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Table of Contents
Year : 2020  |  Volume : 9  |  Issue : 2  |  Page : 110-115

Acute epiglottitis – A life-threatening clinical entity

1 Department of Otorhinolaryngology, IMS and SUM Hospital, Siksha ‘O’ Anusandhan University, Bhubaneswar, Odisha, India
2 Department of Oral Pathology and Microbiology, IDS and SUM Hospital, Siksha ‘O’ Anusandhan University, Bhubaneswar, Odisha, India

Date of Submission25-Nov-2019
Date of Decision13-Mar-2020
Date of Acceptance17-Mar-2020
Date of Web Publication4-Aug-2020

Correspondence Address:
Santosh Kumar Swain
Professor, Department of Otorhinolaryngology, IMS and SUM Hospital, Siksha ‘O’ Anusandhan University Kalinga Nagar, Bhubaneswar 751 003, Odisha
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JCSR.JCSR_120_19

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Acute epiglottitis (AE) is an acute inflammatory life-threatening clinical condition which can lead to obstruction of the airway. AE is a bacterial infection of the supraglottic structures. Breathing difficulties are often thought of as a strong predictor of the intervention to the airway. AE is considered an emergency due to the chance for airway narrowing. Clinical presentations are alone insufficient for the diagnosis of AE. Fibreoptic nasopharyngolaryngoscopic examination should be performed as soon as possible for confirmation of diagnosis. As AE is a life-threatening infection, it warrants immediate diagnosis and treatment. Antibiotics are the mainstay of the initial treatment along with corticosteroids which act as potential adjuncts. This review article describes the aetiopathology, epidemiology, clinical presentations, diagnosis and current treatment of AE.

Keywords: Acute epiglottitis, airway obstruction, stridor, supraglottitis

How to cite this article:
Swain SK, Shajahan N, Debta P. Acute epiglottitis – A life-threatening clinical entity. J Clin Sci Res 2020;9:110-5

How to cite this URL:
Swain SK, Shajahan N, Debta P. Acute epiglottitis – A life-threatening clinical entity. J Clin Sci Res [serial online] 2020 [cited 2020 Oct 31];9:110-5. Available from: https://www.jcsr.co.in/text.asp?2020/9/2/110/291366

  Introduction Top

Acute epiglottitis (AE) is an inflammatory condition affecting the supraglottic structures which mainly involve the epiglottis. AE is a potentially life-threatening infective condition where inflammation occurs at the supraglottic structures such as epiglottis and adjacent structures such as aryepiglottic folds (AEFs) and arytenoids leading to airway obstruction. Although it is common in paediatric age group, it has been documented that its incidence has been raised in adult age group in recent years. The most common pathogen causing AE is Haemophilusinfluenzae type B (Hib). Previously, it was thought that AE is commonly seen among children, B ut nowadays, the incidence of AE among paediatric age is reduced due to massive immunisation against Hib.[1] In case of immunocompromised patients, AE may be due to a wider spectrum of micro-organisms than AE among immunocompetent children. The effective treatment needs prompt diagnosis of the disease, airway intervention and early antibacterial treatment of the aetiological agent.

We searched SCOPUS, Medline and PubMed databases using search terms included “acute epiglottitis” and “supraglottitis” and identified the abstracts of the published articles. other articles were identified manually from citations. This review summarises the aetiology, epidemiology, clinical presentations, diagnosis and current treatment of AE.

  Epidemiology Top

The epidemiology of AE has now changed with an increasing number of adults being affected. In adult age group, AE differs from that in paediatric age group, and in adults, it is a less severe, non-bacterial infection and has longer days of the symptoms with a chief complaint of throat pain.[2] The incidence of AE among adults is around 1–4/100,000 per year, and it is described as having less morbidity and mortality.[3] The mortality in adult AE ranges from 7%,- 20%.[4] Another study[5] also reported a high mortality in paediatric age group AE. Although AE in adults is unpredictable and sometimes leads to catastrophic result, conservative treatment is still preferable.[6] After introducing Hib vaccinations in childhood immunisation programs, there is a significant decline in the incidence of AE among paediatric age group along with an increase among adults.[7] In post-vaccination era, the annual incidence of paediatric AE is 0.3–0.7/100,000 patients with the frequency among adult age group now greater than paediatric age group.[8]

  Etiopathology Top

The epiglottis has a high vascularity on the anterior/lingual surface of the epiglottis. At the time infection, an exudate with inflammatory cell leakage from the vascular network from the anterior surface of the epiglottis leads to oedema and swelling of the lingual surface of the epiglottis and surrounding area such as lingual tonsils and pre-epiglottic space. AE is traditionally related to the H.influenzae infection, but its isolation is more commonly found in children (68%–72%) than adult age group (21%–23%).[9] There are also other pathogens which have been implicated with AE of adult age group and also caused due to thermal injuries by smoking and illicit drug abuse.[10] A patient may show signs of sepsis in case of severe infections. In paediatric age group, H.influenzae is almost invariable the aetiology associated with AE.[11] Other less commonly identified pathogens in AE are Group A streptococci and Streptococcus pneumoniae. The decreased incidence of the paediatric age group with AE might be due to effective vaccination program against H. influenzae. Previously, 75%–90% of cases of AE were due to Hib, but the vaccination introduced in the year 1985 significantly lowered the incidence of this disease.[12] In adults in addition to H. influenza e S. pneumonia e, haemolytic streptococci and Staphylococcus aureus are also seen in throat or blood culture samples obtained from AE patients.[13] Immunocompromised patients are more prone to AE, and there should be a low threshold of suspicion for the diagnosis of epiglottitis along with presenting symptoms and neutropenia.[14] One study reviewed cases of AE in immunocompromised hosts where 50% were immunocompromised secondary to chemotherapy medications, 25% had immunodeficiency virus and around 38% were neutropenic count with white blood cell count <1000 per cubic millimetre.[14]

  Risk Factors Top

The risk factors for AE are middle- or elderly-age caucasians, tobacco smoking and co-morbid situations such as diabetes mellitus.[15] The other risk factors for AE are male sex, pre-existing epiglottic cyst, obesity and impaired immunity of the host.[15] Impaired immunity and epiglottic cysts have been reported to enhance the risk for recurrent episodes of AE.[16] Adults with AE often have pre-existing medical conditions such as diabetes mellitus, hypertension and alcohol abuse which usually weaken the immunity of the patients and lead to susceptibility of the infections such as AE.[7] The upper airway is usually rigid and wider in adult age than in paediatric patients, so adults have a lower chance of the upper airway obstruction.

  Clinical Presentation Top

AE or acute supraglottitis is a rare disease which may be seen at any age group.[17] AE though earlier thought to be a disease of children, is increasingly being seen in adults as well.[18] In children AE is seen in the age group of 1–11 years; children present with symptoms such as sore throat and fever, followed by breathing difficulty.[12] The clinical presentations of AE begin like other upper airway infections with complaints of sore throat and malaise. AE is a clinical entity of infection to the supraglottis leading to the clinical symptoms such as sore throat, odynophagia, muffled speech or hot potato voice, fever, drooling of saliva and stridor. Because of the minor symptoms, AE is often overlooked in patients and allowing the disease to unknowingly progress to breathing difficulty. The progression of the diseases occurs rapidly over the span of hours in paediatric patients whereas a span of days in adults. The incidence of AE in adults is significantly higher than children in the present day and seems to be rising in adult age group. The average age of adult patients wit AE is around 45 years, with a reported male-to-female ratio being 1.8:1–4:1.[4] The incidence of adult AE is around 1–4/100,000/year.[4] Adult patients with AE usually present with sore throat and odynophagia. Stridor and drooling are rarely found in adult patients. In fact, the presence of stridor and dyspnoea are documented as predictors of airway compromise in adults with epiglottitis.[19] The clinical course of AE in adults is often unpredictable and sometimes be catastrophic.[20] The diagnosis of AE in adults is essential based on the clinical findings and supported by indirect laryngoscopy. There is typically diffuse swelling of the aryepiglottic structures unlike the typical reddish (cherry red) epiglottis in paediatric patients.[21]

This fatal disease of the larynx may lead to sudden airway obstruction to inflammatory response to the supraglottic. Unlike in adult patients, examination of the larynx with indirect laryngoscope or laryngeal fibroscope is usually avoided in children with AE as these procedures often trigger sudden obstruction of the laryngeal airway.[6] Other than supraglottis, sometimes, AE is associated with oedemas in other parts such as tongue, oral cavity, uvula and hypopharynx.[22] If a patient presents with breathing difficulties, he or she often leant forwards with outstretched arms into a tripod position. This helps to decrease chocking sensation as swollen and oedematous epiglottis moves forwards. This tripod position is an impending sign for airway obstruction in AE.[23] Adults have less likelihood of sudden airway obstruction in comparison to paediatric patients. It has been documented that acute AE is more commonly seen in the summer season.[24] However, no predilection for time or season has been reported.[25] Anticipating airway obstruction during managing AE is an important part of the patient care. Predictors for impending airway obstruction in AE include presence of drooling, history of diabetes mellitus, rapid onset of the clinical presentations and abscess formation.[10]

The respiratory distress in AE patients has been classified into Stage I to IV by Friedman's classification [Table 1]. It is a life-threatening infective condition which may be fatal secondary to the sudden onset of airway obstruction. The time lag between the onset of symptoms and physician visit is usually two to three days.[26] AE can also present as a self-limiting disease with a chance of developing a rapid and fulminant course. The differential diagnoses of AE are infective tracheitis, heat-induced epiglottitis due to scald burn from smoke or hot beverages, angioneurotic oedema of the epiglottis, retropharyngeal abscess or peritonsillar abscess, diphtheria and uvulitis.
Table 1: Friedman classification of acute epiglottitis

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  Diagnosis Top

Detail history taking and clinical examination are important for the diagnosis of AE. Co-morbidities such as diabetes mellitus, hypertension, addiction to alcohol, addiction to smoking and upper respiratory tract infection must be ruled out as these may play a role in the progress of the disease as well as seen in patients of AE.[27] The diagnosis of AE is based on clinical presentation supported by laryngoscopic examination. Typically, there is classic cherry-red appearance of the epiglottis [Figure 1] along with swelling of the AEFs in indirect laryngoscopic examination. The lateral soft tissue of the neck radiography may show a thickening of the epiglottis, called as 'thumb sign' [Figure 2]. One study proposed the 'vallecula sign' for better accuracy of the diagnosis of the soft-tissue radiographs of the neck.[28] The absence of deep and well-defined vallecula which supports the diagnosis of AE has been referred to as 'vallecula sign'. X-ray neck (lateral view) shows bulging of epiglottis (thumb sign), which was documented to be present in 71% of the cases with AE.[7] Laryngoscopy is considered to be the standard method for the diagnosis of AE and should be done in all cases of AE. Direct fibreoptic laryngoscopic examination of the larynx shows inflamed oedematous epiglottis, and direct manipulation of the larynx should be avoided as it can lead to rapid airway compromise. Direct laryngoscopy shows diffuse erythematous swelling of the epiglottis, AEFs and pooling of saliva in the pyriform sinus in some cases. Radiographic imaging such as lateral neck X-ray and computed tomography (CT) can be helpful for the diagnosis of AE, especially in patients who show signs of airway obstruction. The lateral view of the X-ray of the neck shows a classical 'thumb sign' which is evidence of the swollen epiglottis. However, the use of fibreoptic nasopharyngolaryngoscopy follows a more confirmatory and faster way for assessing the laryngeal airway, so imaging nowadays is often delayed. Hence, after patients become stable or when the presentation is subacute, the imaging may be indicated for the evaluation of AE and its differential diagnosis.[29] X-ray of the lateral soft tissue of the neck shows a swollen epiglottis and pre-vertebral soft-tissue swelling. direct laryngoscopy by an expert is however, the gold standard investigation.[30],[31] CT scan shows diffuse thickening of the epiglottis and AEFs. Laryngoscopic examination requires special training this facility is usually available in emergency department s. X-ray neck with lateral view is less price and easily available and often used as a screening test in the emergency department for suspected AE. Lateral neck X-ray or CT scan is useful for the diagnosis of AE. The findings of AE have vallecula sign, the thumb sign, thickened AEFs, enlargement of the widening of the soft tissue and ballooning of the hypopharynx. However, these imaging findings of epiglottitis are subjective. Around 79% of the cases of AE are diagnosed on the basis of lateral neck radiology.[32] To increase the specificity and sensitivity for the confirmation of AE, several studies have proposed quantitative criteria such as width of the epiglottis.
Figure 1: Endoscopic picture of the larynx showing cherry-red appearance of the epiglottis in acute epiglottitis

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Figure 2: X-ray neck (lateral view) showing ‘thumb sign’ indicating inflamed and oedematous epiglottis in a patient with acute epiglottitis epiglottis (arrow)

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Blood cultures can be done by taking blood taken from patients of AE to confirm the bacteriological agent. In a study[33] blood cultures that were obtained from 17 patients did not show any growth of the bacteria in 16 of them. Patients of AE show raised leucocytes with an increase in white blood cell (WBC) count with comparison to patients without AE. Therefore, WBC count may serve as an effective screening parameter for the diagnosis of AE.

  Treatment Top

When the patient is suspected for the diagnosis of AE, it is necessitate for taking the patient to a high dependency zone like the resuscitation facilities along with emergency airway kit nearest to the patient's bed. The patient will be started a high flow of oxygen and intravenous access along with immediate airway, breathing and circulation. Arterial blood gas analysis, total blood count and bacterial cultures help for taking decisions towards the requirement for intubation and later treatment of the patient but are not often helpful immediately to confirm the diagnosis. The essence of the management of AE is to safeguard patient's airway and protect the airway obstruction. The treatment of AE includes intravenous broad-spectrum antimicrobial agents with additional corticosteroids for reducing inflammation and oedema of the supraglottic.[8] If the diagnosis is done for AE and compromised airway, then intervention should be started immediately without delaying for imaging or cultures. Treatment should be prompt and begin with intravenous antibiotics. Benefits of the steroids and epinephrine, either nebulised or intramuscular, have yet to be confirmed.[19] The administration of second- and third-generation cephalosporins (ceftazidime or cefotaxime) along with corticosteroids, omeprazole and/or oxygen therapy is often commonly prescribed treatment in AE. Third-generation intravenous cephalosporins are administered in case of intensive care unit (ICU) patients of AE, provided that the patients are not allergic to beta-lactams. Supplementation of hydration and 30% oxygen (humidified) was given through facemask to ease laboured breathing. Corticosteroids are often administered for reducing the oedema and inflammation of the supraglottis and so decreases the chance of airway obstruction. It also reduces the duration of the hospital stay. Intubation or tracheostomy may be required in case of AE with stridor due to collapsed airway. In case of abscess formation along with AE, surgical drainage or debridement is also required. Isolated necrosis of the supraglottis or epiglottis may be seen in some cases of AE.[34] Arterial oxygen saturation of the patient is monitored by finger pulse oxymetry. According to the treatment protocol of AE, the glottic and supraglottic airway should be assessed by an otolaryngologist by a fibreoptic laryngoscopy and found whether the airway is patent or compromised. The decision for securing the airway is decided on the basis of the clinical symptoms and airway appearance. In case of respiratory difficulties such as stridor, oxygen desaturation, cyanosis and sitting erect, airway intervention is required immediately. In some situations where patients lack symptoms and signs of airway obstruction but with narrowed airway also need airway intervention. The causes for latter protocol are due to the fickle nature of the disease which can land on imminent respiratory distress at any time. If possible, patients of AE are shifted to the operating room for endotracheal intubation for maintaining airway. If endotracheal intubations fail after repeated attempt, tracheostomy or cricothyrotomy is performed. After securing the airway, patients are usually transferred to the ICU. Those patients of AE with patent laryngeal airway are admitted in the ward with closely supervised by an otolaryngologist and trained staff nurse. Airway protection is essential during the management of AE, but prophylactic orotracheal intubation or tracheostomy is avoided and also not advised. Intravenous antibiotics are needed and corticosteroids may be beneficial in AE. The key to the treatment of AE is awareness of the disease and close monitoring of the airway.[30] In case of 50% narrowing of the airway, tracheal intubation may be done depending on the severity of the patient's condition.[35] Management of the airway in patients of AE is very crucial, particularly in severe cases of AE, but the airway procedure is needed in cases of <10% of the patients.[36] The presence of clinical findings, such as, stridor, tachypnoea, hypoxia and drooling of the saliva at the time of diagnosis of AE indicate the requirement of an airway procedure.[37] In addition to these, older age, male sex, body mass index over 25 kg/m2 and presence of diabetes mellitus increase the chance for the airway intervention.[38] Hence, instead of prophylactic intubation, treatment must be focused on the patient's needs and his or her conditions.

  Complications Top

The complications of AE are epiglottic abscess and systemic bacteraemia. The other complications of AE are retropharyngeal abscess, cervical necrotising fasciitis, sepsis, sudden airway obstruction with respiratory obstruction and pulmonary oedema.[38] The mortality rate in AE is reported 6%–7% among adult age group in comparison to 1.6% case fatality rate in paediatric age group.[39] The difference between adult and paediatric age groups may be due to wrong diagnosis and improper treatment.[6] Oropharyngeal and nasopharyngeal manipulation might provoke complete airway obstruction, so a conservative protocol is required in case of mild-to-moderate clinical symptoms. Epiglottic abscess is considered as an uncommon sequelae of AE.[40] Anticipating airway obstruction during managing AE is an important part of the patient care. There are four predictors for impending airway obstruction such as drooling, diabetes mellitus, sudden onset of the clinical presentations and abscess formation.[23]

AE is an infectious clinical condition which may lead to abrupt, total blockage of the airway, and this is a medical emergency. Hence, it needs early diagnosis of the disease and prompt treatment for avoiding life-threatening complication such as airway obstruction. The use of the flexible nasopharyngolaryngoscope facilitates reliable visualisation of the larynx and evaluation of possible obstructed airway than lateral X-ray of the neck. Although AE has often non-specific clinical presentations, it may lead to sudden airway obstruction and stridor, so high index of clinical suspicion and early diagnosis can be life-saving.

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  [Table 1]


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