Epiglottitis is characterized by acute inflammation of the epiglottis and surrounding supraglottic structures, leading to life-threatening airway obstruction. The pathophysiology of epiglottitis primarily involves infectious or, in some cases, traumatic causes, which result in rapid swelling and edema of the upper airway tissues. This swelling can lead to progressive airway compromise, respiratory distress, and in severe cases, complete airway obstruction.
Differences in Pediatric vs. Adult Airway Anatomy
The anatomy of the airway in pediatric patients differs significantly from that of adults, and these differences have a substantial impact on the presentation and progression of epiglottitis in children. In pediatric patients, the epiglottis is positioned more superiorly and anteriorly compared to adults. This anatomical arrangement makes the pediatric airway more susceptible to early obstruction in the event of inflammation. Additionally, the pediatric epiglottis is more pliable due to immature cartilage, which increases its risk of collapsing when inflamed. In such cases, the swollen epiglottis may act like a one-way valve, worsening airway obstruction during inspiration.
Another key difference is that the narrowest fixed point of the pediatric airway is the subglottic cricoid ring, whereas in adults the glottis is the narrowest area (imaging in living children shows the glottis is actually narrowest side to side, but it stretches and the rigid cricoid does not). Inflammation in the pediatric subglottic space can therefore lead to rapid and significant airway narrowing, which is why the same small airway makes croup so much more severe in young children. On the other hand, the epiglottic cartilage in adults is stiffer and more resilient. While this rigidity can offer some resistance to isolated infections of the epiglottis, inflammation involving the surrounding supraglottic structures can still cause critical airway narrowing. Due to the rigidity of the adult epiglottis, infections in adults may present with a more gradual onset of symptoms compared to children, where airway compromise can occur quickly.
| Feature | Pediatric | Adult |
|---|---|---|
| Epiglottic position | More superior and anterior | Less superior and anterior than in children |
| Epiglottic cartilage | Pliable and immature; prone to collapse when inflamed | Stiffer and more resilient; offers some resistance to isolated epiglottic infection |
| Narrowest fixed point of the airway | Subglottic cricoid ring (rigid, cannot stretch) | Glottis |
| Effect of edema | Swollen epiglottis acts as a one-way "ball-valve," worsening obstruction with each inspiration | Wider supraglottic involvement can still cause critical narrowing despite the stiffer epiglottis |
| Pace of airway compromise | Rapid — early obstruction once inflamed | More gradual onset, but extensive swelling can still cause sudden decompensation |
| Signs of dynamic collapse | Stridor and chest retractions | Sudden, severe respiratory distress when swelling becomes extensive |
Infectious Causes and Pathogenesis
Epiglottitis is most commonly caused by bacterial infections, although viral, fungal, and non-infectious causes are also recognized. Historically, Haemophilus influenzae type B (Hib) was the leading cause of epiglottitis, especially in children. However, with the widespread use of the Hib vaccine, the incidence of Hib-related epiglottitis has drastically decreased. Nowadays, other bacterial pathogens are more frequently implicated in cases of epiglottitis. These include Streptococcus pneumoniae, Staphylococcus aureus, and Streptococcus pyogenes (Group A Streptococcus).
In immunocompromised patients, the range of potential pathogens expands and may include organisms such as Pseudomonas aeruginosa, Candida species, and even Mycobacterium tuberculosis. These infections result in inflammation and swelling of the epiglottis and adjacent tissues. The acute inflammatory response leads to the accumulation of inflammatory cells and fluid, causing the epiglottis to swell and potentially obstruct the airway. The infection and inflammation can also extend to nearby structures, including the arytenoids, aryepiglottic folds, and vallecula, further compromising the airway.
Edema and Airway Obstruction
A defining feature of epiglottitis is the rapid accumulation of inflammatory edema in the supraglottic region, including the epiglottis. The mucosa on the lingual (anterior) surface of the epiglottis and over the aryepiglottic folds is loosely attached, so fluid pools there quickly, whereas the mucosa over the vocal cords is tightly bound to the underlying tissue, which is why the swelling stays above the glottis and the cords themselves usually look normal. This edema increases the size and weight of the epiglottis, which can collapse during inspiration, effectively blocking the airway. In pediatric patients, the pliability of the epiglottic cartilage exacerbates this collapse, creating a "ball-valve" effect in which the inflamed tissue obstructs airflow during each breath. This dynamic collapse of the airway during inspiration leads to the classic signs of respiratory distress in epiglottitis, such as stridor and chest retractions.
In adult patients, although the inflammation and edema tend to involve a wider area of the supraglottic structures, the relatively stiff epiglottis provides more stability. As a result, symptoms of airway obstruction may develop more gradually compared to children. However, when the swelling becomes extensive, even adults can experience rapid airway decompensation, with a sudden onset of severe respiratory distress.
Spread of Infection
Once the infection causing epiglottitis is established, inflammation and edema can spread to adjacent structures in the larynx and upper trachea. In severe cases, this can result in diffuse swelling throughout the upper airway, significantly increasing the risk of respiratory failure. As the infection extends beyond the epiglottis, it may cause supraglottic swelling that involves the arytenoids, aryepiglottic folds, and false vocal cords. In some cases, the infection can progress to laryngotracheitis, where inflammation spreads down into the trachea, a condition more often associated with croup but also seen in advanced epiglottitis. An epiglottic abscess forms in a minority of adults and markedly raises the likelihood that an airway intervention will be needed, and Hib epiglottitis in particular is a bacteremic illness that can seed pneumonia, meningitis, or septic arthritis.
Severe airway obstruction is a dangerous consequence of the widespread infection and swelling. If left untreated, the progressive obstruction can lead to hypoxia, cyanosis, and ultimately respiratory arrest. Rapid recognition and treatment of airway compromise are essential to prevent these life-threatening outcomes in both pediatric and adult patients with epiglottitis.
