bubble_chart Overview

The pharynx is the essential pathway for swallowing and breathing. Burns in the pharynx often involve the larynx simultaneously, and if they extend into the esophagus, esophageal burns occur. In addition to local symptoms, these injuries can lead to complex systemic pathological changes and toxic symptoms. Early diagnosis and prompt treatment are crucial.

bubble_chart Etiology

Throat burns can be classified into two categories: thermal burns and chemical burns. Most pharyngeal burns occur in children, primarily due to inadequate care, such as accidentally drinking boiling water or consuming overheated food. In adults, these burns are often caused by flames, high-temperature steam, or other hot liquids, and are usually accompanied by severe burns to the head, face, and neck. Chemical burns are typically caused by accidental ingestion of corrosive substances such as strong acids, strong alkalis, heavy metal salts, ammonia, etc., and often involve burns to the mouth and esophagus. When mucous membranes come into contact with alkaline corrosive agents, fats are saponified and proteins dissolve, leading to tissue liquefaction and necrosis, with lesions that penetrate deeply and tend to spread to deeper layers. Upon contact with acidic corrosive agents, the primary pathological changes include water absorption and protein coagulation, resulting in localized tissue coagulative necrosis. The penetration ability is slightly weaker, but high concentrations can still cause severe injury.

bubble_chart Pathological Changes

The extent of injury to the throat tissue depends on the temperature (degree of heat) and the nature of the corrosive agent, the amount ingested, and the duration of contact. The injurious agent tends to linger longer in the physiological narrow areas of the throat, resulting in more severe damage to the palatoglossal arch, uvula, lingual surface of the epiglottis, arytenoid cartilage and its folds, and the pharyngoesophageal junction. Throat burns are classified into three grades based on the severity of injury: **Grade I** burns are the most common, presenting as diffuse congestion of the pharyngeal mucosa, followed by edema. Cases involving the larynx are often more severe, but no scar formation occurs after healing. **Grade II** burns involve both the mucosal and muscular layers, with more pronounced mucosal edema. The mucosal surface is covered with necrotic pseudomembranes or scabs, which may appear white, yellow, or gray depending on the causative agent. **Grade III** burns are the most severe and are commonly seen in chemical burns (e.g., ammonia or caustic soda). Caustic soda burns can cause deep mucosal necrosis, prolonged inflammation, and necrotic pseudomembranes that may take 3–4 weeks to resolve. While mild cases may recover, **Grade III** burns often lead to scar tissue proliferation after scab detachment and necrotic tissue formation, resulting in various deformities.

bubble_chart Clinical Manifestations

The main symptoms after injury include oral and throat pain, swallowing pain, dysphagia, drooling, etc. Subsequently, symptoms such as high fever, salivation, cough, dysphonia, wheezing, or dyspnea may occur. Chemical injuries, due to the toxicity of the compounds, can cause lethargy, dehydration, high fever, shock, and even death. In children, it may be accompanied by difficulty sucking and dysphoria. Additionally, symptoms may include listlessness, drowsiness, poor appetite, elevated body temperature, and varying degrees of poisoning symptoms. Dyspnea is caused by laryngeal edema and the retention of secretions in the throat, blocking the respiratory tract, which is the main cause of death in throat burns. Dyspnea mostly occurs 5–10 hours after the injury, and close observation is required during this period. If dyspnea does not occur within 24 hours, the patient can be considered to have passed the critical period of respiratory distress.

Examination reveals blisters, erosions, or white membranes on the soft palate, uvula, posterior pharyngeal wall, and lingual surface of the epiglottis. Chemical burns have more typical manifestations; for example, ingestion of alkaline substances results in vomitus that is viscous, oily, and contains fragments of mucous membranes. Caustic alkalis act on tissues, dissolving and destroying proteins, forming gelatinous masses with soft, deep scabs that appear as turbid gray membranes. Nitric acid burns often produce yellow, brown, or dark-colored scabs, sulfuric acid burns result in black scabs, while vinegar acid and carbonic acid burns produce white scabs. Iodine, ammonia, and vinegar acid poisoning in seasonal disease patients often cause noticeable odors in exhaled breath.

Many toxins can cause damage to the kidneys, liver, central nervous system, and electrolyte imbalances, manifesting as reduced renal function, failure, bleeding tendencies, etc.

In severe cases of pharyngeal burns, the advanced stage may lead to scar stenosis and adhesions in the affected organs, resulting in respiratory and swallowing difficulties.

bubble_chart Diagnosis

The diagnosis is usually straightforward based on medical history, clinical presentation, and oral and pharyngeal examinations. Pediatric pharyngeal burns with an unclear seasonal disease history are prone to misdiagnosis and should be differentiated from pharyngeal contusion, diphtheria, laryngotracheal foreign bodies, and acute laryngeal obstruction. Respiratory burns have a high mortality rate, requiring early diagnosis, prompt treatment, and close monitoring for signs of respiratory distress. Residual toxic substances and containers from chemical burns should be preserved for examination. In some cases, testing vomitus, urine, or feces for toxins may be necessary to aid diagnosis. For cases involving esophageal burns, early diagnosis and treatment are essential to prevent esophageal scar stenosis or atresia.

bubble_chart Treatment Measures

Burns limited to the oral cavity and pharynx, classified as grade I, without secondary infection, will see the white membrane resolve on its own within 3 to 5 days, and the wound will heal. For grade II or III burns, or burns involving the laryngopharynx and larynx, corresponding rescue measures should be taken based on the specific circumstances, with close collaboration among relevant departments.

(1) Acute Phase Management

1. Neutralization Therapy For burns of the throat caused by strong acids or alkalis, if the patient seeks medical attention within 3 to 4 hours after the injury, neutralizers should be administered according to the type of poison ingested. For those who ingested strong alkalis, vinegar, orange juice, lemon juice, milk, or egg whites can be used for neutralization. For acids, aluminum hydroxide gel, soapy water, or dilute magnesium oxide emulsion can be used. However, avoid using baking soda or calcium carbonate for neutralization to prevent the carbon dioxide produced from causing rupture of the injured esophagus and stomach. For cases involving a large amount of ingested poison, gastric lavage may be cautiously performed, though many experts consider it contraindicated for acid or alkali corrosive injuries.

2. Management of Dyspnea Complications such as laryngeal edema and laryngeal obstruction can be life-threatening, so close attention should be paid to any signs of dyspnea to avoid delaying emergency treatment. For extensive grade III burns of the head, face, and neck, or cases with obvious respiratory tract burns, a tracheotomy should be performed before symptoms of respiratory obstruction appear. For burns within grade II and without signs of respiratory obstruction, temporary observation may suffice. The occurrence of dyspnea in throat burns follows a certain pattern. Reports indicate that the more severe the burn, the earlier dyspnea appears. Cases where dyspnea occurs within 12 hours of the burn, even if mild at the time of examination, are often progressive and should undergo early tracheotomy. Dyspnea occurring more than 12 hours after the burn is less likely to progress to a severe degree and can be closely monitored for the time being.

3. Antibiotic Use Broad-spectrum antibiotics in sufficient doses should be selected to prevent and control infection.

4. Use of Adrenocorticosteroids Corticosteroids have anti-shock effects, reduce edema, avoid the need for tracheotomy, and inhibit the growth of granulation and connective tissue, thereby reducing scar stenosis. Their drawback is the potential to cause esophageal perforation and spread infection. Corticosteroids should be used early in throat burns, in sufficient doses, and administered intravenously if oral intake is difficult.

5. Systemic Therapy Measures such as keeping warm, blood transfusion, fluid infusion to counteract shock, and correcting electrolyte imbalances should be taken. Sedatives, pain relievers, and vitamins should also be administered.

6. Local Treatment Maintain oral hygiene. The wound surface can be sprayed with bismuth subcarbonate or painted with gentian violet, or olive oil or paraffin oil can be swallowed to dry the wound, providing antiseptic, lubricating, and protective effects. Swallowing 15 ml of 1% procaine before meals can alleviate dysphagia, which is beneficial for increasing nutritional intake and improving overall condition.

(2) Management of Scar Stenosis Phase After the acute phase of 1 to 3 weeks post-injury, for cases with severe pharyngeal or esophageal injuries, antibiotics and corticosteroids should continue to be used. Atropine and dibazol may be administered to prevent spasms, or preventive dilation may be performed to avoid scar stenosis. Grade I scar stenosis can be treated with dilation. For cases where dilation is ineffective or for multiple, extensive stenoses or occlusions, surgical repair may be necessary.