Chemical burn injury refers to tissue damage caused by various chemical substances. A wide range of chemicals can cause burns, and treatment methods vary accordingly. This section briefly outlines general treatment principles and approaches for more common types of chemical burns.
General Treatment Principles
Contaminated clothing should be removed promptly, and the wound should be irrigated with copious amounts of water to remove or dilute residual chemicals, with rinsing lasting no less than 30 minutes. Priority should be given to rinsing if the cornea or other sensory organs are involved.
If conditions allow, neutralization or antagonistic treatment may be applied to prevent deeper tissue penetration and damage by the chemical. If no contraindications exist, surgical removal of necrotic and chemically contaminated tissue should be performed as early as possible to avoid further chemical invasion and systemic toxicity.
Many chemicals can be absorbed into the bloodstream through the wound, respiratory tract, or digestive tract, potentially causing systemic toxicity. Early administration of antidotes should be provided where applicable. For critically ill patients where the antidote is unavailable or the toxic agent is unidentified, supportive treatments such as intravenous hypertonic glucose and vitamin C, oxygen therapy, fluid resuscitation, transfusion of fresh blood, plasma exchange, blood purification, and diuretics may be used.
Other aspects of care should follow the protocols used for thermal burns.
Treatment of Common Chemical Burns
Acid Burns
Acid burns, including those caused by sulfuric acid, nitric acid, hydrochloric acid, and hydrofluoric acid, result in tissue dehydration, protein precipitation, and coagulation. Blisters typically do not form, and eschar develops rapidly. Sulfuric acid burns produce dark brown to black eschar, nitric acid burns yellow-brown eschar, and hydrochloric acid burns yellow eschar. In general, the deeper the acid burn, the darker and harder the eschar, with deeper indentations. However, the color of the eschar may obscure accurate early assessment of burn depth compared to thermal burns.
Superficial and deep second-degree acid burns often heal beneath the eschar. Deep burns exhibit delayed eschar separation and slow granulation tissue formation after eschar removal, which can result in more significant scarring than thermal burns. Wound care generally follows the principles for thermal burns.
Hydrofluoric acid burns cause not only the typical effects of acid burns but also dissolve fat and decalcify bone. Early skin signs may include erythema or charred eschar with severe pain, progressing to tissue necrosis and deep, spreading injury that may reach bone, resulting in wounds that are difficult to heal. After hydrofluoric acid burns, copious water irrigation or soaking is needed. If possible, immersion in saturated calcium chloride or 25% magnesium sulfate solution, or wet dressings or soaking with 10% ammonia solution may be applied. Repeated local injections of 10% calcium gluconate (0.5 ml/cm²) can help alleviate pain and limit progressive tissue damage. Blisters should be removed promptly, and fingernails or toenails should be extracted if subungual injury occurs. Early surgical debridement should be performed for deep burns.
Phenol (carbolic acid) burns are highly corrosive and penetrate tissues, with systemic absorption potentially causing kidney damage. Initial treatment involves copious water irrigation followed by dressing or irrigation with 70% alcohol to mitigate tissue damage. Early surgical excision of necrotic tissue is required for deep burns.
Alkali Burns
Common causes of alkali burns include sodium (or potassium) hydroxide, sodium bicarbonate, ammonia, lime, and calcium carbide. Strong alkalis cause dehydration of tissue cells and saponification of fats, with alkali ions binding to proteins and forming soluble compounds that penetrate deeper tissues. Without timely initial treatment, the wound may continue to enlarge and deepen, causing severe pain.
After strong alkali burns, early and prolonged irrigation with large amounts of water or tap water is essential, preferably for at least 30 minutes. If feasible, 2% boric acid compresses may be applied. Further treatment generally follows the protocols used for thermal burns.
Phosphorus Burns
Phosphorus burns result not only from direct contact of phosphorus on the skin, which ignites in air, but also from the formation of phosphorus pentoxide during combustion, which dehydrates and oxidizes cells. When phosphorus pentoxide contacts water, it generates phosphoric acid and heat, which further deepens the wound. Phosphorus and phosphorus compounds can be absorbed systemically from the wound, causing liver and kidney damage. Systemic symptoms depend on the severity of phosphorus poisoning and may include headache, dizziness, and fatigue. Wounds are typically deep, sometimes extending to muscle or bone, and may appear brown, bronze, or black. Burning phosphorus emits smoke with a garlic-like odor and blue-green fluorescence in the dark.
On-site treatment involves extinguishing flames, removing contaminated clothing, and thoroughly rinsing the wound and surrounding skin with copious water to eliminate visible phosphorus particles. In the absence of ample water, moist dressings can be used to isolate the wound from air and prevent ongoing combustion.
After hospital admission, continued irrigation with large volumes of water or soaking is indicated, followed by irrigation with 1%–2% copper sulfate solution. Copper sulfate binds phosphorus to form black copper phosphide, which does not burn and can be easily identified and removed with forceps. To minimize copper sulfate toxicity, 5% sodium bicarbonate solution or clean water should be used to rinse the wound after copper sulfate irrigation. Early eschar removal and skin grafting are needed for deep phosphorus burns.
There is currently no highly effective treatment for inorganic phosphorus poisoning. Prevention is key, along with supportive care to protect liver and kidney function. If poisoning occurs, intravenous administration of 50% glucose solution, large doses of vitamin C, and hepatoprotective agents may be given. Severe cases may require plasma exchange.