Trauma Kimia

01Pathophysiology

Chemical burns differ fundamentally from thermal burns in one critical way: the injuring agent continues destroying tissue as long as it remains in contact with the body. In thermal burns, the damage is essentially instantaneous upon removal from heat. In chemical burns, the chemical reaction is ongoing, making time-to-decontamination the single most important prognostic factor.

The mechanisms of tissue injury can be broadly divided by the nature of the chemical agent. Acids (pH < 2) act as proton donors. They denature and coagulate tissue proteins, producing coagulative necrosis. The coagulated protein forms a tough, leathery eschar that paradoxically acts as a barrier, limiting further penetration of the acid into deeper tissues. This is why acid burns, while painful and destructive, tend to be more self-limiting in depth. The exception to this rule is hydrofluoric acid (HF), which behaves unlike other acids and instead produces liquefactive necrosis with deep tissue penetration.

Alkalis (pH > 11.5) act as proton acceptors. They cause injury through three concurrent processes. First, saponification of cell membrane lipids disrupts the permeability barrier of the skin, allowing the agent to penetrate deeper. Second, alkaline hydrolysis of structural proteins produces liquefactive necrosis, in which cells liquefy and dissolve rather than forming a protective barrier. Third, hygroscopic tissue dehydration extracts water from cells, compounding the destruction. Because liquefactive necrosis does not create a coagulum to stop the agent, alkali burns penetrate far deeper and are generally more severe than acid burns at equivalent concentrations and contact times. The wound often has a characteristic "soapy" or slippery texture due to the saponification of subcutaneous fat.

Beyond dermal injury, chemical burns can produce systemic toxicity depending on the agent. HF acid exposure causes the fluoride ion to chelate serum calcium and magnesium, resulting in hypocalcemia, hypomagnesemia, and hyperkalemia, which can lead to fatal cardiac arrhythmias. Burns involving more than 25 square inches (approximately 160 cm${}^2^2$) of HF exposure or any concentration above 50% carry a high risk of systemic toxicity. In burns covering more than 30% total body surface area (TBSA), the systemic inflammatory response leads to capillary leak, massive fluid shifts, and hypovolemic shock, following the same pathophysiology as severe thermal burns. Additionally, rhabdomyolysis can occur in deep chemical burns, with myoglobin precipitating in renal tubules and causing acute kidney injury.

02Classification of Chemical Burns

Burn Depth Classification

A critical exam point: chemical burns often appear deceptively superficial on initial presentation. The full depth of the injury may not declare itself for 48 to 72 hours, especially with alkali burns. Cement burns are notorious for this, as workers may be unaware of the alkaline injury until hours after exposure, by which time deep dermal or full-thickness injury has already occurred.

Roper-Hall Classification (Ocular Chemical Burns)

This is the most tested classification for ocular chemical injuries. It grades severity based on corneal haze and perilimbal ischemia.

The Dua classification subdivides the old Grade IV into Grades IV, V, and VI based on the clock hours of limbal involvement and percentage of conjunctival involvement, providing a more nuanced prognosis for severe injuries. For exam purposes, know both systems, but Roper-Hall is the more commonly tested framework.

Classification by Causative Agent

03Diagnostic Workup

The Best Initial Step for any chemical burn is not a diagnostic test at all. It is immediate copious irrigation with water. Do not delay decontamination to perform any diagnostic workup. The only exception is elemental alkali metals (lithium, sodium, potassium, magnesium), which react exothermically with water and should instead be covered with mineral oil and physically removed with forceps.

The workup proceeds in parallel once irrigation is initiated. For cutaneous burns, wound pH should be checked periodically during irrigation using litmus paper. The goal is a neutral pH of 7.0. For acid burns, irrigation for 15 to 30 minutes is often sufficient. For alkali burns, irrigation may need to continue for 60 minutes or longer because the liquefactive mechanism allows the chemical to persist in deeper tissue layers.

For ocular burns, the irrigating fluid should flow from nasal to lateral to prevent contamination of the unaffected eye. Up to 20 liters of irrigation fluid may be required. After pH normalization (checked in the inferior conjunctival fornix), proceed to slit-lamp examination with fluorescein staining to assess corneal epithelial defects, stromal haze, and limbal ischemia, then grade using the Roper-Hall or Dua classification.

For HF acid burns, the workup prioritizes electrolytes and cardiac monitoring. An ECG must be obtained immediately. Serum calcium and magnesium should be checked and trended. Even a burn that looks minor can produce fatal systemic toxicity through fluoride-ion-mediated hypocalcemia and hyperkalemia. A QTc prolongation or widened QRS on ECG is an ominous sign requiring emergent IV calcium replacement.

04Management and Treatment

Acute Management Summary

Agent-Targeted Therapy

Hydrofluoric Acid Burns:
The treatment of HF burns is unique and frequently tested. Standard water irrigation alone is insufficient because the fluoride ion has already penetrated into deeper tissues. After initial decontamination with water for at least 30 minutes, apply 2.5% calcium gluconate gel to the affected area and massage continuously. The calcium gluconate reacts with the fluoride ion to form insoluble, non-toxic calcium fluoride, neutralizing the ongoing toxicity. The endpoint of treatment is complete relief of pain, which is why analgesics should be avoided early on. If topical gel fails to relieve pain, subcutaneous or intradermal injection of 5% calcium gluconate (0.5 mL per cm${}^2^2$ of burn area, using a 27 or 30-gauge needle) may be required. For digital burns or large area burns unresponsive to topical or local injection therapy, intra-arterial calcium gluconate infusion (10 mL of 10% calcium gluconate diluted in 40 mL of D5W, infused over 4 hours through the radial or brachial artery) can be performed. For inhalational HF exposure, administer nebulized 2.5 to 5% calcium gluconate (4 mL). Monitor serum calcium, magnesium, and potassium; replete as needed. Obtain serial ECGs. Avoid succinylcholine if intubation is required, as hyperkalemia from fluoride toxicity can be worsened.

Alkali Burns (General):
Alkali burns require the most prolonged irrigation. Continue until wound pH reaches 7.0 and remains stable for at least 15 minutes after stopping irrigation. Cement (calcium hydroxide) burns are a common trap: the insidious onset means the patient often presents late with already-deep burns. After decontamination, wound care follows standard burn protocols.

Ocular Chemical Burns:
Irrigation is the cornerstone. Begin immediately, even before a formal eye examination. Use normal saline or lactated Ringer's via a Morgan lens or IV tubing placed in the fornix. Irrigate until the pH of the tears (checked in the inferior fornix) is 7.0 to 7.4. After irrigation, the medical treatment includes: topical antibiotics (e.g., erythromycin ointment or fluoroquinolone drops), cycloplegics (e.g., cyclopentolate 1% or atropine 1% to reduce ciliary spasm and pain), topical corticosteroids (prednisolone acetate 1%, used in the first 7 to 10 days only; avoid after 10 to 14 days as they impair collagen synthesis and increase the risk of corneal perforation), preservative-free artificial tears, and ascorbic acid (vitamin C, 2 g orally daily and 10% topically every 2 hours) to promote collagen synthesis. For Roper-Hall Grade III and IV injuries, amniotic membrane transplantation and limbal stem cell transplantation may be required.

Referral Criteria (Per KMK No. HK.01.07/MENKES/555/2019)According to KMK No. HK.01.07/MENKES/555/2019 (Pedoman Nasional Pelayanan Kedokteran Tata Laksana Luka Bakar), the Indonesian national guideline adopts referral criteria aligned with the ANZBA (Australian and New Zealand Burn Association) framework. Chemical burns are explicitly listed as one of the criteria mandating referral to a burn center (pusat perawatan luka bakar), regardless of TBSA percentage. Additional referral criteria include burns involving the face, hands, feet, genitalia, perineum, or major joints; electrical burns; burns with concomitant inhalation injury; circumferential burns; burns in patients with preexisting comorbidities; and burns in extremes of age. The guideline also mandates that before transfer, the referring facility must complete initial stabilization including airway management, fluid resuscitation using the Parkland formula, and adequate pain control. RSUP Cipto Mangunkusumo (RSCM) Jakarta serves as the primary national burn referral center.

For fluid resuscitation, the PNPK follows the Parkland formula:

$$Fluid(mL)=4\times \mathrm{\%}TBSA\times bodyweight(kg)Fluid\backslash \; (mL)\; =\; 4\; \backslash times\; \backslash \%TBSA\; \backslash times\; body\backslash \; weight\backslash \; (kg)$$

Deliver 50% of the calculated volume in the first 8 hours from the time of injury (not from time of presentation), and the remaining 50% over the next 16 hours. Use lactated Ringer's solution. Titrate to urine output: 0.5 to 1 mL/kg/hr in adults, 1 to 2 mL/kg/hr in children. If pigmented urine is present (suggesting myoglobinuria), increase the target urine output to 70 to 100 mL/hr in adults and 2 mL/kg/hr in children.

Indonesian Occupational Safety Regulations for Chemical Hazards

Several overlapping regulations govern the workplace prevention and first-aid response to chemical injuries:

05Special Agents and Considerations

Hydrofluoric Acid (HF)

HF is the single most important "exception" chemical for exam purposes. Unlike other acids, HF produces liquefactive necrosis and causes deep tissue injury that appears mild externally. The fluoride ion penetrates cells, chelates intracellular calcium and magnesium, and disrupts enzymatic function. Systemic absorption leads to hypocalcemia, hypomagnesemia, and hyperkalemia, which can trigger fatal ventricular fibrillation. Any burn involving concentrated HF (above 50%) or covering an area larger than 25 square inches requires immediate cardiac monitoring and serial electrolyte checks. The antidote is calcium gluconate, applied topically as a 2.5% gel, injected locally as 5% solution, or given intra-arterially for refractory cases. The endpoint of treatment is pain relief, not visual wound improvement. Avoid analgesics in the early phase to preserve this clinical endpoint.

White Phosphorus Burns

White phosphorus ignites spontaneously on contact with air. The particles continue to burn as long as they are exposed to oxygen. Management requires continuous submersion of the wound in water or saline to prevent re-ignition. Particles should be identified using a Wood lamp (they fluoresce) or by darkening the room (they glow). Remove particles with forceps. After removal, apply a 1% copper sulfate solution, which reacts with phosphorus to form a dark, easily identifiable copper phosphide coating, facilitating complete removal. Avoid using copper sulfate on large areas due to the risk of copper toxicity (hemolysis, hepatorenal failure).

Phenol (Carbolic Acid) Burns

Phenol causes both coagulative necrosis and systemic toxicity (CNS depression, hepatotoxicity, cardiac arrhythmias). The wound initially appears painless and white, then progresses to brown or black gangrene. Phenol is lipophilic and poorly soluble in water, so water irrigation alone is less effective. The preferred decontamination method is wiping the affected area with polyethylene glycol (PEG 300 or 400) or, if unavailable, isopropyl alcohol to dissolve the phenol, followed by water irrigation.

Elemental Alkali Metal Burns (Sodium, Potassium, Lithium, Magnesium)

These metals react violently and exothermically with water, producing thermal burns on top of chemical injury. Do NOT irrigate with water. Instead, cover the area with mineral oil, remove metal fragments with dry forceps, and then proceed with standard wound care.

Cement (Calcium Hydroxide) Burns

Cement is a common cause of alkali burns in construction workers. The injury is insidious because cement is not perceived as a caustic agent, and workers often remain in contact with wet cement for hours before symptoms develop. By the time the patient presents, the burn is frequently deep dermal or full-thickness. The lower extremities are most commonly involved. After removal of all cement-contaminated clothing and footwear, irrigate the area extensively and treat as a standard alkali burn.

06Differential Diagnosis and Distractors

07Traps and High-Yield Pearls

The most common way students lose points on chemical burn questions falls into three categories.

First, the reflexive neutralization error. When presented with an acid burn, many students instinctively choose "apply a base to neutralize the acid" as the first step. This is wrong and dangerous. Neutralization reactions are exothermic and produce a secondary thermal injury on top of the existing chemical injury. The correct first step is always copious irrigation with plain water. The only exception to water irrigation is burns from elemental alkali metals (sodium, potassium, lithium, magnesium), where water causes an exothermic reaction and mineral oil coverage is required instead.

Second, the HF acid trap. Test-writers love hydrofluoric acid because it breaks the rules. It is an acid that produces liquefactive necrosis (not coagulative). It causes systemic toxicity (hypocalcemia, hyperkalemia, cardiac arrest) through a mechanism unique among acid burns. And it has a treatment that differs from all other chemical burns (calcium gluconate rather than irrigation alone). When a vignette describes a chemical burn with "pain out of proportion to the visible wound" in a glass etcher, electronics worker, or semiconductor plant employee, think HF immediately. The next best step after irrigation is topical calcium gluconate, not silver sulfadiazine. If the question asks about monitoring, the answer is serial calcium, magnesium, potassium, and ECG, not wound culture.

Third, the delayed presentation of alkali burns. Cement burns are the classic exam scenario. A construction worker presents hours after exposure with what appears to be a superficial wound. The trap is underestimating the depth of injury. The test is asking whether you understand that alkali burns (liquefactive necrosis) continue to penetrate tissue and that the wound will evolve to become much deeper over 48 to 72 hours. The correct answer involves prolonged irrigation (at least 60 minutes for alkali), close follow-up with re-evaluation of burn depth, and referral to a burn center.

The core competency being tested across all chemical burn questions is prioritization: can you recognize that decontamination comes before diagnostics, that water irrigation is the universal first step (with narrow exceptions), and that certain agents (HF, alkali metals, phosphorus, phenol) require agent-targeted therapies on top of standard burn care?