Throat burns: first aid and treatment

A pharyngeal burn is damage to the mucous membrane of the oropharynx and nasopharynx caused by chemically corrosive substances (acids, alkalis, oxidizing agents) or thermal factors (hot food/liquid, steam, fire). The damage may be limited to the oral cavity and pharynx or extend more distally to the larynx, esophagus, and stomach. Early assessment of the airway and the extent of the damage is critical, as laryngeal edema can worsen over the course of hours. [1]

Chemical burns are most often associated with household cleaning products based on hypochlorite, alkalis (e.g., sodium hydroxide), acids (hydrochloric, sulfuric, acetic acid), and industrial reagents. Alkalis cause liquefactive necrosis with deep penetration, while acids cause coagulative necrosis and eschar, sometimes limiting depth. Thermal burns of the pharynx in adults are less common, but severe cases with life-threatening laryngeal edema have been described after swallowing very hot food/drinks. [2]

First-line management today includes: airway control if obstruction is a concern; avoidance of emesis induction and "neutralization"; early endoscopy if significant ingestion has occurred; selective use of computed tomography to search for transmural necrosis and perforation; symptomatic therapy, nutritional support, and stricture prophylaxis when indicated. [3]

Code according to ICD-10 and ICD-11

In ICD-10, a thermal burn of the oropharynx is coded as T28.0 "Burn of the mouth and pharynx"; a chemical burn (corrosion) is coded as T28.5 "Corrosion of the mouth and pharynx." For clarification, the external cause is indicated (X codes, Y92 - site). If the esophagus is involved, there are separate entries T28.1 (burn of the esophagus) and T28.6 (corrosion of the esophagus). [4]

In ICD-11, internal burns are coded in the NE00-NE0Z block "Burns of the Eye and Internal Organs," with mandatory post-coordination of the anatomical location (mouth, pharynx) and the external cause. This improves the accuracy of statistics, routing, and payment. Detailed codes are selected from the ICD-11 electronic tool (browse11) with the addition of anatomical extensions. [5]

Table 1. Codes (ICD-10/ICD-11) for burns of the pharynx

Situation	ICD-10	Notes	ICD-11 (principle)
Thermal burn of the mouth/pharynx	T28.0 (±7th character XXA/XXD/XXS)	Add external cause (X00-X19, Y92). [6]	NE0* “Burns of internal organs” + post-coordination of place (mouth/pharynx) and cause. [7]
Chemical burn (corrosion) of the mouth/pharynx	T28.5 (± 7th character)	For the esophagus - T28.6. [8]	Similarly: code NE0* + anatomy + external cause. [9]

Epidemiology

Acid-base ingestion is less common than other poisonings but carries a high risk of complications. In a large French database from 2010 to 2019, the proportion of adults admitted with caustic ingestion was approximately 0.016% of all emergency hospitalizations; complications occurred in 34% of patients, surgery for necrosis was required in 11%, and the in-hospital mortality rate was 8%. [10]

According to global surveys, approximately 68% of cases occur in children and are typically accidental; the proportion of adults with intentional (suicidal) intoxications is higher, and their severity is greater. Alkalis and household cleaning products are prevalent in the pediatric population; in adults, industrial acids are often the cause. [11]

Poison control center data indicate that most calls for chemical exposure occur at home; unintentional exposures predominate among young children. Although aggregated reports include a wide range of toxicological incidents, they reflect a general risk pattern for household corrosives. [12]

Table 2. Epidemiological landmarks

Indicator	Value/Range	Source
Proportion of adult hospitalizations with caustics	≈0.016% of all emergency receipts	[13]
Complications in adults	≈34%	[14]
Operations for necrosis	≈11%	[15]
Hospital mortality	≈8%	[16]
Proportion of children among all cases	≈68% (world samples)	[17]

Reasons

Chemical burns are caused by acids (hydrochloric, sulfuric, and acetic acid), alkalis (sodium and potassium hydroxide), and oxidizing agents (permanganate and hypochlorite). Alkalis produce deep liquefactive necrosis with the risk of perforation; acids produce coagulative necrosis with eschar. In industry, the risk is associated with high concentrations and volumes; in everyday life, it is associated with the availability of products and improper sealing. [18]

Thermal burns of the pharynx occur when swallowing extremely hot foods/drinks or inhaling hot steam/smoke. Severe cases of "thermal epiglottitis" with rapid development of respiratory failure requiring early airway management have been described. [19]

Risk factors

The severity of injury is determined by the concentration of the substance, the volume, and the time of contact. Intentional ingestion in adults is associated with higher doses and a worse prognosis. Concomitant medical conditions, late presentation, and lack of specialized care increase the risk of complications and mortality. [20]

For the thermal variant, the key risk is laryngeal edema in the first few hours; in children, due to their anatomy, the airways decompensate more quickly. With chemical damage to the airways and aspiration, a mixed picture of "chemical" and "thermal" damage develops. [21]

Table 3. Factors of severe course

Factor	Why is it dangerous?
Large volume, high concentration	Deep necrosis, perforations, strictures. [22]
Intentional ingestion	Often large doses, combined lesions. [23]
Delay in appeal	Missed window of early endoscopy and airway protection. [24]
The airways are involved (laryngeal burn)	Risk of rapid obstruction. [25]

Pathogenesis

Alkalis saponify fats and dissolve proteins, leading to liquefaction necrosis and deep penetration of damage through the submucosa. Acids form coagulative necrosis with an eschar, which partially limits the depth but does not exclude perforation and late strictures. Spread to the esophagus and stomach depends on the volume and duration of contact. [26]

Thermal trauma to the mucosa triggers an inflammatory cascade, swelling, and barrier dysfunction, which in the larynx can quickly lead to critical narrowing of the lumen. With massive ingestion of hot liquids, the esophagus and stomach are also affected. [27]

Symptoms

Chemical burns are characterized by intense pain in the mouth and throat, hypersalivation, dysphagia, and often vomiting and blood. Signs of severity include progressive shortness of breath, hoarseness, stridor, hematemesis, severe chest or abdominal pain, and signs of perforation. The absence of visible lesions in the oral cavity does not exclude deep esophageal/stomach damage. [28]

Thermal burns of the pharynx cause pain, a scratchy sensation, and dysphagia; with damage to the epiglottis, rapidly increasing shortness of breath and the risk of obstruction. Any respiratory symptoms warrant immediate evaluation of the airways. [29]

Table 4. Red Flags

Sign	What does it involve?
Stridor, progressive hoarseness	Laryngeal edema → risk of obstruction. [30]
Cutting pain behind the breastbone/abdomen, free gas	Perforation. [31]
Hematemesis, severe dysphagia	Deep lesions, possible necrosis. [32]

Classification, forms and stages

The Zargar classification is used to assess the severity of esophageal and gastric lesions based on endoscopy data: from 0 (normal) to 3B (extensive necrosis) and 4 (perforation). The risk of strictures increases sharply at grades 2B-3. There is no formal "score" for the oropharyngeal mucosa; it is practical to divide lesions into superficial (erythema/edema), moderate (vesicles/fibrin), and severe (necrosis, black eschar) - with a key emphasis on airway patency. [33]

Thermal burns of the oropharynx are often superficial and self-limiting, however, if the epiglottis is affected, a rapid transition to critical stenosis is possible - this is a separate clinical form requiring an “airway first” tactic. [34]

Table 5. Classification (simplified)

Segment	Light	Moderate	Heavy
Mouth/pharynx	Erythema, pain	Plaques/blisters	Necrosis, scab, deep defects
Esophagus (according to Zargar)	1	2A/2B	3A/3B, 4 (perforation) [35]

Complications and consequences

Early: laryngeal edema with airway obstruction, esophageal/gastric perforation, mediastinitis, peritonitis, aspiration. Late: cicatricial strictures of the pharynx and esophagus, dysphagia, reflux, nutritional deficiency. In adults, serious complications after severe swallowing occur in a third of patients, and the mortality rate reaches 8% in large series. [36]

Strictures develop predominantly in Zargar grades 2B-3; the risk is higher with alkalis and intentional ingestion. Oromaxillofacial scarring deformities and voice disorders are possible if the larynx is involved. [37]

When to see a doctor

Immediately - for any respiratory symptoms (hoarseness, stridor, shortness of breath), ingestion of highly corrosive substances, severe chest/abdominal pain, bloody vomiting, inability to swallow saliva, in children - at any suspicion of ingestion of caustics. Contacting a poison control center/poison control point is also recommended. [38]

Even with “mild” symptoms, evaluation by a specialist is essential: the severity of esophageal/gastric damage cannot be reliably predicted based on the condition of the oral cavity alone. [39]

Diagnostics

Step 1. Initial ABCDE assessment. Check the airway; if signs of a threat are present, perform early intubation by an experienced team. Do not induce vomiting; do not "neutralize" at home. [40]

Step 2. Laryngoscopy/fibroendoscopy of the ENT organs, if indicated. This is necessary to assess swelling of the epiglottis and larynx if there are vocal/respiratory symptoms. In severe cases, first ensure the airway. [41]

Step 3. Esophagogastroduodenoscopy. In cases of significant ingestion, this should be performed within the first 12-24 hours (possibly up to 48-96 hours in some centers). From the 5th to the 15th day, endoscopy is generally not recommended due to tissue fragility. The endoscopist performs a careful assessment and grades the lesions according to Zargar. [42]

Step 4. Computed tomography of the chest and abdomen. This helps identify transmural necrosis, perforation, and mediastinitis when endoscopy is potentially hazardous or the results are questionable; in some algorithms, CT is performed within the first 24 hours, parallel to endoscopy. [43]

Step 5. Laboratory and monitoring. Complete blood count, electrolytes, blood gases, inflammatory markers; in case of poisoning with specific reagents, a profile according to chemical incident protocols. [44]

Table 6. When to do what

Situation	Action/Exploration	Window
Respiratory tract threat	Intubation	Immediately. [45]
Significant ingestion	Endoscopy	12-24 hours (up to 48-96 hours in the center). [46]
Suspected perforation/necrosis	CT scan of the chest and abdomen	Urgent. [47]
Period 5-15 days	Endoscopy	Usually avoided. [48]

Differential diagnosis

Thermal burns of the larynx differ from infectious epiglottitis by an acute thermal trigger and the absence of an infectious prodrome; however, management remains equally focused on airway patency. Hemorrhagic pain syndrome and perforations following bone/foreign body ingestion require different management. In cases of chest pain, acute coronary syndrome, spontaneous esophageal perforation, and drug-induced esophagitis are differentiated. Context, history, and imaging are important. [49]

Table 7. What is confused with what?

State	"For"	"Against"
Infectious epiglottitis	Fever, slower increase	No thermal/caustic factor
Foreign body	Local pain, feeling of being stuck	There is no chemical burn of the mucous membrane
Spontaneous perforation	Vomiting "to" pain, subcutaneous emphysema	No contact with caustic

Treatment

First, the airway. In cases of stridor, hoarseness, progressive dyspnea, and laryngeal burns, a low threshold for early intubation by an experienced specialist is necessary; "hot" differentiation from epiglottitis does not change the priority. Oxygen, monitoring, warming, analgesia, and antiemetics to prevent vomiting and repeated mucosal exposure to caustic sores are recommended. [50]

What not to do: Do not induce vomiting, do not administer activated charcoal (it is ineffective and interferes with endoscopy), do not perform blind nasogastric intubation in the prehospital setting, do not attempt to "neutralize" acid with alkali or vice versa, and do not force the patient to drink milk "to dilute" the acid. These actions do not improve outcomes and may worsen the injury. [51]

Endoscopic management. In cases of significant ingestion, endoscopy is performed in the first 12-24 hours to stratify the patient according to Zargar and determine nutritional management. Mild lesions (0-1 and part of 2A) are managed conservatively; for 2B-3, early nutritional support and closer monitoring are considered. Endoscopy is avoided during the "danger window" of days 5-15. [52]

The role of computed tomography. CT helps detect transmural necrosis and perforation and, according to current studies, complements endoscopy in severity stratification; in some algorithms, it is performed on all patients with severe clinical symptoms within the first 24 hours. The decision is individualized. [53]

Medication support. Pain relief, antiemetics, proton pump inhibitors for acid protection, antibiotics – as indicated (suspected perforation/mediastinitis). The effect of systemic glucocorticosteroids remains controversial: many reviews do not recommend routine use; some European guidelines allow a short course of high doses for grade 2B to reduce the risk of strictures, but not for grades 1, 2A, or 3. The decision is made by the specialized team. [54]

Barrier agents. Sucralfate as a "film former" has shown potential to reduce the risk of strictures in small studies (especially in children with 2B), but the evidence base is limited; use as part of combination therapy may be considered by a gastroenterologist/pediatrician. [55]

Nutrition. For mild lesions, early oral fluid intake is permitted after swallowing has been assessed. For 2B and higher lesions, enteral feeding is often initiated through a thin tube under control (after integrity assessment) or parenteral nutrition is given until stabilization. Vomition is actively managed. [56]

Surgery. Signs of perforation, mediastinitis, and wall necrosis are indications for emergency surgery. In late stages, strictures are treated with bougienage/balloon dilation, sometimes with adjuvants (for example, local mitomycin-C, according to individual studies), and in refractory strictures, reconstructive surgery is performed. [57]

Thermal burns of the pharynx. Most cases are treated conservatively with pain relief, cooling by drinking room-temperature water in small sips, a soft diet, and observation. If signs of laryngeal damage are present, priority is given to maintaining the airway, and sometimes short-term systemic steroids are given to reduce swelling for ENT indications (the evidence base is limited and the decision is individualized). [58]

Multidisciplinary and centralized. National series show better outcomes in centers with a high case volume; in cases of severe disease, transfer to experienced institutions is justified. [59]

Table 8. Treatment goals and monitoring

Target	What to track	Landmark
Respiratory tract	Voice, stridor, saturation	Early provision of patency. [60]
Pain/vomiting	Pain scales, vomiting episodes	Adequate pain relief, antiemetics. [61]
Risk of perforation	Pain, fever, CT signs	Low threshold for visualization/consultation. [62]

Prevention

Store cleaning products in their original child-resistant containers; do not transfer to food containers. Provide training, PPE, and labeling at the production facility. Keep reagents out of reach of children and provide safety training. [63]

In households and catering establishments, hot drinks and soups should not be served at temperatures that could cause mucous membrane burns; pauses should be observed after microwave heating. In case of fire, avoid inhaling hot smoke and steam. [64]

Forecast

The prognosis depends on the type of reagent, volume, time to treatment, and the level of the center. Adults with severe swallowing have a complication risk of up to 34% and a mortality rate of approximately 8%, according to large series; in children, most accidental episodes have a favorable outcome with early assessment and management. Late outcomes are determined by the presence of strictures and the quality of their endoscopic correction. [65]

FAQ

Is it possible to neutralize an acid with an alkali (or vice versa) at home? No. Neutralization can cause an exothermic reaction and worsen the burn; it is not recommended. Do not induce vomiting or give activated charcoal. [66]

When to perform endoscopy? In cases of significant ingestion, it is usually performed within the first 12-24 hours (in some centers, up to 48-96 hours). From the 5th to the 15th day, endoscopy is avoided due to tissue fragility. [67]

Are steroids necessary to prevent strictures? Routinely, no. Some guidelines allow a short course of high doses for grade 2B; other reviews show no convincing benefit. The decision is made by a multidisciplinary team. [68]

Does sucralfate help? There are small studies (including in children) showing a reduced risk of strictures in grade 2B cases, but the data are limited. This is discussed on a case-by-case basis. [69]

What should you do immediately if someone has swallowed the corrosive? Ensure safety and seek immediate medical attention; if breathing symptoms occur, call emergency services. Poison control centers are available for advice. Do not induce vomiting or "neutralize." [70]

Table 9. Thermal vs. chemical burn of the pharynx - key differences

Parameter	Thermal	Chemical
Trigger	Hot food/liquid, steam	Acids, alkalis, oxidizing agents
The main risk	Laryngeal edema, early obstruction	Deep necrosis, perforations, strictures
First line	Maintaining airway, symptomatic therapy	Airway, early endoscopy/CT, avoidance of "neutralization"
Further measures	Observation, soft diet	Nutritional support, prevention of strictures as indicated