Epiglottitis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

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 that prevents 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 closes off the windpipe.

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]

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]

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]

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.

Epiglottitis must be differentiated from other upper respiratory diseases and conditions that may cause throat pain and airway obstruction examples:^[15][16] Croup (Laryngotracheobronchitis), Foreign body obstruction, Subglottic stenosis, pharyngitis, Tonsilitis, Angioedema, uvulitis, retropharyngeal or peritonsilar abscesses and Bacterial tracheitis. For example, although patients with croup and epiglottitis both have stridor, in epiglottitis there is associated drooling without a cough whereas in croup there is cough but no drooling.^[17]

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.^{[18][19][20][21]} 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.^[22]

There is no screening modality available for epiglottitis.

Risk factors in the development of epiglottitis include the absence of immunization, immunocompromised state, smoking, and postsplenectomy.^[8][23]

Epiglottitis if left untreated may result in respiratory obstruction and death within few hours.^[24] Acute epiglottitis may be complicated by the following:^{[25][26][26][27][28]} 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]

Epiglottitis presents differently in children and adults. 80 to 95% of adults with epiglottitis present with sore throat and dysphagia^{[2] [21]} whereas the predominant symptoms in infected children are high fever, muffled or hoarse voice, drooling and difficulty swallowing.^{[2] [29]} 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.^[30] Other common symptoms may include:^{[31][8][32][33]} abnormal breathing sounds (stridor), chills, rigor, cyanosis, and Difficulty breathing

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][21][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.^[34]

Although there is no specific laboratory test for epiglottitis, the following nonspecific test are helpful. These include blood culture, complete blood count, arterial blood gases and throat culture.^[34][26] Throat culture should only be done in intubated patients.^{[35][36][37][38]}

On lateral soft tissue X-ray of the neck, the thumbprint sign a finding that suggests the diagnosis of epiglottitis is seen.^[39][40][41] The thumbprint sign is a manifestation of swollen and edematous epiglottis. This shows as a hemispherical mass at the base of the tongue replacing the normal slender coma shape of the epiglottis.^[33]

There is no ECG finding in epiglottitis.

Computed tomography of the neck in epiglottitis shows swelling and edema of the epiglottis at the base of the tongue.^[42]

MRI in a patient with epiglottitis shows thickening of the epiglottis and aryepiglottic fold. However, it is unnecessary to do imaging in this life-threatening condition unless the diagnosis is uncertain or when an abscess or other complication is suspected.^[43]

The bedside ultrasonography is a safe and noninvasive study that is very useful in evaluating a patient in the emergency department when acute epiglottitis is suspected. The alphabet “P” sign is formed by acoustic shadow of hyoid bone and swollen epiglottis at the level of thyrohyoid membrane in a longitudinal orientation.^[44]

There are no other imaging findings of epiglottitis.

Other diagnostic studies involve the use of fibreoptic laryngoscope which shows the omega sign. This refers to the thickened aryepiglottic folds and epiglottis observed in epiglottitis, when the larynx is seen endoscopically or via laryngoscope as shown below.^[45][46]

Epiglottitis is a medical emergency and warrants immediate establishment of a patent airway. Once the airway has been secured, cultures of blood and epiglottic surface should be obtained before administration of antimicrobial therapy. Administering high-flow oxygen, establishing intravenous access, and calling an ENT specialist are standard first-line interventions for epiglottitis.^[47] An appropriate antibiotic regimen that covers Streptococcus pneumoniae, beta-hemolytic streptococci, and Staphylococcus aureus includes parenteral Cefotaxime or Ceftriaxone in combination with Vancomycin (or Levofloxacin in combination with Clindamycin for Penicillin-allergic patients). Adjuvant therapy is commonly used in the management of stridor associated with acute epiglottitis. Adjuvant therapy includes corticosteroids and racemic Epinephrine.^[34][48]

Epiglottitis requires urgent endotracheal intubation to protect the airway. Ideally, this should be performed in the theater by an experienced anesthesiologist or respiratory therapist, with otolaryngologist back-up in case of failed intubation.^[33] If intubation fails, tracheotomy is required.

Immunization with the Hib vaccine protects children from epiglottitis.^[9] Postexposure prophylaxis with rifampin should be given to selected household contacts when a Haemophilus influenzae epiglottitis is diagnosed. 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.^[9]

Template:WS Template:WH

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

One remarkable incident 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. A few hours later, he was found to be in respiratory distress. Washington died few hours later of acute epiglottitis.^[1][2][3] In the 1980s, Haemophilus influenza type b vaccine was introduced. Prior to this, epiglottitis used to be mostly found in pediatric age group between 3 to 5 years.^[4] However, recent trends in North America have shown adults to be the most commonly affected individuals.^[5]

• On December 13, 1799, George Washington, the United States’ first president, 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.
• The physicians who attended to him tried all treatment modalities but were unsuccessful and by 10:20 PM was declared dead of what was most likely due to bacterial epiglottitis after a review of the signs, symptoms, and clinical course of his fatal illness. It is likely that if he had lived in recent times, the sequela would have been different.^[1][2][3]

• Before 1960, acute epiglottitis was classified under several headings.^[6]

• In the 1980s Haemophilus influenza type b vaccine was introduced. Prior to this,^[4] H. influenza was the most common culprit of epiglottitis.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

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^[1] On the basis of disease duration, epiglottitis is almost always acute in presentation requiring emergency treatment else the outcome is fatal.^[2]

Epiglottitis is almost always an acute condition and may be classified according to the etiology of the disease.

Infectious epiglottitis is a soft tissue swelling of epiglottis,^[3] and the surrounding structures example; plica aryepiglottica, arytenoids, sinus piriformis and vestibular folds usually caused by bacteria and occasionally viruses.^[4] Infectious epiglottitis may be subclassified into:

Prior to the introduction of Haemophilus influenza type b vaccine,^[5] 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.^[6] Other pathogens such as escherichia coli, kingella kingae may be encountered in immunocompromised hosts. Other common bacterial causes of epiglottitis include:^[7][8][9] Staphylococcus aureus and Streptococcus pneumoniae.

This mostly happen in immunocompromised people commonly resulting in necrotizing epiglottitis usually involving infection with CMV or EBV. 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 superimposed infections. The causative organism of necrotizing epiglottitis is unclear.^[10]

Fungi are rare cause of epiglottitis. Notable among them are aspergillus spp and candida albicans.^[1]

This includes all other factors resulting in the development of epiglottitis aside pathogenic organism. These include trauma from foreign objects inhalation and chemical burns^[1]

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

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.^[1] 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. ^[2] 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.^[3] 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 with the laryngeal surface. The extravasation of fluid leads to remarkable tissue swelling that may lead to respiratory obstruction and the other symptoms of epiglottitis.^[4] 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 superimposed infections. The causative organism of necrotizing epiglottitis is unclear.^[5]

Infectious epiglottitis is a soft tissue swelling of epiglottis,^[6] and the surrounding structures example; plica aryepiglottica, arytenoids, sinus piriformis and vestibular folds.^[7] Understading the pathogenesis of epiglottitis involves a good knowlegde of the causative organisms. The only known reservoirs for H. influenzae in humans include:^[1]

• Respiratory tract
• Conjunctival
• Genital surfaces.

Healthy people are normal carriers of the organism. 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.^[2] IgA antibody accords the mucosa surface protection again attachement 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.^[3]

Acute epiglottis pathogenesis is well exemplified by H. influenzae, with the ability to colonize mucosal surfaces and to spread contiguously or invade epithelial cells, to disseminate within the bloodstream, and to localize to selected tissues among these is the epiglottis. The H. influenza like other infectious agents cause epiglottis mostly via invasion of the bloodstream by the help of its virulence factors. These include:^[8]

• Capsular polysaccharide
• Lipopolysaccharide
• Outer-membrane proteins
• Pilus proteins
• IgA proteases
• Histamine
• Factors affecting cilial

The tissues surrounding the epiglottis have rich blood and lymphatic supply. Microbial invasion of the bloodstream around the epiglottis lead 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.^[4]

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.^[5]

On gross pathology the epiglottis and the surrounding structures appear erythematous and swollen as shown below.^[9][10][7]

​

The dissected anatomy of the epiglottis is shown below: ^[11]

The potential space between the mucosal epithelium of the epiglottis and the epiglottic cartilage consists of adipose tissue, fibrous tissue and glands. This space becomes occupied with extravasated fluid resulting from the inflammatory process. Nuetrophilic chemotaxis as well as other inflammatory molecules are responsible for the tissue response to the infectious agents.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Alonso Alvarado, M.D. [2]; Ogheneochuko Ajari, MB.BS, MS [3] Prince Tano Djan, BSc, MBChB [4]

Prior to the introduction of Haemophilus influenza type b vaccine,^[1] 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.^[2] 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.

Prior to the introduction of Haemophilus influenza type b vaccine,^[3] H. influenza was the 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.^[2]

Life-threatening conditions may result in death or permanent disability within 24 hours if left untreated. Epiglottitis is a life-threatening condition and must be treated as such irrespective of the causes.^[4]

Common causes of epiglottitis include:^[5][2]

• Beta-hemolytic streptococci
• Haemophilus influenzae serotype B infection
• Staphylococcus aureus
• Streptococcus pneumoniae

Less common causes of epiglottitis include:^[6][7]

• Noninfectious causes examples include:
  • Trauma from foreign objects inhalation
  • Chemical burns
• Viruses (including herpes simplex)
• Fungi (Aspergillus spp and Candida albicans)

Cardiovascular	No underlying causes
Chemical/Poisoning	Chloramines in pool water, smoking illicit drugs
Dental	No underlying causes
Dermatologic	No underlying causes
Drug Side Effect	No underlying causes
Ear Nose Throat	Vallecular cyst
Endocrine	No underlying causes
Environmental	No underlying causes
Gastroenterologic	Gastroesophageal reflux
Genetic	Hereditary angioedema
Hematologic	Bone marrow transplantation
Iatrogenic	Laryngeal mask airway, tonsillectomy complication
Infectious Disease	Aeromonas hydrophilia, aspergillus, bacteroides melaninogenicus, beta-hemolytic streptococcus, candida albicans, citrobacter diversus, cytomegalovirus, eikenella corrodens, enterobacter cloacae, Epstein-Barr virus, escherichia coli, fusobacterium, haemophilus influenzae, haemophilus parainfluenzae, herpes simplex virus, histoplasma capsulatum, influenza B virus, kingella kingae, klebsiella pneumoniae, moraxella catarrhalis, mycobacterium tuberculosis, neisseria meningitidis, parainfluenza virus, pasteurella multocida, peptostreptococcus, propionibacterium, pseudomonas aeruginosa, serratia marcescens, staphylococcus aureus, stomatococcus mucilaginosus, streptococcus pneumoniae, streptococcus pyogenes, streptococcus viridans, streptococcus milleri, varicella-zoster virus, vibrio vulnificus
Musculoskeletal/Orthopedic	No underlying causes
Neurologic	No underlying causes
Nutritional/Metabolic	No underlying causes
Obstetric/Gynecologic	No underlying causes
Oncologic	Laryngeal lymphangioma
Ophthalmologic	No underlying causes
Overdose/Toxicity	No underlying causes
Psychiatric	No underlying causes
Pulmonary	Foreign body ingestion
Renal/Electrolyte	No underlying causes
Rheumatology/Immunology/Allergy	Allergic reactions
Sexual	No underlying causes
Trauma	Foreign body ingestion, thermal injury
Urologic	No underlying causes
Miscellaneous	Blind finger sweep, caustic ingestion, chloramines in pool water, hot water ingestion, Foreign body ingestion, smoking illicit drugs, thermal injury, vallecular cyst

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

Epiglottitis must be differentiated from other upper respiratory diseases and conditions that may cause throat pain and airway obstruction examples:^[1][2] Croup (Laryngotracheobronchitis), Foreign body obstruction, Subglottic stenosis, pharyngitis, tonsilitis, angioedema, uvulitis, retropharyngeal or peritonsilar abscesses and bacterial tracheitis. For example, although patients with croup and epiglottitis both have stridor, in epiglottitis there is associated drooling without a cough whereas in croup there is cough but no drooling.^[3]

Epiglottitis must be differentiated from other upper respiratory diseases and conditions that may cause throat pain and airway obstruction:^[1][2]

• Croup (Laryngotracheobronchitis)
• Foreign body obstruction
• Subglottic stenosis
• Pharyngitis
• Tonsilitis
• Angioedema 
• Uvulitis
• Retropharyngeal or peritonsilar abscesses
• Bacterial tracheitis

Some simialrities and differences between these differentials are shown below:^[4][3]

Variable		Croup	Epiglottitis	Pharyngitis	Bacterial tracheitis	Tonsilitis	Retropharyngeal abscess	Subglottic stenosis
Presentation	Cough	✔	—	Sore throat, pain on swallowing, fever, headache, abdominal pain, nausea and vomiting	Barking cough, stridor, fever, chest pain, ear pain, difficulty breathing, headache, dizziness.	Sore throat, pain on swallowing, fever, headache, cough	Neck pain, stiff neck, torticollis fever, malaise, stridor, and barking cough	Depends on severity. May have respiratory distress at birth, exercise-induced dyspnea, intermittent wheezing. Inspiratory stridor. [5]
	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	Parainfluenza virus		H. influenza type b, beta-hemolytic streptococci, Staphylococcus aureus, fungi and viruses.	Group A beta-hemolytic streptococcus.	Staphylococcus aureus	Most common cause is viral including adenovirus, rhinovirus, influenza, coronavirus, and respiratory syncytial virus. Second most common causes are bacterial; Group A streptococcal bacteria,[6]	Polymicrobial infection. Mostly; Streptococcus pyogenes, Staphylococcus aureus and respiratory anaerobes (example; Fusobacteria, Prevotella, and Veillonella species)[7][8][9][10][11][12]	Congenital, trauma
Physical exams findings	Suprasternal and intercostal indrawing,[13] Inspiratory stridor[14], expiratory wheezing,[14] Sternal wall retractions[15]		Cyanosis, Cervical lymphadenopathy, Inflammed epiglottis	Inflammed pharynx with or without exudate	Subglottic narrowing with purulent secretions in the trachea[16][17]	Fever, especially 100°F or higher.[18][19]Erythema, edema and Exudate of the tonsils.[20] cervical lymphadenopathy, Dysphonia.[21]	Child may be unable to open the mouth widely. May have enlarged cervical lymph nodes and neck mass.	Signs of respiratory distress, intermittent wheezing. Inspiratory stridor. [5]
Age commonly affected	Mainly 6 months and 3 years old rarely, adolescents and adults[22]		Used to be mostly found in pediatric age group between 3 to 5 years, however, recent trend favors adults as most commonly affected individuals[23] 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.[24]	Mostly during the first six years of life	Primarily affects children between 5 and 15 years old.[25]	Mostly between 2-4 years, but can occur in other age groups.[26][27]	May be congenital congenital or acquired. Mean age in acquired is 54.1 years[28]
Imaging finding	Steeple sign on neck X-ray		Thumbprint sign on neck x-ray	—	Lateral neck xray shows intraluminal membranes and tracheal wall irregularity.	Intraoral or transcutaneous USG may show an abscess making CT scan unnecessary.[29][30][31]	On CT scan, a mass impinging on the posterior pharyngeal wall with rim enhancement is seen[32][33]	Bronchoscopy reveals subglottic stenosis. Computed tomography may reveal a concentric stenotic tracheal segment.[34]
Treatment	Dexamethasone and nebulised epinephrine		Airway maintenance, parenteral Cefotaxime or Ceftriaxone in combination with Vancomycin. Adjuvant therapy includes corticosteroids and racemic Epinephrine.[35][36]	Antimicrobial therapy mainly penicillin-based and analgesics.	Airway maintenance and antibiotics	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.	Endoscopic balloon dilation for patients with low-grade subglottic stenosis,[37] glucocorticoid injections, and resection.[38]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

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.^[1][2][3][4] December is observed to be the month with highest number of cases whilst April is the least.^[5] Males are more commonly affected with epiglottitis in USA than females. The male to female ratio is approximately 3:2.^[5] 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^[6] 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.^[5] In USA, epiglottitis is more prevalent in the caucasian race in urban communities accounting for over 2/3rd of all epiglottitis admissions.^[5] Epiglottitis occurs more commonly in developing countries.^[7]

With the advent of Haemophilus influenza type b vaccine, the prevalence of epiglottitis has reduced by >90%.^[8]

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.^[1][2][3][4]

December is observed to be the month with highest number of cases whilst April is the least.^[5]

Males are more commonly affected with epiglottitis in USA than females. The male to female ratio is approximately 3:2.^[5]

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^[6] 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.^[5]

In USA, epiglottitis is more prevalent in the caucasian race in urban communities accounting for over 2/3rd of all epiglottitis admissions.^[5]

Epiglottitis occurs more commonly in developing countries.^[7]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

There is no screening modality available for epiglottitis.

There is no screening modality available for epiglottitis.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

Risk factors in the development of epiglottitis include:^[1][2] absence of immunization, immunocompromised state, smoking and postsplenectomy.

Some risk factors in the development of epiglottitis include the following:^[1][2]

• Absence of immunisation
• Immunocompromised state
• Smoking
• Postsplenectomy

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

If left untreated, epiglottitis may result in respiratory obstruction and death within a few hours.^[1] Acute epiglottitis may be complicated by the following:^{[2][3][3][4][5]} 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.^[6]

If left untreated, epiglottitis may result in respiratory obstruction and death within a few hours.^[1]

Acute epiglottitis may lead to the following complications:^{[2][3][3][4][5]}

• Epiglottic abscess
• Emphysematous epiglottitis
• Septic epiglottic chondritis with or without abscessation
• Pneumonia
• Septic arthritis
• Airway obstruction

Epiglottitis can be a life-threatening emergency. However, with appropriate and timely diagnosis and treatment usually results in a complete recovery.^[6]