bubble_chart Overview

In our daily life, military research, and industrial and agricultural production, there are over 25,000 chemical substances that can cause harm to the human body. Due to the rapid development of modern industry, the incidence of chemical burns has also gradually increased.

bubble_chart Pathogenesis

The Mechanism of Chemical Burns　When chemicals come into contact with the human body, they can cause both local and systemic damage. The extent of the damage depends on factors such as the nature of the chemical, dose, concentration, duration and area of contact, and whether treatment is timely and effective.

1. Local Damage

Chemicals can cause local tissue damage through oxidation, reduction, corrosion, protoplasmic poisoning, dehydration, and blistering effects. These effects are determined by the nature of the chemical. A single chemical may exhibit several of these effects simultaneously. Some chemicals cause burns due to their own combustion, such as phosphorus burns. Others may not harm healthy skin initially, but once ignited, they cause skin burns, allowing the chemical to be absorbed through the wound and trigger toxic reactions.

In general, acid burns cause tissue protein coagulation, forming a scab that can prevent further damage. Alkali burns lead to fat saponification and produce soluble alkaline proteins, resulting in ongoing damage to the local wound. Phosphorus burns form phosphoric acid, which continues to damage tissues.

2. Systemic Damage

Chemical agents can be absorbed through normal skin, wounds, the respiratory tract, or the digestive tract, leading to poisoning and damage to internal organs. The mortality rate of chemical burns is significantly higher than that of general burns, primarily due to poisoning and complications caused by chemical toxins. Since most chemicals are excreted by the liver and kidneys, liver and kidney damage are more common. Typical conditions include toxic hepatitis, acute liver necrosis, acute renal failure, and tubular nephritis. Certain chemical vapors directly irritate the respiratory tract, causing injury. Many volatile substances are expelled through the respiratory tract and also irritate the alveoli and airways, leading to pulmonary edema and inhalation injury. Some chemicals can suppress bone marrow function, destroy red blood cells, and cause anemia or hemolysis. Others may induce toxic encephalopathy, cerebral edema, nerve damage, gastrointestinal ulcers, and bleeding.

bubble_chart Clinical Manifestations

1. Acid Burns

Common types include sulfuric acid, hydrochloric acid, and nitric acid burns. Others include hydrofluoric acid, carbolic acid, and oxalic acid. Their characteristic effect is tissue dehydration and protein precipitation or coagulation, leading to rapid eschar formation with clear boundaries, which limits further deep tissue erosion.

① Sulfuric acid, hydrochloric acid, and nitric acid burns: These are the most frequent, accounting for 80.6% of acid burns. Sulfuric acid burns appear black or dark brown; hydrochloric acid burns are yellow; nitric acid burns are tan or brown. The color also correlates with burn depth: bright red indicates superficial burns, while gray, tan, or black suggest deeper injury. Due to eschar formation, early depth assessment is more challenging than with typical burns. The absence of blisters does not necessarily indicate a superficial burn.

Liquid sulfuric, hydrochloric, or nitric acid can cause skin burns, while their vapors may lead to inhalation injuries. Among the three, liquid sulfuric acid is the most corrosive at the same concentration, while gaseous nitric acid is the most harmful. Inhalation of nitric acid vapor can cause pulmonary edema within hours. Ingestion of these acids may result in upper digestive tract burns, laryngeal edema, respiratory distress, or even ulcer perforation.

Management follows general principles for chemical burns. After rinsing, neutralize residual hydrogen ions with 5% sodium bicarbonate solution, magnesium oxide, or soapy water, followed by further rinsing. Expose the wound for treatment. For confirmed third-degree burns, perform escharectomy and skin grafting as needed. Inhalation injuries require standard care. After ingesting strong acids, administer milk, egg whites, aluminum hydroxide gel, soy milk, or magnesium hydroxide orally. Avoid gastric lavage or emetics, and never use sodium bicarbonate, as it may cause gastric perforation. Oral prednisone may reduce fibrotic complications.

② Hydrofluoric acid burns: Hydrofluoric acid is an aqueous solution of hydrogen fluoride, colorless and highly corrosive, with fat-dissolving and decalcifying properties. Initial burns may show only erythema or leathery eschar, but necrosis soon spreads laterally and deeply, potentially damaging bones and causing persistent ulcers with severe pain. Even 10% hydrofluoric acid can cause significant injury, while 40% solutions penetrate skin more slowly.

Immediate and thorough rinsing with copious flowing water for at least 30 minutes (some recommend 1–3 hours) is critical. After rinsing, apply magnesium oxide-glycerin (1:2) ointment or soak in saturated calcium chloride or 25% magnesium sulfate to precipitate residual hydrofluoric acid as calcium or magnesium fluoride. Avoid ammonia, which forms corrosive ammonium bifluoride. For severe pain, infiltrate the wound periphery with 5–10% calcium gluconate (0.5ml/cm²) mixed with 1% procaine to limit progressive damage. Beijing Jishuitan Hospital developed a topical cream applied every 2–4 hours (with optional bandaging until pain resolves), showing excellent results. Hayashi reported corticosteroids may also help. Remove blisters and excise fingernails/toenails if subungual burns occur. Early escharectomy and grafting are needed for third-degree burns.

③ Carbolic acid burns: Carbolic acid primarily damages kidneys after absorption. Its strong corrosion and penetration cause progressive tissue injury. Emergency care involves copious cold-water rinsing followed by 70% alcohol rinsing or bandaging. Deep burns require early eschar excision or debridement.

④ Oxalic acid burns: Contact with skin or mucous membranes forms stubborn white ulcers. Oxalic acid binds calcium, lowering serum levels. While rinsing extensively with water, administer calcium locally and systemically.

2. Alkali Burns

Clinically common alkali burns include caustic alkalis, lime, and ammonia, with a higher incidence rate than acid burns. The characteristic of alkali burns is their combination with tissue proteins to form alkaline protein compounds, which are easily soluble, further deepening the wound; saponifying fatty tissues; causing cell dehydration and death, and generating heat to exacerbate the injury. Therefore, the injury caused by alkali burns is more severe than that by acid burns. ①Caustic alkali burns: Caustic alkalis refer to sodium hydroxide and potassium hydroxide, which are highly corrosive and irritating. After such burns, the wound appears as a sticky or soap-like eschar with a reddish color, generally deeper, usually above deep II degree, accompanied by intense pain. After the necrotic tissue falls off, the wound becomes depressed with undermined edges, often persisting for a long time without healing.

The key to treatment lies in early and prompt rinsing with flowing cold water for an extended period. Some advocate rinsing for 24 hours and discourage the use of neutralizing agents. Deep wounds should also undergo early escharotomy. After ingesting caustic alkalis, gastric lavage and induced vomiting are contraindicated to prevent gastric and esophageal perforation. Small doses of olive oil, 5% acetic acid, edible vinegar, or lemon juice can be administered orally. For necrotic tissue that naturally sloughs off and forms granulation wounds, applying a 1% citric acid solution as a wet compress for 24 hours can lower the pH and improve skin graft survival rates.

② Lime burns: Quicklime (calcium oxide) reacts with water to form calcium hydroxide (slaked lime), releasing a significant amount of heat. Lime burns typically present as dry, brownish, and relatively deep wounds. Before rinsing with water, ensure all lime powder is wiped away to avoid additional heat generation that could worsen the injury.

③ Ammonia burns: Ammonia solution is highly volatile and releases ammonia, which is irritating. Inhalation can lead to laryngeal spasms, laryngeal edema, pulmonary edema, and other inhalation injuries. Superficial ammonia burns may exhibit blisters, while deeper burns appear dry and black, resembling leather-like eschar.

The wound management for these burns follows the same principles as general alkali burns. For cases involving inhalation injuries, treatment should adhere to the guidelines for inhalation injuries.

3. Phosphorus burns with poisoning

Phosphorus burns rank third among chemical burns, following acid and alkali burns. In addition to burns caused by phosphorus igniting in air, phosphorus oxidation generates phosphorus pentoxide, which dehydrates cells and deprives them of oxygen. Phosphorus pentoxide reacts with water to form phosphoric acid, releasing heat in the process and further deepening the wound. Inhalation of phosphorus vapor can cause inhalation injuries, while phosphorus and its compounds absorbed through wounds and mucous membranes can lead to phosphorus poisoning.

Phosphorus is a protoplasmic toxin that inhibits cellular oxidation processes. After absorption, it accumulates in the liver and kidneys, causing widespread damage to these organs. Patients with phosphorus burns primarily exhibit symptoms such as headache, dizziness, weakness, and nausea. Severe cases may involve liver and kidney dysfunction, hepatomegaly, liver pain, jaundice, oliguria or anuria, and proteinuria with casts. Inhalation injuries and phosphorus poisoning can cause rapid breathing, irritating cough, dry or wet rales in the lungs, and, in severe cases, pulmonary dysfunction and ARDS. Chest X-rays may reveal interstitial pulmonary edema or bronchopneumonia. Some patients may also experience hypocalcemia, hyperphosphatemia, arrhythmias, psychiatric symptoms, or cerebral edema. Phosphorus burns are often deep, potentially affecting bones, and present as brownish wounds. Third-degree burns may appear bronze or black when exposed.

After a phosphorus burn, immediately extinguish flames and remove contaminated clothing. Rinse the wound extensively with water or immerse it in water. Carefully remove phosphorus particles from the wound to prevent contact with air. If large amounts of water are unavailable, cover the wound with a wet cloth. To avoid inhalation injuries, both the patient and rescuers should cover their noses and mouths with wet handkerchiefs or masks. Upon hospital admission, rinse the wound with 1% copper sulfate to form black copper phosphide, facilitating removal, and then rinse again with water or immerse in water. Monitor the amount of copper sulfate used to ensure no white smoke is produced from the wound. Residual copper phosphide should be meticulously removed with forceps, followed by rinsing with water and applying a 5% sodium bicarbonate solution as a wet compress to neutralize phosphoric acid. After 4–6 hours, switch to a dressing, avoiding oily materials. Deep wounds should undergo early escharotomy and skin grafting. Regardless of burn size, protecting internal organ function is crucial. Provide a high-carbohydrate, high-calorie, high-protein diet, administer early fluid therapy with slightly increased volume, and promptly administer alkaline agents, diuretics, and energy-protective agents. Early calcium supplementation can prevent phosphorus poisoning. For patients already poisoned, calcium alleviates symptoms, promotes phosphorus excretion, and aids in the recovery of affected organs.

4. Cyanide burns and associated poisoning

Cyanides can be divided into inorganic cyanides and organic cyanides based on their chemical structure, with the latter also referred to as nitrile compounds. After cyanides enter the body, cyanide ions rapidly bind to the trivalent iron of oxidized cytochrome oxidase, preventing the reduction of cytochrome to the reduced form of cytochrome oxidase containing divalent iron. This deprives cells of sufficient oxygen, leading to "intracellular asphyxia." In cases of acute poisoning, the arteriovenous oxygen difference can drop from the normal 4-5% to 1%-1.5%, which easily causes respiratory center paralysis and results in death.

The main clinical manifestations of cyanide poisoning include lack of strength, chest pain, chest tightness, dizziness, tinnitus, difficulty breathing, arrhythmia, constricted or dilated pupils, paroxysmal or tonic spasm, unconsciousness, and ultimately respiratory and cardiac arrest leading to death.

The treatment involves administering amyl nitrite and sodium nitrite as early as possible. At the scene or during transport, the patient can inhale 0.2–0.4 ml of amyl nitrite every 15–30 seconds to a few minutes, not exceeding 5–6 doses, until intravenous sodium nitrite is administered. A 30% sodium nitrite solution (10–20 ml, 6–12 mg/kg) should be injected intravenously at a rate of 2–3 ml/min, followed by 50 ml of 25% sodium thiosulfate through the same needle. If necessary, repeat the injection after one hour. The injection speed should not be too fast to avoid causing hypotension. For local wounds, rinse thoroughly with running water first, then wash with 0.01% potassium permanganate, followed by 5% sodium thiosulfate. It should be noted that sodium nitrite and sodium thiosulfate have no detoxifying effect on organic cyanide poisoning, and sodium nitrite itself can be harmful to the body.

5. Asphalt Burns

Asphalt, commonly known as tar, has strong adhesive properties and is widely used in construction, engineering for corrosion and moisture resistance, and road paving. Liquid asphalt causes skin burns purely due to thermal effects, without chemical injury. Its characteristics include difficulty in removal, high heat retention, and slow heat dissipation, often resulting in deeper burns, mostly occurring on exposed skin areas such as hands, feet, and face.

For large-area asphalt burns, avoid scrubbing with gasoline to prevent acute lead poisoning. Immediately after an asphalt burn, cool the affected area in cold water, then use olive oil or sesame oil to remove the asphalt from the wound. Alternatively, knotty pine wood oil can be used for wiping, but it is irritating and thus more suitable for small to medium-sized wounds.

Asphalt evaporation produces small amounts of photosensitive substances such as acridine, anthracene, and phenanthrene, which increase pain upon light exposure. Therefore, patients should avoid sunlight and photosensitizing drugs such as sulfonamides, chlorpromazine, and promethazine. Avoid using merbromin or gentian violet on the wounds.

bubble_chart Treatment Measures

First aid treatment for chemical burns

1. Quickly remove the contaminant and immediately rinse with flowing cold water for 20-30 minutes or more. Sometimes, the chemical substance on the wound surface (such as dry lime powder) should be wiped off first before rinsing with water to avoid generating excessive heat upon contact with water, which could cause further damage to the wound. After rinsing, a neutralizing agent can be applied, but the neutralization time should not be too long. Rinse again with flowing water shortly afterward.

2. Promptly determine whether chemical poisoning is present and treat it according to the appropriate principles. If a detoxifying agent or the specific toxic substance cannot be identified immediately, administer a large amount of hypertonic glucose and vitamin C intravenously, provide oxygen, and transfuse fresh blood, among other measures. If there are no contraindications, apply diuretics early, and then select a detoxifying agent based on the situation.

3. Treat burn toxins using standard burn treatment methods, including shock resuscitation and wound management. Early excision of third-degree eschar and removal of necrotic tissue from deep second-degree wounds can help cut off the source of toxins.

4. Address any complications or concurrent conditions promptly, and consult relevant departments for diagnosis and treatment if necessary.