Acid burn: first aid and treatment

An acid burn is a chemical injury to the skin, eyes, or mucous membranes caused by contact with solutions of inorganic and organic acids. In everyday life, this most often occurs when using descaling agents, plumbing cleaners, and automotive chemicals, while in industrial settings, it occurs when working with sulfuric, hydrochloric, nitric, acetic, and hydrofluoric acids. Acids typically cause coagulative necrosis: proteins coagulate, forming a dense "scab," which partially limits the depth of further penetration of the substance. This distinguishes them from alkalis, which tend to destroy tissue more deeply. [1]

Despite their apparent "local" nature, acid burns can be insidious. Strong and concentrated solutions generate heat when diluted with water and, with prolonged contact, damage deeper layers. Hydrofluoric acid is an exception: it quickly penetrates tissue, binds calcium and magnesium, and can cause arrhythmias and systemic toxicity, requiring special antidote therapy with calcium salts. [2]

The basic principles of caring for chemical burns remain unchanged: immediate, copious irrigation with clean water, removal of contaminated clothing, and avoiding attempts to "neutralize" the acid with alkali. Water remains a universal and proven means of initial decontamination in most scenarios, with rare exceptions such as phenol and a number of specialized industrial solutions. Early irrigation reduces the depth of damage and decreases the risk of complications. [3]

Clinics focus on combined injuries: acid splashes in the eyes, inhalation of vapors with respiratory irritation, and accidental ingestion. Additional algorithms exist for each of these scenarios, but the cornerstone always remains early, prolonged, and proper decontamination and timely referral to specialists. [4]

Code according to ICD 10 and ICD 11

To code acid burns, the International Classification of Diseases, Tenth Revision, uses the T20-T28 "Burns and Corrosion" categories, where "corrosion" denotes a chemical burn. The choice of specific code depends on the body region and depth of the lesion, and the burn area is recorded using separate codes T31-T32, where T32 indicates corrosion, with the percentage of surface area assessed using the "rule of nines." If necessary, codes for external causes are added to describe the circumstances of the injury. [5]

In cases of severe systemic toxicity, codes from block T54 "Toxic effect of corrosive substances" are additionally used, including T54.2 "Toxic effect of corrosive acids and acid-like substances," with clarifications as appropriate. In the International Classification of Diseases, Eleventh Revision, chemical burns of the external integument are classified under the section "Burns of the external surface of the body, specified by location," while burns of the eye and internal organs are classified under a separate section, with the possibility of further detailing using expansion codes. [6]

Table 1. Examples of codes for acid burns

System	Code example	What is being encoded?	Comment
ICD 10	T23.601A	Corrosion of the hand and wrist, initial treatment	Localization and depth of damage. [7]
ICD 10	T32.11	Corrosion area of 10-19% of the body surface	Assessment of the affected area. [8]
ICD 10	T54.2	Toxic effect of corrosive acids	Complements local diagnosis in case of systemic toxicity. [9]
ICD 11	ND90-ND9Z	Burns of the external surface by localization	Selection by anatomical region. [10]
ICD 11	NE00-NE0Z	Burns of the eye and internal organs	Separate block for eyes and internal organs. [11]

Epidemiology

The proportion of chemical burns among all burn injuries varies by region and observation conditions. Surveys of industrial medicine and safety data indicate that approximately 10% of burns are associated with chemicals, including acids. The prevalence is higher in industries that use corrosive solutions, as well as in households where cleaning products are improperly stored and mixed. [12]

The severity of outcomes is determined not only by the reagent concentration but also by the time before the start of irrigation. In centers that standardize early decontamination at the prehospital stage, the proportion of deep lesions is lower and healing times are shorter. This emphasizes the importance of staff training and the availability of water sources and protective equipment. [13]

Acid eye burns are less common than alkaline burns, but they account for a significant proportion of severe chemical corneal injuries in both domestic and industrial settings. The visual prognosis is most dependent on the time before irrigation and the achievement of a neutral pH on the ocular surface. [14]

Hydrofluoric acid injuries are particularly common in the microengraving, glass, and chemical industries. Such cases may appear harmless in the first few hours, but are accompanied by a late increase in pain and systemic electrolyte disturbances, requiring vigilance and readiness for antidote therapy. [15]

Table 2. Epidemiological landmarks

Indicator	Grade	Practical conclusion
The share of chemical burns in the total number	Up to 10%	Prevention and education are critical.[16]
The deciding factor in the outcome	Time before the start of rinsing	Provide immediate irrigation with water. [17]
Acid eye burns	A significant proportion of severe injuries	Rinsing to neutral pH. [18]
Special risk	Hydrofluoric acid	Calcium salts and monitoring are needed. [19]

Reasons

The most common sources are sulfuric and hydrochloric acids in household and industrial cleaning products, nitric acid in pickling compounds, high concentrations of acetic acid in food and laboratory applications, and organic acids in specialized chemicals. Contact occurs through spills, spraying, splashes, improper mixing with other reagents, and unlabeled storage. [20]

Acid vapors and aerosols pose an additional hazard, especially in poorly ventilated areas and when heated. Inhalation of irritating vapors can cause burns to the upper respiratory tract, bronchospasm, and chemical tracheobronchitis, requiring a simultaneous assessment of respiratory function. Eye damage often accompanies skin splashes. [21]

Hydrofluoric acid is classified as a separate substance due to its dual mechanism: in addition to the destructive action of hydrogen ions, fluoride binds calcium and magnesium, penetrates deeply, and causes severe pain, late necrosis, and systemic cardiac arrhythmias. Contact is possible even through intact skin at high concentrations. [22]

Phenol and phenol-containing solutions are sometimes mistakenly classified as "acids" in everyday life, although they are a separate class. It's important to understand that the initial treatment of phenol is different: water is ineffective; low-molecular-weight polyethylene glycols or glycerin are preferred, followed by standard care. [23]

Table 3. Common agents and features

Agent	Where it is found	Risk characteristics	First steps
Sulfuric and hydrochloric acids	Household and industrial cleaning	Coagulation necrosis, risk of heat generation during dilution	Rinse immediately with water. [24]
Nitric acid	Metal etching	The burn may have a yellowish discoloration.	Water, eye and breathing protection. [25]
High concentration acetic acid	Food and laboratory sphere	Risk of vapors, eye burns	Water and ventilation. [26]
Hydrofluoric acid	Microengraving, glass industry	Deep penetration, systemic hypocalcemia	Water and calcium-containing antidotes. [27]
Phenol	Laboratories, production	Poor water washability	Polyethylene glycol or glycerin. [28]

Risk factors

The most common organizational factors are lack of personal protective equipment, poor ventilation, overfilling into unlabeled containers, and storage near food products. Such errors greatly increase the likelihood of skin and eye contact, as well as accidental ingestion. Safety planning reduces these risks. [29]

Individual risk factors include childhood and old age, as these groups have thinner skin and a more pronounced reaction to chemical agents. Other factors include underlying skin conditions, medications that thin the stratum corneum, and the length of time spent under contaminated clothing, which can contribute to the reaction. [30]

Lack of immediate access to water greatly increases the severity of the outcome. The longer the active acid remains on the surface, the deeper the coagulative necrosis develops. Therefore, it is advisable to install wash stations and train employees in first aid procedures at production facilities. [31]

Work with hydrofluoric acid requires particular caution: even a small area of damage can lead to systemic electrolyte imbalances and arrhythmias. Calcium gels and solutions, along with protocols for their use, should be readily available in such areas. [32]

Table 4. What increases the risk of severe disease

Factor	Why is it dangerous?	What to control
Working without protection	Direct contact, splashes	Gloves, glasses, screens. [33]
Poor ventilation	Aerosols and vapors	Local exhaust, ventilation. [34]
Delayed flushing	Deepening necrosis	Access to water and trained personnel. [35]
Contact with hydrofluoric acid	Systemic hypocalcemia	The presence of calcium-containing antidotes. [36]

Pathogenesis

Acids cause coagulative necrosis: proteins coagulate, forming a dense scab that partially limits diffusion into the depths. However, at high concentrations and prolonged contact, damage can reach the dermis and subcutaneous tissue. The release of heat during dilution intensifies the initial injury. [37]

Acid vapors and aerosols, settling on mucous membranes, initiate inflammation and swelling, causing pain, coughing, and bronchospasm. If exposure is significant, chemical tracheobronchitis and subsequent secondary infection may develop. Eye damage follows a similar pattern, but corneal tissue is more vulnerable. [38]

Hydrofluoric acid acts differently: the fluoride ion penetrates deep into tissue, binds calcium and magnesium, causing pain, necrosis, and can lead to life-threatening arrhythmias and seizures. Toxicity can increase after the initial decontamination is complete, so dynamic monitoring and electrolyte control are required. [39]

For phenolic lesions, lipophilicity and poor water solubility are key: the substance remains on the skin, penetrates quickly, and causes systemic toxicity. Therefore, the initial choice of solvent for rinsing differs from the standard aqueous regimen. [40]

Symptoms

Skin lesions typically experience burning, soreness, redness, and sometimes blisters and a moist surface. Color and appearance depend on the specific agent and concentration. With deep lesions, pain may be less due to the destruction of nerve endings, but the risk of scarring is higher. Often, the visible area does not reflect the true depth. [41]

Eye damage is accompanied by severe pain, photophobia, lacrimation, eyelid spasms, and corneal clouding. This condition requires immediate and prolonged irrigation until the surface pH returns to normal and an ophthalmologist's examination. The sooner irrigation is initiated, the better the visual prognosis. [42]

Inhalation of vapors may cause irritation, coughing, wheezing, shortness of breath, and a feeling of shortness of breath. Symptoms may worsen over several hours. Respiratory function should be assessed and lower respiratory tract infection should be ruled out. [43]

Contact with hydrofluoric acid may be accompanied by increasing pain, muscle cramps, a mottled sensation on the skin, and dizziness. These are warning signs of possible hypocalcemia, requiring immediate administration of calcium-containing agents and monitoring of electrolytes and heart rate. [44]

Table 5. Symptoms by localization

Localization	Typical manifestations	Priority of actions
Leather	Burning, erythema, blisters	Water, bandage, pain relief. [45]
Eyes	Pain, photophobia, tears	Rinse to neutral pH and inspect. [46]
Respiratory tract	Cough, wheezing, shortness of breath	Respiratory assessment and support. [47]
Hydrofluoric acid	Severe pain, cramps, arrhythmia	Calcium-containing therapy. [48]

Classification, forms and stages

In practice, superficial, partial, and deep burns are classified based on clinical characteristics: color, moisture content, presence of blisters, pain sensitivity, and capillary refill rate. The chemical nature of the burn does not change the basic principles of depth assessment, but it does influence the risk of progression. The degree of depth determines the choice of dressings and the need for surgical intervention. [49]

Based on the time course of the disease, an early inflammatory phase is conventionally distinguished within the first 24 hours, a necrotic scab formation phase and secondary changes within 2-5 days, and a reparative phase after 7-10 days. Each stage has its own priorities: from decontamination and pain relief to infection prevention and assessment of the need for surgery. [50]

Eye lesions are classified separately according to clinical scales, where the outcome is most strongly influenced by the time to flushing and the degree of limbal damage. Acid eye lesions have a better prognosis on average than alkaline eye lesions, but at high concentrations the outcome can be severe. [51]

The affected area is recorded separately, since even a small area in critical areas - face, hands, perineum - changes the tactics of observation and treatment, including earlier involvement of specialized specialists. [52]

Table 6. Quick depth references

Sign	Superficial	Partial	Deep
Pain	Expressed	Strong	May decrease
View	Erythema, moist surface	Blisters, oozing	Pale gray dense crust
Capillary filling	Saved	Slowed down	Absent
Tactics	Home care and monitoring	Specialized dressings	Surgical evaluation
[53]

Complications and consequences

The main early complications are increased pain and swelling, wound infection, necrosis, and progression of wound depth in the first two days with inadequate decontamination. Even shallow lesions on the face and hands can cause significant functional and cosmetic discomfort. Eye lesions pose a risk of persistent vision loss. [54]

Medium-term sequelae include delayed epithelialization, formation of a coarse eschar, and the need for surgical debridement. At this stage, the risk of secondary bacterial colonization and pneumonia increases in cases of combined inhalation injuries. Care and pain management are key. [55]

Hypertrophic scarring, contractures, chronic sensitivity, and cosmetic defects are possible in the long term. Ocular lesions include persistent dryness, photophobia, and corneal clouding, especially if irrigation is delayed. Prevention involves early irrigation and proper dressing selection. [56]

Specific effects of exposure to hydrofluoric acid include hypocalcemia, hypomagnesemia, arrhythmias, and rare cases of cardiac arrest. Such patients require observation and laboratory monitoring, even if the affected area is small. [57]

When to see a doctor

Burns to the face, eyes, hands, or perineum, large areas, severe pain, blisters, oozing, and signs of deep crusting require immediate attention. Any eye injury is an emergency: irrigation should be started immediately and continued en route until an ophthalmologist can examine the burn. Delay worsens the prognosis. [58]

Seek medical attention if pain does not subside after prolonged rinsing, numbness in the area occurs, swelling and redness increase, or signs of infection appear. If vapor inhalation occurs—cough, wheezing, shortness of breath—respiratory assessment and observation are necessary. [59]

If contact with hydrofluoric acid is suspected, seek immediate medical attention, even if the lesion appears minor. Early application of a calcium-containing gel and medical observation, including monitoring of electrolytes and heart rate, are necessary. [60]

If you come into contact with phenol or if the chemical agent is unknown, it's also best to consult a specialist: some substances require special initial treatment with other solvents before switching to water. This reduces the depth and accelerates healing. [61]

Diagnostics

The first step is a clinical assessment of the severity and immediate decontamination: remove contaminated clothing, remove dry powder, and begin copious rinsing with clean water. At the same time, the contact time, type of substance, and concentration, if known, are recorded. This allows for the early selection of specific measures for individual agents. [62]

Vital signs and pain are then assessed. In case of ocular lesions, irrigation is continued until the pH of the conjunctival sac returns to approximately 7.0-7.2, with repeated checks. Once the condition stabilizes, the eyes are examined by an ophthalmologist, stained with fluorescein, and the extent of the lesion is assessed. [63]

For skin lesions of significant area and depth, basic laboratory tests are performed, the need for tetanus prophylaxis is assessed, and photo documentation is obtained for progress. In cases of contact with hydrofluoric acid, calcium, magnesium, and potassium levels are monitored, and an electrocardiogram is recorded for the early detection of arrhythmias. [64]

If vapor inhalation occurred, respiratory function is assessed, chest X-rays are performed as indicated, and symptoms of irritation and bronchospasm are monitored. If acid ingestion is suspected, early endoscopy in specialized settings within the first 24 hours helps assess the depth of damage to the esophagus and stomach. [65]

Table 7.

Step	Action	Target
1	Immediately begin rinsing with water	Reduce concentration and depth. [66]
2	Remove contaminated clothing and remove dry particles	Stop exposure. [67]
3	For eyes - rinse until pH is neutral	Preserve vision. [68]
4	Assess pain, vital signs, and take photographic documentation	Treatment plan and dynamics.
5	For hydrofluoric acid - electrolyte control and antidote	Prevention of arrhythmias. [69]

Differential diagnosis

Acid burns should be distinguished from thermal burns caused by boiling water and steam, which often present with typical blisters and a less pronounced crust. The chemical history, odor, specific coloration, and rapid response to rinsing with water help verify the chemical nature. When in doubt, rely on the circumstances and laboratory data. [70]

Skin irritation with phenol and other organic solvents can mimic acid injury, but differs in the initial treatment strategy. If phenol is suspected, polyethylene glycols or glycerin are preferred before switching to water. This accelerates removal of the substance and reduces the depth of penetration. [71]

Acid-induced eye injuries are differentiated from alkaline injuries. Acids, on average, cause less stromal damage due to protein coagulation, but the clinical situations overlap, and the tactics are the same: immediate irrigation to a neutral pH and prompt examination. The speed of irrigation, rather than the agent, is more important. [72]

In respiratory tract lesions, chemical irritation is differentiated from infections and exacerbations of bronchial hyperreactivity. The association with vapor exposure, chemical odor, and dynamics after evacuation and lavage support the diagnosis of chemical injury. [73]

Treatment

The mainstay of treatment remains immediate and prolonged irrigation with clean, cool water. For the skin, most guidelines recommend irrigation for at least 20-30 minutes, and longer if irritation is persistent. For the eyes, irrigation is continued until the pH of the conjunctival sac returns to normal, and the test is repeated after a few minutes, as acid may be released from the fornices. The sooner irrigation is started, the shallower the depth and the better the outcome. [74]

Attempts to "neutralize" acid with alkali at home are not recommended due to heat generation and the risk of further damage. The best neutralizer remains a large volume of water. In industrial settings, amphoteric solutions are sometimes used for emergency flushing; however, if these are unavailable, time must be wasted and water must be used first. After initial irrigation, switching to a specialized solution is possible according to local protocol. [75]

Superficial skin lesions after decontamination are treated with a "moist healing" method: a thin layer of an inert ointment base and a non-adherent dressing, changed daily. This reduces pain and accelerates epithelialization. Prophylactic antibiotics are usually not required and may contribute to contact dermatitis. Tetanus prophylaxis is administered as indicated. [76]

Pain control is achieved through a stepwise approach: oral analgesics, cold compresses over the dressing, and gentle support. Harsh alcohol-based antiseptics, concentrated peroxides, and powdered dressings inhibit healing and are not recommended. Care should be gentle, emphasizing cleanliness, moisture, and the absence of friction. [77]

If contact with hydrofluoric acid is suspected, in addition to water, immediately apply a calcium-containing gel with calcium gluconate, gently rubbing it into the affected area and repeating the application until pain subsides. For severe pain or a large area, use injection or intra-arterial calcium administration techniques, and for inhalation exposure, inhalation of a calcium gluconate solution. Monitoring of calcium, magnesium, potassium, and cardiac electrical activity is essential. [78]

For phenol burns, initial treatment differs: contaminated clothing is removed, and the skin is repeatedly wiped or irrigated with low-molecular-weight polyethylene glycol or glycerin until the phenol odor disappears, then switched to water. This reduces the concentration of phenol on the surface and prevents deep necrosis. Further treatment is similar to that for conventional chemical burns. [79]

Eye lesions are treated by an ophthalmologist: after the pH level has returned to normal, topical antibiotics are prescribed to prevent infection, cycloplegics to reduce pain, and sometimes a short course of supervised steroid drops to limit the inflammatory response. The decision on additional treatments is made individually, taking into account the depth and extent of the damage. Observation is mandatory until the epithelium stabilizes. [80]

In cases of significant skin damage or depth, dense scab formation, and slow epithelialization, surgical debridement and early excision with skin grafting are considered. Current guidelines for burn wound care indicate that early surgery within the first one to two weeks after injury can shorten hospital stay and improve outcomes, but this decision is made on an individual basis. Dressing selection and frequency depend on the exudate and the area. [81]

Antibacterial therapy is indicated only if signs of infection are present. Concurrent treatment includes thrombosis prophylaxis, nutritional support, and rehabilitation. If respiratory tract lesions are present, humidification is provided, bronchodilators are administered as indicated, and gas exchange is monitored. In cases of acid ingestion, interventions are performed only in a specialized hospital with early endoscopy capabilities. [82]

Table 8. First aid: what to do and what to avoid

Step	Do	Do not do
Decontamination	Remove clothing, remove dry powder, rinse with water for a long time	Do not try to “neutralize” with household alkalis. [83]
Eyes	Rinse until the pH is neutral, then see an ophthalmologist.	Do not stop irrigation prematurely. [84]
Hydrofluoric acid	Apply calcium gluconate gel, monitor electrolytes	Do not use calcium chloride intradermally.[85]
Phenol	Use polyethylene glycol or glycerin, then water	Don't limit yourself to water from the start. [86]

Prevention

At home, store acids in their original, clearly labeled containers, out of the reach of children. Do not mix cleaning products. Wear gloves and safety glasses. Work in ventilated areas. Before starting, carefully read the manufacturer's instructions. Simple measures reduce the risk of contact and splashes. [87]

In production, personnel training, rapid decontamination procedures, availability of water sources and eyewash stations, personal protective equipment, and local protocols for special substances such as hydrofluoric acid are essential. Regular training and audits help maintain readiness. [88]

For the eyes, it's important to get into the habit of rinsing immediately when in doubt and know the location of the nearest irrigation station. It's important to be able to monitor the surface pH and continue irrigation until it returns to normal. This significantly improves visual outlook. [89]

When working with phenol, have polyethylene glycol or glycerin nearby, and when working with hydrofluoric acid, have calcium-containing gels and clear instructions for their use. These are critical details that change the outcome. [90]

Forecast

Most superficial acid burns heal within 1-3 weeks without significant scarring with early and prolonged irrigation. The key determinant of outcome is the time to initiation of irrigation. The sooner irrigation is initiated, the lower the risk of deep crusting and subsequent surgery. [91]

Acid burns to the eye have a better prognosis than alkali burns, but with high concentrations and delayed irrigation, the outcome can be serious. The duration of observation is determined by the extent of corneal damage and limbal involvement. [92]

In cases of hydrofluoric acid, the prognosis depends on early application of calcium gluconate gel and electrolyte correction. Even small lesions require monitoring due to the risk of late arrhythmias. [93]

Factors for poor outcome include delayed decontamination, large area and depth, involvement of critical areas, and concomitant ocular or respiratory involvement. In these scenarios, early referral to a specialized center is desirable.[94]

Frequently Asked Questions

How long should you rinse your skin with water after contact with acid?
A guideline is at least 20-30 minutes of continuous irrigation, and longer if the burning sensation persists. The sooner and longer the rinsing, the better the outcome. [95]

Can you "quench" acid with baking soda?
No. Neutralization at home is dangerous due to heat generation and delays rinsing. The standard is large volumes of water. [96]

What to do if it gets into your eyes?
Immediately begin rinsing and continue until the pH of the eye surface is neutral, then consult an ophthalmologist immediately. Time is critical. [97]

What's special about hydrofluoric acid?
It penetrates deeply and binds calcium and magnesium, which can lead to arrhythmias. In addition to water, calcium-containing therapy and electrolyte monitoring are required. [98]

Are there any exceptions to the "water only" rule for primary processing?
Yes. For phenol, polyethylene glycols or glycerin are preferred, followed by water. Otherwise, water remains the standard. [99]

Table 9. Brief checklist

Situation	First steps	Key feature
Skin and clothing are contaminated with acid	Remove clothing, remove dry particles, rinse with water	Do not neutralize with household products. [100]
Acid got into my eyes	Rinse until pH is neutral, consult an ophthalmologist.	The time before irrigation begins determines the outcome. [101]
Suspected hydrofluoric acid	Water plus calcium gluconate gel, monitoring	Control of calcium, magnesium, potassium and rhythm. [102]
Unclear agent, possibly phenol	Polyethylene glycol or glycerin, then water	Special primary decontamination. [103]