Laryngeal burns: first aid and treatment

Laryngeal burns are injuries to the mucous membrane and underlying structures at the entrance to the respiratory tract, caused by inhalation of hot gases and smoke, vapors and aerosols of caustic substances, or by ingestion of hot liquids or chemicals. The danger of such burns is that even with seemingly "minor" symptoms, laryngeal swelling can increase over the first 24-48 hours and lead to acute airway obstruction. Therefore, early assessment and, if necessary, immediate airway management are key. [1]

Based on the mechanism, a distinction is made between thermal injuries (hot air, steam, flame, hot drinks/food) and chemical injuries (acids, alkalis, irritating gases). In adults, inhalation injuries from fires in enclosed spaces are more common; in children, cases of "thermal epiglottitis" have been described after hot drinks and food. The clinical picture ranges from hoarseness and pain when swallowing to stridor and respiratory failure. [2]

In contrast to older approaches, modern tactics do not recommend "prophylactic" systemic antibiotics and routine glucocorticoids for inhalation trauma: these interventions do not improve outcomes and may increase the risk of complications. Instead, the emphasis is on oxygen, careful monitoring, targeted antidote therapy for carbon monoxide and cyanide poisoning, bronchoscopic debridement when necessary, and individualized use of adjuvant techniques. [3]

Finally, it's important to understand that laryngeal burns are often associated with tracheal and bronchial damage and generalized burn damage to the skin. Inhalation injury is an independent factor in increasing mortality in patients with skin burns, with the risk increasing significantly with larger burn areas. This necessitates early consultation with a burn center and an otolaryngologist. [4]

Code according to ICD-10 and ICD-11

In the International Classification of Diseases, Tenth Revision (ICD-10), burns of the internal respiratory organs are classified under block T27, "Burns and corrosion of the respiratory tract." The most relevant codes are: T27.0, "Thermal burn of the larynx and trachea," T27.1, "Thermal burn of the larynx and trachea with lung damage," and chemical injuries T27.4 and T27.5. For document management, extended entries are often used, indicating the type of contact (primary, subsequent, consequences). [5]

In the eleventh revision (ICD-11), these conditions are coded in the NE00-NE0Z block "Burns of the eye or internal organs" using post-coordination: anatomical expansion codes from Chapter X (e.g., "Larynx" XA2RH5, "Epiglottis" XA1PB3) and other clarifying features are added to the "core" code for burns of internal organs. This cluster approach allows for more precise recording of localization (larynx, trachea), etiology (thermal, chemical factor), and severity. [6]

Table 1. Corresponding codes

Classification	Code	Description
ICD-10	T27.0	Thermal burn of the larynx and trachea (variants T27.0XXA and others for the type of treatment)
ICD-10	T27.1	Thermal burn of the larynx and trachea with lung damage
ICD-10	T27.4	Chemical burn of the larynx and trachea
ICD-10	T27.5	Chemical burn of the larynx and trachea with lung damage
ICD-11	NE00-NE0Z + XA codes	Burns of internal organs with postcoordination: "Larynx" XA2RH5, "Epiglottis" XA1PB3, other specifications (code cluster)

Epidemiology

Inhalation injury of the respiratory tract occurs in approximately 20-30% of hospitalized burn patients; the risk is increased with central facial burns. The presence of inhalation injury significantly increases the risk of mortality and complications, including pneumonia and respiratory failure. [7]

According to research and registries, the proportion of inhalation injury among all burn patients ranges from 10% to 35%, and its contribution to mortality is disproportionately large: in patients with inhalation injury, mortality is several times higher than in patients without it, especially with a large area of skin burn. [8]

In children, thermal injury to the epiglottis ("thermal epiglottitis") has been described as a rare but potentially serious cause of acute upper airway obstruction, often associated with the ingestion of hot drinks or foods. Recent publications emphasize the need for active inquiry about hot liquids and monitoring for swelling progression. [9]

In fires in enclosed spaces, the risk of laryngeal damage increases due to the combination of heat and toxic gases (carbon monoxide, cyanide). Such cases require not only respiratory support but also a search for signs of poisoning and targeted antidote therapy. [10]

Table 2. Key epidemiological figures

Indicator	Range/Value
Prevalence of inhalation injury among hospitalized burn patients	10-35%
Typical level for major burns and/or facial burns	20-30%
Impact on mortality	Increase several times, especially with large areas of skin burns
Thermal lesions of the epiglottis in children	Rare, but with a risk of rapid obstruction

Sources for the table: [11]

Reasons

Thermal burns of the larynx occur from exposure to hot air, steam, and combustion products, especially in enclosed spaces, as well as from accidental ingestion or aspiration of very hot liquids or food. Common scenarios include indoor fires, inhalation of vapors from explosions, and scalding of the upper respiratory tract with boiling water. [12]

Chemical burns are caused by the inhalation of irritating gases (ammonia, chlorine, sulfur dioxide), as well as by the aspiration and ingestion of acids and alkalis. Alkalis cause "liquation" necrosis with deep penetration, while acids cause coagulation necrosis with scab formation. Chemical inhalations often result in combined damage to the larynx, trachea, and bronchi. [13]

Mixed fire injuries are a separate category: a combination of thermal burns and the toxic effects of carbon monoxide and cyanide. In such cases, the determining factors are exposure to the fire in a confined space, traces of soot, altered consciousness, and high levels of carboxyhemoglobin or severe lactic acidosis. [14]

In children and the elderly, pain thresholds and avoidance responses may be different, and the laryngeal lumen may be narrower, so even moderate temperatures or irritant concentrations can cause clinically significant obstruction. This explains the more severe course of the disease in children in seemingly "everyday" scenarios. [15]

Table 3. Causes and proposed mechanisms

Cause	Damage mechanism
Fire in a confined space	Thermal burn of the mucous membrane + toxic gases
Steam, hot air	Thermal denaturation of proteins, edema
Hot drinks/food	Point thermal lesion of the epiglottis and entrance to the larynx
Acids/alkalis (inhalation/aspiration)	Coagulative or liquative necrosis
Irritating gases (ammonia, chlorine)	Chemical burn, inflammatory edema

Risk factors

The risk increases with exposure to smoke in a confined space, loss of consciousness during a fire, facial burns, scorched eyebrows and eyelashes, soot in the mouth or nasal passages, hoarseness, stridor, and dysphagia. These are classic predictors of inhalation injury to the upper respiratory tract. [16]

In children, risk factors include access to very hot drinks and food, as well as lack of adult supervision. In the elderly and in people with underlying respiratory diseases, edema develops more quickly and is more severe. [17]

Occupational exposures (chemical vapors, cryogenic and thermally aggressive environments) and the lack of personal protective equipment also increase the risk of laryngeal burns. In everyday life, non-functioning smoke alarms and the absence of an evacuation plan add to the risk. [18]

Finally, deep burns of large areas of skin, especially the head and neck, are often accompanied by inhalation injury, requiring early consultation with a burn center.[19]

Table 4. Risk factors

Category	Specific factors
Scenario	Fire in the room, prolonged exposure to smoke, loss of consciousness
Signs on examination	Facial burn, burnt hair, soot in mouth/nose, hoarseness, stridor
Vulnerable groups	Children, the elderly, people with respiratory diseases
Wednesday	Industrial chemicals, lack of protective equipment, non-functioning smoke detectors

Pathogenesis

Thermal exposure of the laryngeal mucosa leads to protein denaturation, increased microvascular permeability, and rapid edema formation. Peak edema often occurs within the first 24-48 hours, which explains the delayed deterioration in breathing after a "quiet" onset. [20]

Chemical burns, especially alkali burns, cause deep tissue melting with destruction of the submucosa and the risk of perichondritis and chondronecrosis. In the lower respiratory tract, smoke inhalation causes fibrin "clots" and debris to form, creating "casts" that are dangerous for ventilation, especially in the distal regions. [21]

Toxic components of smoke act systemically: carbon monoxide causes hypoxic tissue injury via carboxyhemoglobin, and cyanides block cellular respiration, resulting in severe lactic acidosis. These mechanisms require targeted antidote therapy and affect the prognosis. [22]

The inflammatory response is accompanied by bronchoconstriction and airway hyperreactivity; symptomatic inhaled bronchodilators are appropriate. Routine steroids have not been shown to be effective and may increase the risk of infection, so their prophylactic use in inhalation trauma is not recommended. [23]

Table 5. Chronology of pathophysiology

Time	Key events
0-6 hours	Thermal/chemical injury, initial swelling
6-24 hours	Increasing swelling of the larynx, the onset of bronchial detritus
24-48 hours	Peak edema, risk of obstruction; formation of fibrin "casts"
3-7 days	Resorption of edema, risk of infection; beginning of scarring
Weeks-months	Scars, granulomas, stenoses, dysphonia

Symptoms

Early signs include pain when swallowing, a sore throat, hoarseness, a sensation of a "foreign body" in the throat, and a dry cough. As swelling increases, inspiratory dyspnea, stridor, salivation, and an inability to swallow saliva occur. Any increasing stridor is a danger sign. [24]

Indirect "marker" signs of inhalation injury include facial burns, scorched hair, soot in the mouth and nose, and "black" sputum. However, their absence does not rule out laryngeal damage. [25]

In children, symptoms often develop more rapidly: pronounced salivation, anxiety, a "croup-like" appearance without fever and without typical infectious markers. This should suggest thermal damage to the epiglottis. [26]

In case of chemical damage, there is a burning sensation, metallic taste, chemical smell from the mouth, and in case of systemic toxicity - headache, confusion, pink-cherry coloration of the skin with carbon monoxide poisoning. [27]

Table 6. Common symptoms and red flags

Symptom	Significance
Hoarseness, pain when swallowing	Early signs of laryngeal damage
Stridor, salivation, inability to swallow	High risk of obstruction, urgent care required
Soot in the mouth/nose, black phlegm	Suspected inhalation injury
Altered consciousness, severe headache	Possible carbon monoxide/cyanide poisoning

Classification, forms and stages

Based on etiology, a distinction is made between thermal and chemical burns, as well as mixed injuries. A separate clinical form is "thermal epiglottitis" in children. [28]

Based on the depth of mucosal damage, lesions are conventionally classified as superficial (erythematous), partial, and deep (with ulceration, necrosis, and risk of perichondritis). This helps predict scarring and stenosis of the laryngeal inlet. (There is no generally accepted "grade" scale for the larynx.)

Bronchoscopic assessment using abbreviated injury scales is widely used for stratification of inhalation injury in general; a number of protocols link the stages to the tactics of sanitation and respiratory care. [29]

The staging of the course includes the acute phase of edema (the first 48 hours), the phase of resorption and recovery (days), then the reconstructive stage (weeks/months), when persistent dysphonia and stenosis appear.

Table 7. Classification (practical view)

Axis	Categories
Etiology	Thermal, chemical, mixed
Localization	Epiglottis, folds, entrance to the larynx, subglottic space
Depth	Superficial, partial, deep (with necrosis/perichondritis)
Phase	Acute (0-48 hours), subacute (3-7 days), late (weeks-months)

Complications and consequences

Early complications include progressive edema and obstruction, the need for intubation or surgical access to the airway, aspiration, and pneumonia. In cases of combined inhalation injury, acute respiratory failure and acute lung injury syndrome may occur. [30]

Long-term sequelae include granulation and scarring, anterior-posterior and posterior commissural stenosis, persistent dysphonia, chronic "respiratory" cough, and dysphagia. Long-term voice impairments requiring phoniatric rehabilitation are possible.

Systemic complications are associated with smoke toxins: hypoxic brain damage from carbon monoxide, lactic acidosis and organ damage from cyanide intoxication.[31]

Chondronecrosis of the larynx after deep chemical burns can lead to lumen deformation and the need for reconstructive surgery.

Table 8. Complications

Period	Complications
Early	Obstruction, pneumonia, need for intubation/tracheostomy
Subacute	Bronchial "casts", atelectasis, infection
Remote	Cicatricial stenosis, dysphonia, chondronecrosis
Systemic	Hypoxia (carbon monoxide), lactic acidosis (cyanides)

When to see a doctor

Immediately - with any stridor, increasing shortness of breath, salivation, inability to swallow saliva, blue lips, or impaired consciousness. These are signs of impending obstruction and hypoxia. [32]

Urgently - in case of facial burns, smoke inhalation in closed spaces, soot in the mouth/nose, hoarseness, pain when swallowing, especially in children and the elderly. [33]

In case of chemical exposure, go to hospital immediately, even if the symptoms are moderate: swelling may increase, and systemic toxins act “hidden”. [34]

Patients with significant skin burns, particularly to the head and neck, should be referred to a burn center according to current referral criteria.[35]

Table 9. Red flags for immediate attention

Sign	Action
Stridor, salivation, inability to swallow	Call an ambulance, provide oxygen
Facial burn, soot in mouth/nose	Airway assessment, burn center consultation
Impaired consciousness after a fire	100% oxygen, no carbon monoxide or cyanide
Childhood with a croup-like picture without fever	Examination by an otolaryngologist, fibrolaryngoscopy

Diagnostics

The first step is to assess and manage the airway: monitor saturation, administer humidified oxygen, and prepare for controlled intubation if there are signs of threatened obstruction according to modern clinical criteria. [36]

Next comes targeted visualization of the upper respiratory tract. Flexible fiberoptic laryngoscopy in a stable patient allows assessment of swelling of the epiglottis, folds, and subglottic space. If swelling of the lower airways is suspected, fiberoptic bronchoscopy is performed, which simultaneously allows for debridement. [37]

Laboratory tests include co-oximetry to measure carboxyhemoglobin, arterial blood gases, and lactate levels as an indirect marker of cyanide intoxication. Chest radiography may be normal in the first few hours, and CT scanning of the neck is considered if deep injury and complications are suspected.[38]

The final block is severity stratification and monitoring planning: in patients without severe endoscopy features, a dynamic monitoring tactic with re-evaluation within 24-48 hours is possible; in case of doubt, it is better to choose a more cautious strategy with early airway management. [39]

Table 10. Diagnostic tools and their tasks

Method	What does it give?
Fibrolaryngoscopy	Direct assessment of edema and ulcerative-necrotic changes in the larynx
Fiberoptic bronchoscopy	Assessment of the trachea/bronchi, possibility of sanitation
Co-oxymerism/blood gases	Detection of carbon monoxide, hypoxemia, hypercapnia
Blood lactate	Indirect sign of cyanide intoxication
CT scan of the neck	Indications: deep lesions, perichondritis, abscesses

Differential diagnosis

Infectious epiglottitis can mimic a thermal injury: salivation and stridor are similar, but in the thermal variant there is often a history of hot liquid or smoke and fever and marked inflammatory markers may be absent.[40]

Allergic laryngeal edema and anaphylaxis are typically accompanied by urticaria, hypotension, and allergen exposure; systemic manifestations and response to epinephrine are key.

A foreign body in the larynx or trachea causes sudden obstruction, cough, and wheezing; endoscopy confirms the diagnosis and helps remove the object.

Neck trauma and iatrogenic injuries after intubation are differentiated based on the relationship to the procedure, endoscopic findings, and imaging data.

Table 11. Differential features

State	What does it suggest?
Thermal/chemical burn	Association with hot liquid/smoke, soot, characteristic endoscopic findings
Infectious epiglottitis	Fever, laboratory signs of infection
Allergic edema	Urticaria, allergen history, adrenaline effect
Foreign body	Sudden onset, localized wheezing, visualized by endoscopy

Treatment

First and foremost, the airway is important. If there are signs of impending obstruction (stridor at rest, salivation, progressive dyspnea, severe hoarseness, or edema seen on endoscopy), controlled intubation is performed, preferably under videolaryngoscopy or with fiberoptic assistance. Decision-making criteria are based on the current clinical "Denver" criteria and updated recommendations from specialized societies: it is best not to perform intubation unless indicated to avoid complications. [41]

Humidified oxygen should be administered to all patients. If carbon monoxide poisoning is suspected, high-concentration oxygen is indicated until carboxyhemoglobin levels return to normal; hyperbaric oxygenation is considered in cases of severe hypoxia and neurological symptoms. If cyanide intoxication is suspected, hydroxocobalamin is considered. [42]

In stable patients with limited edema, positioning with the head of the bed elevated, humidified inhalations, and close observation are used. A helium-oxygen gas mixture can be used as a temporary "bridge" measure for upper obstruction to reduce the work of breathing; however, this is symptomatic support and does not replace problem-solving. [43]

Inhaled bronchodilators are used based on symptoms of bronchospasm. Nebulized adrenaline solutions are sometimes used briefly to reduce the severity of stridor (the effect is temporary, especially in children), but the decision to use them is made individually, under observation. [44]

Routine administration of systemic glucocorticoids for inhalation trauma has not been shown to improve outcomes and is not recommended due to the potential for increased risk of infection. Exceptions include specific clinical scenarios (e.g., post-extubation laryngeal edema), where short courses may be discussed on an individual basis. Prophylactic antibiotics are also not recommended without evidence of infection.[45]

Bronchoscopic debridement is indicated for severe airway obstruction with combustion products and mucofibrin deposits. This not only improves ventilation but also allows for objective assessment of the severity and progression of the lesion. A plan for repeat debridement is determined based on clinical and endoscopic findings. [46]

Inhalation protocols with heparin and acetylcysteine are actively debated: meta-analyses and cohort studies yield conflicting results, some studies have shown no clinical benefit, and a number of observations have noted an increased incidence of pneumonia; however, some series have not revealed a significant risk of bleeding. If this technique is used, it should be done according to a local protocol and under strict monitoring. [47]

Pain relief and sedation are tailored individually. Contrary to outdated beliefs, opioid analgesics are not "contraindicated" by definition; they are used cautiously, under respiratory monitoring, especially in cases of multiple trauma.

Surgical airway management (urgent cricothyrotomy or tracheostomy) is used when safe intubation is impossible or when persistent late stenosis requires long-term access. In the long-term, reconstructive interventions for cicatricial deformities of the larynx are possible.

Rehabilitation includes early speech therapy and phoniatric support, scar prevention, reflux control, and breathing exercises. Patients with combined smoke exposure require an assessment of the neurological consequences and psychological support.

Table 12. Treatment options and evidence status (simplified)

Method	Role today
Early airway management	Key, according to clinical criteria
Oxygen, antidotes (hydroxocobalamin), hyperbaric oxygen as indicated	According to indications for toxic components
Bronchoscopic sanitation	By clinic/endoscopy
Bronchodilators	By symptoms
Systemic steroids	Not routine for inhalation injury
Nebulized heparin/acetylcysteine	Conflicting data according to local protocols
Antibiotics	Not prophylactically, only for infection
Helium-oxygen	Temporary support for superior obstruction

Sources for the table: [48]

Prevention

At home, consider installing and regularly testing smoke alarms, creating a family evacuation plan, storing hot drinks and food out of reach of children, and checking the temperature before serving. Simple measures can significantly reduce the risk.

In production, strict ventilation standards, personnel training, respiratory protective equipment, emergency evacuation protocols, and access to emergency showers/rinses for chemical exposures are in place.

Cooking hazards - be careful with 'boiling' drinks and foods with melted cheeses/caramel, which retain heat longer; this is especially important for children. [49]

In educational institutions and nursing homes, training is provided to recognize "red flags" and conduct actions before the arrival of an ambulance.

Table 13. Preventive measures

Sphere	Measures
House	Smoke detectors, evacuation plan, hot beverage monitoring
Production	Protective equipment, ventilation, training
Kitchen	Be careful with "long-hot" foods
Institutions	Training staff in threat recognition

Forecast

The prognosis is determined by the speed and accuracy of early action: timely provision of the airway and targeted correction of toxic effects significantly improve outcomes. [50]

The presence of inhalation injury in extensive skin burns increases mortality and complication rates; however, patients with limited laryngeal lesions and adequate support usually have a favorable outcome. [51]

In children with "thermal epiglottitis," the outcome is good with early airway management and observation, but delayed diagnosis is dangerous.[52]

Long-term consequences (dysphonia, stenosis) depend on the severity of the lesion and the quality of rehabilitation; reconstructive interventions and phoniatric therapy are used when necessary.

Table 14. Prognostic factors

Factor	Influence
Rapid airway management	Improves survivability
Area and depth of skin burns	Worsens the prognosis with increasing
Toxic effects (carbon monoxide, cyanides)	Worsens the outcome, requires antidotes
Age (children, elderly)	More pronounced edema, higher risk of obstruction

Frequently asked questions

Can I "expect" the swelling to go away on its own? No. Laryngeal swelling usually peaks within 24-48 hours. If there is stridor, drooling, or increasing shortness of breath, immediate medical attention is required. [53]

Do all victims need steroids and antibiotics "just in case"? No. Routine steroids and prophylactic antibiotics for inhalation trauma do not improve outcomes and are not recommended without specific indications. [54]

Do heparin and acetylcysteine inhalations help? The data are conflicting: there are reports of no clinical benefit and even an increase in pneumonia; the decision is made by the center's team according to local protocol, weighing the risks and benefits. [55]

When to refer to a burn center? For any suspected inhalation injury, facial burn, or large-area skin burns, or in children, early contact with a specialized center is preferable in accordance with current referral criteria. [56]