Chemical burns

Overview

Chemical burns account for a small but clinically significant proportion of burn center admissions. They differ fundamentally from thermal injuries in that tissue destruction continues as long as the agent remains in contact with tissue. The diversity of causative agents (acids, alkalis, oxidizers, vesicants, specialized industrial compounds) means a single treatment algorithm is insufficient. The clinician must understand agent-specific pathophysiology to provide effective care. Time to decontamination is the single most important variable in outcome.

Epidemiology

The largest early institutional series was reported by Mozingo et al. ^[1], who reviewed 87 chemical burn patients (2.1% of admissions) over 17 years at the U.S. Army Institute of Surgical Research. White phosphorus was the most common agent (49 patients), and overall mortality was 13.8%. They established that reducing exposure time and recognizing systemic toxicity are the two critical variables. Chemical burns carry disproportionately high mortality relative to TBSA when systemic effects are present, reinforcing that these are combined local-systemic injuries requiring agent-specific management.

Hydrofluoric acid burns

Hydrofluoric acid (HF) burns represent the most dangerous subset because of the potential for fatal hypocalcemia from even small exposures. Sheridan et al. ^[2] established the treatment protocol of wound irrigation, subeschar injection of calcium gluconate, serum calcium monitoring, and prompt wound excision, demonstrating that as little as 2.5% TBSA exposure to concentrated HF may be fatal. The debate regarding calcium gluconate delivery route (topical gel versus subeschar injection versus intra-arterial infusion) remains unresolved, with Rutan et al. ^[3] contributing to the discussion of treatment modalities.

Alkali burns

Alkali burns present distinct management challenges. Latenser and Lucktong ^[4] demonstrated with anhydrous ammonia cases that immediate on-scene irrigation is the single most important determinant of outcome. Two patients with identical exposure had dramatically different outcomes based solely on whether decontamination occurred at the scene. Chung et al. ^[5] compiled cement-related injuries across two burn units and the National Burn Repository, finding that cement burns deepen progressively with prolonged contact because workers often fail to recognize the alkaline injury for hours. Reilly and Garner ^[6] reinforced that early water irrigation followed by diligent wound care is the cornerstone approach, with agent-specific modifications for particular compounds.

Emerging and iatrogenic mechanisms

The emergence of lithium-ion battery injuries as a chemical burn mechanism was documented by Palmieri et al. ^[7], who described the spectrum from cutaneous burns and explosions to corrosion injuries from electrolyte leakage. Cancio et al. ^[8] developed chemical injury guidelines for austere conditions, addressing the intersection with blast and radiation injuries where multiple mechanisms may coexist. Saeed et al. ^[9] reviewed respiratory effects of toxic industrial chemicals including chlorine, phosgene, hydrogen sulfide, and ammonia, which may present alongside cutaneous chemical burns.

Iatrogenic chemical burns are an underrecognized category. Cohan et al. ^[10] reviewed contrast material extravasation injuries, which are often underreported and may progress to significant tissue necrosis. Buchanan et al. ^[11] reported a fatal case of chest wall necrosis from hydrochloric acid infusion extravasation, demonstrating that chemical burns from therapeutic agents administered centrally can go unrecognized until tissue destruction is advanced. Pham et al. ^[12] illustrated the challenge of managing compounds with significant systemic toxicity: sodium azide inhibits ATP production, causing hypotension and bradycardia in addition to local injury. Saydjari et al. ^[13] provided a foundational review of chemical burn principles that informed subsequent management approaches.

Controversies and Evidence Gaps

The evidence base is dominated by case series, case reports, and expert reviews, with no randomized controlled trials comparing treatment strategies. The debate over Diphoterine versus water as first-line decontamination remains active: Diphoterine's amphoteric properties theoretically offer advantages for unknown agents, but definitive comparative data are lacking. For hydrofluoric acid burns, the optimal calcium gluconate delivery route (topical, subeschar, intra-arterial) has not been resolved by controlled studies. The growing incidence of lithium-ion battery injuries raises questions about whether existing chemical burn protocols adequately address the combined thermal-chemical-electrical mechanism. The threshold for surgical excision versus conservative management in chemical burns, particularly alkali burns that may continue to deepen for 48 to 72 hours, lacks evidence-based timing guidelines.

References

[1] Mozingo DW et al. (1988). Chemical burns. PMID: 3367407 [2] Sheridan RL et al. (1995). Emergency management of major hydrofluoric acid exposures. PMID: 7718123 [3] Rutan R et al. (2001). Electricity and the treatment of hydrofluoric acid burns--the wave of the future or a jolt from the past? PMID: 11505153 [4] Latenser BA, Lucktong TA. (2000). Anhydrous ammonia burns: case presentation and literature review. PMID: 10661537 [5] Chung JY et al. (2007). Cement-related injuries: review of a series, the National Burn Repository, and the prevailing literature. PMID: 17925652 [6] Reilly DA, Garner WL. (2000). Management of chemical injuries to the upper extremity. PMID: 10791168 [7] Palmieri TL et al. (2018). Lithium batteries: A technological advance with unintended injury consequences. PMID: 29787525 [8] Cancio LC et al. (2017). Guidelines for Burn Care Under Austere Conditions: Special Etiologies: Blast, Radiation, and Chemical Injuries. PMID: 27355658 [9] Saeed O et al. (2018). Inhalation Injury and Toxic Industrial Chemical Exposure. PMID: 30189064 [10] Cohan RH et al. (1996). Extravasation of radiographic contrast material: recognition, prevention, and treatment. PMID: 8756899 [11] Buchanan IB et al. (2005). Chest wall necrosis and death secondary to hydrochloric acid infusion for metabolic alkalosis. PMID: 16144181 [12] Pham T et al. (2001). Sodium azide burn: a case report. PMID: 11403249 [13] Saydjari R et al. (1986). Chemical burns. PMID: 3639877