Delayed fatal upper-airway obstruction due to laryngopharyngeal burns and thermal epiglottis

Introduction

Lethal upper-airway obstruction may be caused by a variety of congenital or acquired lesions, the nature of which varies depending on age. For example, congenital obstructive lesions are far more common in infants and children than they are in adults, whereas obstruction from inhaled food may occur in both the very young, associated with immature dentition, and the old, related to dementia and other neurological conditions. ¹ , ² Occasionally, intrinsic or extrinsic tumours may cause critical airway narrowing, as may anaphylaxis and infections. ³ , ⁴

It is also well recognised that burn injuries to the upper airway may predispose to lethal obstruction from the resultant stenosing oedema. ⁵ While most of these cases result from hot air or steam inhalation, very rarely thermal epiglottitis may arise from the ingestion of hot food. As this is usually not fatal,^6–8 the following case is presented to demonstrate a rare cause of death following ingestion of hot food.

Case report

A 48-year-old man complained of swelling of the throat some hours after eating hot food at dinner. He was reluctant to call an ambulance and opted instead to wait for another member of the household to wake before seeking medical attention. It was later reported that he was drooling because he was no longer able to swallow.

Subsequently, he was found gasping for breath and collapsed in a car before he could be transported to hospital. Cardiopulmonary resuscitation was commenced and continued by attending ambulance personnel to no avail. His past history included insulin-dependent type II diabetes mellitus, hypercholesterolaemia, hypertension, obstructive sleep apnoea and depression.

At autopsy, the body mass index was 50.7 kg/m² (morbidly obese) with cardiomegaly (720 g) and congestion and oedema of the lungs, which were also mildly emphysematous. Significant findings were limited to the upper aerodigestive tract where there was generalised hyperaemia with moderate congestion and oedema of the epiglottis, which showed a focal area of mucosal necrosis over the anterior aspect (Figure 1). There was also marked oedema and swelling of the aryepiglottic folds associated with a 20 mm×30 mm focus of mucosal congestion and necrosis with overlying inflammatory exudate lying in the laryngopharynx over the posterior aspect of the cricoid cartilage (Figure 2). This had resulted in marked narrowing of the glottic inlet. The vocal cords and false cords were not inflamed, and the thyroid cartilage, cricoid cartilage and hyoid bone were intact. Histology showed coagulative necrosis of the squamous epithelium with areas of epithelial loss and a surface coating of fibrinopurulent exudate. The submucosa was markedly oedematous and diffusely infiltrated by neutrophils with vascular congestion and patchy submucosal haemorrhage (Figure 3). The appearances were consistent with a recent burn injury. No other trauma was identified, and there were no underlying organic diseases present which could have caused or contributed to death.

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Figure 1.

A superior view of the markedly oedematous epiglottis with narrowing of the glottic inlet and a focal area of mucosal necrosis anteriorly.

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Figure 2.

A view of the aryepiglottic folds showing marked oedema and swelling with a 20 mm×30 mm focus of mucosal congestion and necrosis and adherent overlying inflammatory exudate over the posterior aspect of the cricoid cartilage (a). A closer view of the area of mucosal burn (b).

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Figure 3.

Photomicrograph of the aryepiglottic folds showing marked oedema with adjacent areas of mucosal inflammation, interstitial haemorrhage and necrosis from the recent burn (hematoxylin and eosin ×30).

A sample of blood was negative for alcohol but contained therapeutic levels of duloxetine and codeine. Additionally, low levels of delta-9-tetrahydrocannabinol (delta-9-THC) and 11-nor-9-carboxy-delta-9-THC were detected, consistent with recent cannabis use. The serum tryptase level was not significantly raised (13 µg/L), with no elevations of total immunoglobulin (Ig)E (166 kIU/L) or allergen-specific IgE (<0.35 kIU/L; for milk, wheat, peanut, soybean and egg). Vitreous biochemistry was unremarkable. Death was therefore attributed to upper-airway obstruction due to glottic inlet oedema associated with laryngopharyngeal and epiglottic burns.

Discussion

Thermal epiglottitis results from the direct application of heat to the mucosa and underlying cartilaginous components of the epiglottis. ⁸ It usually arises from inhalation of hot air or steam, with inhalational burns being documented in 10–47% of burns patients. It has been suggested, however, that the reported range may be skewed by differences in diagnostic criteria. ⁵ On occasion, it has occurred in adults smoking illicit drugs. ⁹ Most thermal injuries are restricted to the supraglottic airways, with <5% of burns patients having injuries to the trachea or bronchi. ¹⁰ Emergency airway management may be required with intubation or tracheotomy. ⁷ , ¹¹

Rarely, such upper-airway injuries may follow the ingestion of hot liquids or food. ¹² For example, a 59-year-old man was reported who developed worsening dyspnoea, drooling and a wheeze after swallowing scalding hot milk. This occurred several hours after ingestion and was associated with erythema of the aryepiglottic folds, arytenoids and false vocal cords with oedema of the epiglottis. ⁷ Similarly, a 21-year-old man who presented to hospital with a sore throat and dysphagia after attempting to eat a portion of a microwaved potato was found to have an erythematous and oedematous hypopharynx and epiglottis. ⁶ Lastly, a 51-year-old man who developed a sore throat, dysphonia and dysphagia shortly after eating a hot stewed tomato had developed an oedematous epiglottis. ⁸ Treatment in these cases included oxygen therapy, empiric antibiotics, corticosteroids and/or nasogastric feeds with resultant full recoveries.^6–8

Airway obstruction may also be caused purely by oral or facial oedema from burns, ¹³ and it has been shown that thermal epiglottitis may even develop in the absence of specific ingestion of hot material, for example in the ‘teapot syndrome’ when a child falls with a hot liquid and suffers scalds to the face and neck. ¹⁴

The current case differs from the above reports in that upper-airway burning by hot food led to critical upper-airway narrowing which proved lethal. There are, however, some similarities in that the symptoms and signs in all cases take some time to develop, with a slow onset sometimes masking the clinical diagnosis. ¹⁵ The case does, however, demonstrate that thermal epiglottitis, not in the setting of a fire or steam inhalation, may be a cause of unexpected death in adults. In a forensic setting, cases should be suspected if there are burns to the mouth, or there is a history of collapse following difficulty swallowing, a sore throat, drooling and/or dyspnoea. A history of recent ingestion of hot fluid or food may also provide a clue to this rare diagnosis. Measures of serum tryptase and IgE may be useful tests to exclude possible anaphylaxis. ¹⁶