Nitrogen burn: help and treatment

Nitric acid is a highly corrosive oxidizing agent. Upon contact with skin, it causes coagulative necrosis; the characteristic symptom is a yellow-brown discoloration of the scab due to a xanthoprotein reaction with proteins. This is neither a thermal burn nor a "cold burn": the mechanism of injury is chemical, and the depth often increases in the first hours and days after exposure. Therefore, early and prolonged irrigation with water is key to reducing severity. [1]

Skin contact isn't the only hazard. Fuming nitric acid vapors contain nitrogen oxides (primarily nitrogen dioxide), which can cause respiratory irritation and delayed pulmonary edema, including acute respiratory distress syndrome (ARDS) 6-48 hours after exposure. Ingestion of concentrated nitric acid can cause burns to the mouth, pharynx, esophagus, and stomach, as well as bleeding and perforation. [2]

A common household mistake is attempting to "neutralize acid with baking soda." This can increase heat generation and injury. Current guidelines recommend rinsing affected areas with running water (or saline solution if water is unavailable) as early and as long as possible, followed by specialized treatment. Amphoteric rinsing solutions (such as diphoterine) are acceptable where available, but there is little evidence that they are superior to water for skin burns. [3]

Finally, to clarify the terminology: liquid nitrogen burns are freezing injuries (cryogenic, essentially "frostbite"), not chemical burns. Their first aid and treatment differ (e.g., controlled rewarming), and they are not accompanied by a yellow eschar from the xanthoprotein reaction. This article briefly mentions this variant for the sake of distinction, but the main focus is on nitric acid burns. [4]

Code according to ICD-10 and ICD-11

In ICD-10, chemical burns of the skin and mucous membranes are coded as "corrosions" by anatomical region and depth: block T20-T25 (for example, T23 for the hand, with a sixth degree symbol - from "first" to "third"). If a significant area is affected, codes T31-T32 are added for the percentage of the surface. For the toxic effect upon inhalation/ingestion, T54.2 is used - toxic effect of corrosive acids and acid-like substances; external causes - range X47 (other gases and vapors, including nitrogen oxides) and X49 (other and unspecified chemicals). [5]

In ICD-11, burns of the external integuments are coded in sections ND90-ND9Z (by location), while burns of the eyes and internal organs are coded in sections NE00-NE0Z. Harmful effects of substances, primarily non-drug ones, are coded as NE61 with post-coordination; the external cause is PE94 for intentional exposure to corrosive substances or the corresponding codes for the section on external causes in case of an accident. For burns of the esophagus/stomach after ingestion, the corresponding codes for burns of internal organs are used. [6]

Table 1. Coding examples

Clinical situation	ICD-10	Commentary (ICD-10)	ICD-11	Commentary (ICD-11)
Second-degree corrosion of the skin of the hand	T23.6-…	The side, episode, and degree are specified	ND95.Y	"Burnt/corrosion of the hand", post-coordination degree
Burn of the facial skin with nitric acid, area 12%	T20.x + T32.11	T32.11 - chemical corrosion 10-19%	ND91 + XS…	Post-coordination of area percentage and depth
Toxic action of corrosive acids (ingestion)	T54.2X1A	With indication of intention and episode	NE61 + XE…	"Harmful effects of corrosive substances", external cause
Inhalation of vapors with lung damage	X47 + additional codes for complications	External cause of exposure	NE61 (gases) + external cause	Nitrogen oxide vapors

Epidemiology

Chemical burns account for approximately 4% of all burn injuries, but their contribution to mortality can reach 30%, due to severe inhalation and esophageal injuries from concentrated substances. In industrial regions, some of these burns are caused by mineral acids, including sulfuric and nitric acids. [7]

Inhalational exposure to nitrogen oxides is well known in agriculture as "silo filler's disease" and in industry due to accidents involving fuming nitric acid. It is characterized by a latent phase and delayed pulmonary edema, which requires observation even when symptoms are initially mild. [8]

Chemical eye burns are a significant cause of ophthalmic trauma. According to reviews, chemical eye injuries account for 10-22% of all eye injuries; the annual incidence worldwide is estimated at 0.02 to 50 per 100,000 population, with a high proportion of occupational cases in young men. [9]

The incidence of corrosive ingestion varies by region. Some studies provide estimates ranging from 1 to 16 cases per 100,000 population per year; in adults, some episodes are associated with intentional self-poisoning, which increases the risk of adverse outcomes. [10]

Reasons

The main etiological factor is contact of the skin, eyes, or mucous membranes with nitric acid solutions of varying concentrations (including "fuming" nitric acid). Industrial risks include metallurgy, electroplating, etching, fertilizer production, laboratory work, and storage and transportation of the reagent. Household risks include overfilling the acid into unauthorized containers and homemade cleaning mixtures. [11]

Inhalation injury occurs when nitrogen oxides and vapors formed from nitric acid are inhaled. This can occur either as an acute episode of high concentrations or as a result of repeated, smaller exposures in poorly ventilated areas. [12]

Ingestion most often occurs accidentally in children or intentionally in adults. Concentration and volume determine the risk of deep necrosis and complications, including perforations, hemorrhages, and late esophageal strictures. [13]

It's important to distinguish between chemical burns caused by nitric acid and cold injury caused by liquid nitrogen. The latter is associated with instantaneous tissue freezing at temperatures around -196°C and leads to microvascular thrombosis and reperfusion injury—a different mechanism and different first aid strategy. [14]

Risk factors

In industrial settings, risks increase when working with concentrates, aerosols, and "fuming" solutions, as well as in the absence of local ventilation, eye and skin protection, and storage and labeling errors. The presence of emergency showers and eye wash stations significantly reduces the severity of outcomes. [15]

In everyday life - pouring into bottles without labeling, storing in a place where children can reach, using acid to clean plumbing and metal surfaces without gloves and glasses. [16]

For the eyes - no protective glasses when pouring and mixing solutions; for the lungs - work in confined spaces without ventilation and without vapor control. [17]

Aggravating factors for outcome: high concentration, prolonged exposure without rinsing, large area, late presentation, concomitant diseases and intentional inhalation/ingestion of large volumes. [18]

Table 2. Key risk factors and impact on outcome

Factor	Risk of severe course	Comment
High concentration of acid	↑↑	Rapid deep necrosis
Long exposure without rinsing	↑↑	The depth increases with time
Lack of eye/skin PPE	↑	Frequent eye and skin lesions
Poor ventilation	↑	Inhalation injury, delayed pulmonary edema
Childhood/intentional injection	↑↑	Severe esophageal and gastric burns

Pathogenesis

Nitric acid causes coagulative necrosis in skin and mucous membranes: protein denaturation forms a "barrier" scab, which sometimes limits further penetration—hence the common but dangerous myth that acid burns are "superficial." In practice, the depth often increases in the first 24-48 hours due to ongoing chemical reactions in the tissues. [19]

The xanthoprotein reaction between aromatic amino acids and nitrating agents gives the scab a yellow-brown hue - a diagnostic clue specifically for nitric acid. [20]

When inhaled, nitrogen dioxide dissolves in the water of the mucous membranes, forming acids and free radicals, damaging the alveolar-capillary membrane. Biphasic lesions are characteristic: early irritation and late non-cardiogenic pulmonary edema; a bronchiolitic obliterative form is possible after 1-4 weeks. [21]

If swallowed, it can cause chemical burns to the oropharynx, esophagus, and stomach, deep necrosis, and risk of perforation. The inflammatory phase is followed by granulation, then scarring and strictures; in the long term, the risk of esophageal carcinoma increases. [22]

Symptoms

Skin: burning, pain, erythema, followed by the formation of a dry, yellow-brown scab, sometimes with clear boundaries; swelling of surrounding tissues. Deep corrosion causes loss of sensitivity. The depth of damage is often underestimated in the first hours. [23]

Eyes: severe pain, lacrimation, blepharospasm, photophobia, decreased vision; in severe cases - limbal ischemia, corneal opacity, increased intraocular pressure. This is an ophthalmologic emergency. [24]

Respiratory tract: cough, shortness of breath, chest pain, hoarseness, irritation; a latent phase with “apparent well-being” and subsequent progression to pulmonary edema is possible. Medical assessment and monitoring are necessary. [25]

Ingestion: pain and burning in the mouth and throat, dysphagia, hypersalivation, vomiting, possibly with blood; in severe cases, signs of perforation and mediastinitis. [26]

Classification, forms and stages

For skin and mucous membranes, corrosion grades are used based on depth, similar to burns: superficial (first degree), partial thickness (second degree), and full thickness (third degree). Chemical burns may increase in depth after the initial assessment, so follow-up examinations are essential. [27]

For the eyes, the Roper-Hall and Dua prognostic scales are used (they assess the degree of corneal opacity and the extent of limbal ischemia/conjunctival damage). Greater limbal and conjunctival ischemia means a worse prognosis and a higher risk of stem cell loss and corneal opacity. [28]

Inhalation injuries are classified according to the clinical presentation and severity of respiratory failure; an early form with pulmonary edema in the first 24 hours and a late bronchiolitic form after 1–4 weeks have been described. [29]

In case of ingestion, the endoscopic classification of Zargar (0-3b) is used in the first 12-24 hours for risk stratification, as well as computed tomography data if perforation is suspected. [30]

Table 3. Classification of chemical eye burns (comparison)

System	Criteria	Gradations	Forecast
Roper Hall	Corneal opacity, limbal ischemia	I-IV	From good (I) to bad (IV)
Dua	Hours of limbal ischemia + % conjunctival damage	I-VI	>6 hours of ischemia and >50% conjunctiva - unfavorable

Complications and consequences

Skin: infection, delayed healing, hypo-/hyperpigmentation, scarring and contractures; in deep lesions - need for skin grafting. [31]

Eyes: persistent corneal opacification, neovascularization, dry eye syndrome, increased intraocular pressure, conjunctival scarring and symblepharon, corneal stem cell deficiency.[32]

Respiratory tract: delayed pulmonary edema, bronchiolitis obliterans, chronic obstructive symptoms with repeated exposures. [33]

Esophagus/stomach: strictures, dysphagia, chronic pain, risk of late malignancy in some patients years later. [34]

Table 4. Frequent complications by organ

Organ/system	Complications
Leather	Infections, scars, contractures, pigmentation
Eyes	Corneal clouding, stem cell deficiency, dry eye, glaucoma
Lungs	Pulmonary edema, obliterating bronchiolitis
Gastrointestinal tract	Esophageal strictures, perforations, bleeding

When to see a doctor

Immediately - in case of any chemical burn of the eye; if concentrated nitric acid comes into contact with the skin over an area larger than the palm of the hand; if blisters, severe pain, decreased sensitivity or signs of deep corrosion appear. [35]

After any inhalation of vapors with or without irritation symptoms - due to the risk of delayed deterioration in breathing for 6-48 hours. [36]

After swallowing acids - always; do not induce vomiting or give activated charcoal; it is permissible to give water or milk in small quantities if the victim is conscious and can swallow. [37]

Children, pregnant women, the elderly, and patients with comorbidities have a lower threshold for seeking treatment; they require assessment and observation. [38]

Diagnostics

Step 1. Decompression and initial assessment. In an emergency setting, the airway, breathing, and circulation are assessed in parallel with ongoing irrigation. During inhalation, oxygen saturation and respiration are monitored, and chest X-ray/CT scanning is performed if necessary. [39]

Step 2. Skin. Inspection of the affected area to assess depth and area; it is important to remember the tendency for the lesion to deepen in the first few hours. Instrumental assessment of perfusion (laser Doppler imaging) helps predict depth and plan treatment (early vs. delayed necrectomy and skin grafting). [40]

Step 3. Eyes. Immediately after irrigation, measure the pH of the tear film, continue irrigation until neutralization, then examine with a slit lamp, check intraocular pressure, the degree of limbal ischemia, and epithelial damage. Classify according to Roper-Hall or Dua for prognosis and treatment planning. [41]

Step 4. Esophagus and stomach. In case of injection, esophagogastroduodenoscopy is performed within the first 12-24 hours for stratification according to Zargar (0-3b). Computed tomography is indicated if perforation or severe wall damage is suspected. Repeated assessment is based on clinical findings. [42]

Table 5. Instrumental and laboratory methods

Situation	Method	For what
Leather	Laser Doppler Imaging	Depth forecast, plastic plan
Eyes	pH measurement, tonometry, slit lamp	Neutralization, degree of damage
Lungs	X-ray/CT scan	Pulmonary edema, bronchiolitis
Gastrointestinal tract	Endoscopy in 12-24 hours	Zargar gradation, nutrition/stent tactics

Differential diagnosis

Chemical burn with acid versus alkali burn: acid more often produces coagulative necrosis with a scab and sometimes less depth; alkali causes liquefactive necrosis with deep penetration. [43]

Nitric acid chemical burn vs. thermal burn: General appearance may be similar, but xanthoprotein yellow-brown coloration indicates nitric acid.[44]

Chemical burn versus cryogenic injury with liquid nitrogen: with cryotrauma there is no chemical scab; frostbite-like blisters are typical, pain on rewarming, and there is a high risk of microthrombosis. [45]

Inhalation injury by nitrogen oxides versus chlorine/ammonia irritation: nitrogen oxides are characterized by a delay in the development of severe respiratory failure. [46]

Treatment

The first and most important measure is immediate and prolonged rinsing of the affected skin or eye with water. This should be started immediately, on the spot, without waiting for medical attention. Running water at room temperature should be allowed on the skin and eyes for at least 15-30 minutes, often longer, until the irritation subsides and, for the eyes, until the pH becomes close to 7. Soaked clothing and jewelry should be removed immediately; rubbing is prohibited. Neutralizers (e.g., soda) should not be used due to the heat generated. Where an amphoteric solution (diphoteric) is available, it can be used in addition, although there is no convincing evidence that it is superior to water for skin; for the eyes, the evidence is stronger. [47]

In case of eye damage, irrigation is carried out using an irrigation device (Morgan lens) or manually; at the same time, the pH of the tear film is monitored and examination is carried out with a slit lamp. After irrigation, antibiotic drops are prescribed (to prevent infection), a cycloplegic for pain, artificial tears without preservatives, and, in case of moderate damage, topical corticosteroids for a short course under the supervision of an ophthalmologist, citrate/ascorbate drops for stromal support; in case of stem cell deficiency, amniotic membrane and reconstructive surgeries are considered. [48]

After irrigation, skin lesions are treated with a mild antiseptic, non-viable tissue is removed (as indicated), and modern atraumatic dressings are applied to support moist healing. Antimicrobial agents are selected individually: silver-containing coatings are used, but their limitations for superficial wounds have been discussed in recent years; alternatives include nanocrystalline silver or iodine-containing dressings, as indicated. Systemic antibiotics are not prescribed prophylactically, but only if signs of infection are present. Pain relief is administered using a stepwise approach. [49]

Deep chemical skin corrosion requires planning for necrectomy and skin grafting after demarcation. In some cases, laser Doppler imaging is used to clarify perfusion, and for complex wounds, a combination of negative pressure and dermal matrices is used to prepare the wound bed for skin grafting. [50]

Treatment for inhalation injury due to nitrogen oxides is supportive: oxygen, inhaled bronchodilators, and observation for at least 24-48 hours due to the risk of delayed pulmonary edema. If symptoms worsen, transfer to the intensive care unit and support ventilation. Glucocorticosteroids are used selectively for inhalation injury; high-level data are insufficient; the physician's decision is based on the clinical presentation. [51]

Following acid ingestion, the priorities are airway protection, fluid therapy, and pain control. Vomiting is not induced, and activated charcoal is not used. Esophagogastroduodenoscopy is performed in the first 12-24 hours to determine the severity and management of nutrition (tube/enteral or parenteral nutrition), as well as to prevent and treat strictures in the long term (balloon dilation, stenting). The role of systemic corticosteroids in stricture prevention remains controversial and is decided on an individual basis. [52]

Local remedies “from folk medicine” (potatoes, tea, etc.) mentioned in the original article are not recommended: they do not dilute the reagent, can introduce an infection, and distract from the main thing - prolonged rinsing with water and urgently seeking help. [53]

During the rehabilitation phase, scar prevention (compression gloves/clothing, silicone gels), physical therapy, stretching exercises to prevent contractures, and ophthalmic medications for dry eye syndrome are used. Planned scar correction and reconstruction are possible after stabilization. [54]

A separate tactic for burns caused by liquid nitrogen (for differentiation): after cessation of exposure - passive rewarming to 37-39 °C, pain relief with ibuprofen (as a thromboxane blocker), perfusion assessment; in severe cases - vascular interventions (iloprost, thrombolysis under strict indications). This does not apply to nitric acid, but it is important to understand the difference in terms. [55]

Table 6. What to do/what not to do for chemical burns from nitric acid

Action	Not really	Explanation
Immediate prolonged rinsing with water	Yes	The key to reducing severity
Removing soaked clothing/jewelry	Yes	Prevents continued exposure
Neutralization with soda/alkali	No	Risk of heat generation and increased injury
"Folk" applications (potatoes, tea)	No	Unreasonable and unsafe
Diphoterine solution	Optional	Where available; there is no further evidence for skin
Induce vomiting/give charcoal if injected	No	Contraindicated
Rinse eyes to pH≈7	Yes	With pH control

Prevention

In production: engineering measures (local exhaust, sealed systems), personnel training, personal protective equipment (goggles, shields, gloves, aprons), emergency showers and eye wash stations, clear labelling and storage. [56]

In everyday life: store chemicals in their original, labeled containers, out of the reach of children; never pour into beverage bottles; use protective goggles and gloves when cleaning with aggressive cleaning agents. [57]

To prevent inhalation injuries - ventilation, gas sensors where provided, work outside of confined spaces, avoid heating and contact with metals that can increase evaporation and reactivity. [58]

Ophthalmoprophylaxis: use closed-type glasses when pouring/mixing solutions, have emergency eye wash facilities ready. [59]

Forecast

For superficial skin corrosions with early irrigation - favorable; depth and risk of scarring directly depend on the time before the start of irrigation and concentration. [60]

Ocular prognosis is determined by the degree of limbal ischemia and the depth of corneal damage according to the Roper-Hall/Dua scales; early irrigation and proper anti-inflammatory therapy improve outcomes. [61]

Inhalation injuries are insidious due to delayed complications; even minimal initial symptoms require observation. Outcomes range from full recovery to severe respiratory failure. [62]

After ingestion, early endoscopic stratification and proper nutritional management are crucial; severe cases are associated with the risk of strictures and long-term complications. [63]

FAQ

Should I neutralize the acid with baking soda? No. This can worsen the damage due to heat generation. The most important thing is to rinse with water as soon as possible and for as long as possible. [64]

How long should you rinse your skin or eyes? At least 15-30 minutes; for eyes, until the pH returns to normal; if irritation persists, longer. [65]

Does a yellow crust mean the burn is superficial? Not necessarily. A yellow-brown color is a sign of a xanthoprotein reaction with nitric acid, but the depth can be significant and "deepen" over the first day. [66]

What to do if you inhale the vapors and are currently "fine"? Seek medical evaluation and observation for 24-48 hours due to the risk of delayed pulmonary edema. [67]

What is the treatment for eye irritation after irrigation? Antibiotic drops, cycloplegic, tear substitutes; if indicated, a short course of steroids, citrate/ascorbate, amniotic membrane, or surgical reconstruction. The decision is made by an ophthalmologist. [68]

Can special solutions be used instead of water? If amphoteric solutions (diphoteric/Previn) are available, they can be used, especially for the eyes. However, for skin burns, convincing superiority over water in clinical outcomes has not yet been demonstrated; water should be started immediately. [69]

What's the difference between a "nitrogen burn" and a "liquid nitrogen burn"? Nitric acid is a chemical corrosive burn with a yellow scab; liquid nitrogen is a cryogenic frostbite-like injury, without xanthoprotein staining, with a different treatment algorithm (warming, not irrigation with water). [70]

Additional tables for practice

Table 7. First aid by context

Context	What to do immediately	What not to do
Leather	Running water ≥15-30 minutes, remove clothes	Neutralization with soda, rubbing
Eyes	Continuous rinsing to pH≈7	Drops without a doctor's examination, delay
Inhalation	Fresh air, observation for 24-48 hours	Ignore the "latency period"
Swallowing	Do not induce vomiting; if able to swallow - 100-200 ml of water/milk; go to hospital	Activated carbon, acid-alkali "neutralization"