Epiglottitis overview

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Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Epiglottitis from other Diseases

Epidemiology and Demographics

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Risk Factors

Natural History, Complications and Prognosis

Diagnosis

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Physical Examination

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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]

Overview

Epiglottitis is a soft tissue swelling of the epiglottis,[1] and the surrounding structures example; plica aryepiglottica , arytenoids, sinus piriformis and vestibular folds mostly caused by bacteria.[2] The epiglottis is a flap of tissue at the base of the tongue, which prevent food from going into the trachea. Due to its place in the airway, swelling of the epiglottis may interfere with breathing and constitutes a medical emergency. especially when it obstructs or completely close off the windpipe.

Historical perspective

One remarkable incidence of epiglottitis has been traced to George Washington; the first president of the United States on December 13, 1799. He was reported to have had sore throat and hoarseness of voice. At dawn the next day, his conditioned worsened with difficulty in breathing. Few hours later he was found to have respiratory distress and died few hours later of what was known to be due to acute epiglottitis.[3][4][5] In the 1980s Haemophilus influenza type b vaccine was introduced. Prior to this,[6] epiglottitis used to be mostly found in pediatric age group between 3 to 5 years. However, recent trend in North America favors adults as most commonly affected individuals.[7]

Classification

Epiglottitis may be classified according to the etiology, and disease duration into infectious and noninfectious causes. Infectious epiglottitis may be subclassified into bacterial, viral and fungal causes. Noninfectious epiglottitis is main due to trauma from foreign objects inhalation and chemical burns[8] On the basis of disease duration, epiglottitis is almost always acute in presentation requiring emergency treatment else the outcome is fatal.[9]

Pathophysiology

Understading the pathogenesis of epiglottitis involves a good knowlegde of the causative organisms. The only known reservoirs for H. influenzae in humans include, respiratory tract, conjunctival and genital surfaces.[10] Pathogenicity of H. influenza is as a result of imbalance between the virulent factors of the organism and the host immune system. This immunity is enhanced when children are vaccinated with the purified polyribosylribitol phosphate (PRP). H. influenza type b capsule is antiphagocytic. Serum anit-purified polyribosylribitol phosphate (anti-PRP) antibody is important in the complement dependent phagocytosis and lyses of the bacteria. [11] IgA antibody accords the mucosa surface protection again attachment of the organism. The strategies deployed by a microbe to assist its survival and proliferation, may or may not lead to disease process. Epiglottitis caused by H. influenza may therefore be considered as an accidental consequence of the microbial factors that permit its survival.[12] Acute epiglottitis pathogenesis is well exemplified by H. influenzae, with the ability to colonize mucosal surfaces and to spread contiguously or invade epithelial cells. It commonly disseminates within the bloodstream, or localizes to selected tissues among these is the epiglottis. Microbial invasion of the bloodstream around the epiglottis leads to inflammatory response and tissue edema most apparent at the lingual surface of the epiglottis compared to the laryngeal surface. The extravasation of fluid leads to remarkable tissue swelling that may lead to respiratory obstruction and the other symptoms of epiglottitis.[13] The pathogenesis of necrotizing epiglottitis involves the infection with CMV or EBV usually in immunocompromised people. Affected patients are usually neutropenic and lymphopenic at presentation. CMV and EBV modulate the host's immune defense facilitating immune evasion and thereby predisposing the patient to a superimposed infections. The causative organism of necrotizing epiglottitis is unclear.[14]

Causes

Prior to the introduction of Haemophilus influenza type b vaccine,[6] H. influenza was the most common culprit of epiglottitis. In recent literature, group A [beta]-hemolytic Streptococci is more commonly observed to be the cause. The disease used to be mostly found in pediatric age group of 3 to 5 years. However, recent trend favors adults as most commonly affected individuals.[7] Other pathogens such as escherichia coli, candida albicans, or kingella kingae may be encountered in immunocompromised hosts. Occasionally, noninfectious causes examples trauma from foreign objects inhalation and chemical burns have been found to cause epiglottitis.

Differentiating epiglottitis from other diseases

Epidemiology and demographics

In North America, approximatley 1.3 per 100,000 children are affected per year. In adults, the incidence is between 1 and 4 per 100,000 per year.[15][16][17][18] December is observed to be the month with highest number of cases whilst April is the least.[1] Males are more commonly affected with epiglottitis in USA than females. The male to female ratio is approximately 3:2.[1] The disease used to be mostly found in pediatric age group between 3 to 5 years. However, recent trend favors adults as most commonly affected individuals[7] with a mean age of 44.94 years. Recent data suggest an increase in those between 45 to 64 years old as well as those over 85 years whilest those below 18 years is decreasing.[1] In USA, epiglottitis is more prevalent in the caucasian race in urban communities accounting for over 2/3rd of all epiglottitis admissions.[1] Epiglottitis occurs more commonly in developing countries.[19]

Screening

There is no screening modality available for epiglottitis.

Risk factors

Risk factors in the development of epiglottitis include:[8][20] absence of immunization, immunocompromised state, smoking and postsplenectomy.

Natural history, complication and prognosis

Epiglottitis if left untreated may result in respiratory obstruction and death within few hours.[21] Acute epiglottitis may be complicated by the following:[22][23][23][24][25] epiglottic abscess, emphysematous epiglottitis, septic epiglottic chondritis with or without abscessation, airway obstruction and pneumonia. With appropriate and timely diagnosis and treatment, the prognosis is usually good.[9]

Diagnosis

History and symptoms

Epiglottitis presents differently in children and adults. 80 to 95% of adults with epiglottitis present with sore throat and dysphagia[2] [18] whereas the predominant symptoms in infected children are high fever, muffled or hoarse voice, drooling and difficulty swallowing.[2] [26] A forward-leaning position with drooling while trying to breathe is typically seen in affected children. The child often appears acutely ill, anxious, and has very quiet and shallow breathing with the head held forward, on insisting on sitting up in bed. Adults usually have milder presentations and less commonly develop airway obstruction with respiratory distress.[27] Other common symptoms may include:[28][8][29][30] abnormal breathing sounds (stridor), chills, rigor, cyanosis, and Difficulty breathing

Physical examination

A definitive diagnosis of acute epiglottitis can be confirmed by direct inspection under laryngoscopy, although this may provoke airway obstruction. The epiglottis and the surrounding structures appear erythematous and swollen. Physical examination may include:[8][18][2] tenderness of anterior neck, high temperature, increased respiratory rate in both children and adults, pharyngeal redness and cervical lymphadenopathy. In addition, patients with epiglottitis may adapt the so called tripod posture with hyper-extension of the neck, chin pointing forward and trunk and arms leaning forward.[31]

Laboratory findings

Xray

ECG

CT scan

MRI

Ultrasound

Other imaging findings

Other diagnostic findings

Treatment

Medical therapy

Surgery

Prevention

References

  1. 1.0 1.1 1.2 1.3 1.4 Shah RK, Stocks C (2010). "Epiglottitis in the United States: national trends, variances, prognosis, and management". Laryngoscope. 120 (6): 1256–62. doi:10.1002/lary.20921. PMID 20513048.
  2. 2.0 2.1 2.2 2.3 Ossoff RH, Wolff AP, Ballenger JJ (1980). "Acute epiglottitis in adults: experience with fifteen cases". Laryngoscope. 90 (7 Pt 1): 1155–61. PMID 6967138.
  3. 6.0 6.1 Schlossberg, David (2015). Clinical infectious disease (Second ed.). p. 202. ISBN 9781107038912.
  4. 7.0 7.1 7.2 Lichtor JL, Roche Rodriguez M, Aaronson NL, Spock T, Goodman TR, Baum ED (2016). "Epiglottitis: It Hasn't Gone Away". Anesthesiology. 124 (6): 1404–7. doi:10.1097/ALN.0000000000001125. PMID 27031010.
  5. 8.0 8.1 8.2 8.3 Charles R, Fadden M, Brook J (2013). "Acute epiglottitis". BMJ. 347: f5235. doi:10.1136/bmj.f5235. PMID 24052580.
  6. 9.0 9.1 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.
  7. 18.0 18.1 18.2 Mayo-Smith MF, Spinale JW, Donskey CJ, Yukawa M, Li RH, Schiffman FJ (1995). "Acute epiglottitis. An 18-year experience in Rhode Island". Chest. 108 (6): 1640–7. PMID 7497775.
  8. Rivers RL (1979). "Acute epiglottitis (supraglottitis)". J Forensic Sci. 24 (2): 470–2. PMID 541622.
  9. Infernuso T, Watts AE, Ducharme NG (2006). "Septic epiglottic chondritis with abscessation in 2 young Thoroughbred racehorses". Can Vet J. 47 (10): 1007–10. PMC 1571119. PMID 17078251.
  10. 23.0 23.1 Rohrbach MR, Shabani S, Wieland A (2016). "Airway Obstruction Secondary to Emphysematous Epiglottitis: A Case Report". Am J Case Rep. 17: 834–836. PMC 5102242. PMID 27821835.
  11. Chang HW, Lin WJ, Hu SY (2013). "Acute epiglottitis complicating an emphysematous abscess". CJEM. 15 (3): 184–5. PMID 23663468.
  12. Hsieh JK, Phelan MP, Wu G, Bricker A, Anne S (2015). "Epiglottic abscess". Am J Emerg Med. 33 (5): 734.e5–7. doi:10.1016/j.ajem.2014.10.036. PMID 25456339.
  13. Cohen SR, Chai J (1978). "Epiglottitis. Twenty-year study with tracheotomy". Ann Otol Rhinol Laryngol. 87 (4 Pt 1): 461–7. PMID 686588.
  14. 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.


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