology of a cohort of 795 pediatric patients”. Int. J. Pediatr. Otorhinolaryngol. 79 (12): 2137–41. doi:10.1016/j.ijporl.2015.09.035. PMID 26478108.
Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahshid Mir, M.D. [2]

Overview

The most potent risk factor in the development of adenoiditis is being a young child. Other risk factors include immuno-deficiencies, living in an urban environment with more exposure to viruses or bacteria and usage of immuno-suppressant drugs.

Risk factors

Risk factors for adenoiditis involve increasing the risk of invasion by pathogenic viruses or bacteria.[1][2][3]

  • Living or working in close proximity to children
  • Living in an urban environment with more exposure to viruses or bacteria
  • Young child or elderly adult
  • Immunocompromised
  • Living or working in close proximity to airborne pollutants, such as smoke
  • Living in colder climates[4]
  • Excessive and prolonged use of corticosteroids
  • Obesity or overweight[5]
  • Living with someone who suffers the disease

References

  1. Capper R, Canter RJ (2001). “Is the incidence of tonsillectomy influenced by the family medical or social history?”. Clin Otolaryngol Allied Sci. 26 (6): 484–7. PMID 11843928.
  2. “Stopping the Spread of Germs at Home, Work & School | Seasonal Influenza (Flu) | CDC”.
  3. Graham NM (1990). “The epidemiology of acute respiratory infections in children and adults: a global perspective”. Epidemiol Rev. 12: 149–78. PMID 2286216.
  4. Erling V, Jalil F, Hanson LA, Zaman S (1999). “The impact of climate on the prevalence of respiratory tract infections in early childhood in Lahore, Pakistan”. J Public Health Med. 21 (3): 331–9. PMID 10528962.
  5. Early GJ, Seifried SE (2012). “Risk factors for community-associated Staphylococcus aureus skin infection in children of Maui”. Hawaii J Med Public Health. 71 (8): 218–23. PMC 3419822. PMID 22900237.
Natural history, complications and prognosis


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Charmaine Patel, M.D. [2]

Introduction to the Natural History, Complications and Prognosis Page

  • The page name should be “(Disease name) natural history, complications and prognosis”, with only the first letter of the title capitalized.
  • Goal: To provide information on the natural progression of the disease without treatment, complications that occur as a result of the disease and its treatment, and the anticipated and actual outcomes of treatment.
  • As with all microchapter pages linking to the main page, at the top of the edit box put {{CMG}}, your name template, and the microchapter navigation template you created at the beginning.
  • Remember to create links within Wikidoc by placing [[square brackets]] around key words which you want to link to other pages. Make sure you make your links as specific as possible. For example if a sentence contained the phrase anterior spinal artery syndrome, the link should be to anterior spinal artery syndrome not anterior or artery or syndrome. For more information on how to create links click here.
  • Remember to follow the same format and capitalization of letters as outlined in the template below.
  • Remember this is not the section to put the history of the disease in time. This would be detailed in the historical perspective section.
  • Remember this is not the section to put the history of the patient. This would be detailed in the diagnosis section, under history.
  • You should include the name of the disease in the first sentence of every subsection.
A guide on how to write the Natural History, Complications and Prognosis Page contents

Overview

  • The overview section should include the disease name in the first sentence.
  • The goal is to summarize the entire page in several sentences. This section can be the same as the natural history, complications and prognosis segment on the overview page.
  • To see an example, click here.

Template

  • First Sentences:
If left untreated, [#]% of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3]. Common complications of [disease name] include [complication 1], [complication 2], and [complication 3]. Prognosis is generally excellent/good/poor, and the 1/5/10-year mortality/survival rate of patients with [disease name] is approximately [#]%.
OR
Depending on the extent of the tumor at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as poor/good/excellent.
  • Examples:
Example 1: If left untreated, 20% to 30% of patients with IgA nephropathy may progress to develop ESRD. Common complications of IgA nephropathy include pro-thrombotic states, such as stroke and myocardial infarction. Prognosis is generally good, and the 5-year mortality rate of patients with IgA nephropathy is approximately 5%.
  • Additional Sentences:
[Disease/malignancy] is associated with a 5 year survival rate of [#]%.
The presence of metastasis is associated with a particularly poor prognosis among patients with [disease/malignancy]. The 5 year event free survival rate is less than [#]%.
The [Subtype of disease or malignancy] is associated with the most favorable prognosis.
The prognosis varies with the [characteristic] of tumor: [subtype of disease/malignancy] have the most favorable prognosis.
  • Examples:
Example 1: Rhabdomyosarcoma is associated with a 5 year survival rate of 72%.
Example 2: The presence of metastasis is associated with a particularly poor prognosis among patients with rhabdomyosarcoma. The 5 year event free survival rate is less than 30%.
Example 3: The embryonal subtype of rhabdomyosarcoma is associated with the most favorable prognosis.
Example 4: The prognosis varies with the location of tumor: orbital and genitourinary tract rhabdomyosarcomas have the most favorable prognosis.

Preferred Template Statements

  • If left untreated, [#]% of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].
  • Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].
  • Prognosis is generally excellent/good/poor, and the 1/5/10-year mortality/survival rate of patients with [disease name] is approximately [#]%.
  • Depending on the extent of the [tumor/disease progression/etc.] at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as poor/good/excellent.

 

Additional Sentences

  • The presence of [characteristic of disease] is associated with a particularly [good/poor] prognosis among patients with [disease/malignancy].
  • [Subtype of disease/malignancy] is associated with the most favorable prognosis.
  • The prognosis varies with the [characteristic] of tumor; [subtype of disease/malignancy] have the most favorable prognosis.

Natural History

  • The natural history of disease details how the disease progresses without treatment.
  • Here are a few template sentences you can use: “The symptoms of (disease name) usually develop in the first/ second/ third decade of life, and start with symptoms such as ___. The symptoms of (disease name) typically develop ___ years after exposure to ___. Without treatment, the patient will develop symptoms of ___, which will/ may eventually lead to ___.

Complications

  • Using lists can be helpful for describing this section.
  • You can use these template sentences;
    • “Complications that can develop as a result of (disease name) are ___ (describe in list form)”.
    • “Complications that can develop as a result of the treatment of (disease name) are ___ (describe in list form).
    • Next to each complication, provide a brief one sentence description detailing the complication.
  • For an example of the complications section in a natural history, complications and prognosis page, click here.

Prognosis

  • This section should detail the prognosis of the disease, both treated and untreated.
  • Here are some template sentences; “The prognosis of (disease name) is poor/good with treatment. Without treatment, (disease name) will result in ___. (Disease name) is associated with a 1/5/10 year mortality of __ among patient with ______ (for example high grade lesions). The presence of ___ is associated with a particularly poor prognosis among patients with (disease name).
  • For an example of a prognosis section within a natural history, complications and prognosis page, click here.

References

  • References should be cited for the material that you have put on your page. Type in {{reflist|2}}.This will generate your references in small font, in two columns, with links to the original article and abstract.
  • For information on how to add references into your page, click here.


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