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Ростовский Государственный Медицинский Университет

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Chapter19

163

Chemical burns

Introduction to chemical burns 164 Classication 165 Pathophysiology 166 Clinical features 166 General features 166 Workup 167 General management principles 168 Subsequent care 170 Complications 170 Further reading 170

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CHAPTER19 Chemical burns

Introduction tochemical burns

Chemicals cause 2.4– 10.7% of all burn injuries worldwide; burns from chemicals are seven times more common in males than females. Although relatively rare, these injuries account for up to 30% of burn deaths, and therefore demand careful and timely management. Recent studies suggest that improved health and safety measures may be reducing the incidence of industrial injuries but domestic injuries are increasing. Head and neck structures, including eyes, and extremities are most commonly aected. The most important step in the intial management of a chemical burn is the immediate removal to halt further injury. Thereafter, the management is similar to other burn injuries although some chemicals require specic management steps, discussed below.

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CLASSIFICATION

Classiﬁcation

Chemicals which cause burns can be grouped into six main classes according to their mechanism of action. These are summarized in Table 19.1.

However, the most important clinical distinction is between acidic and alkalotic burns. Acids (pH 1– 7) donate protons (H+) in solution and alkalis (pH 8– 14) accept hydroxyl ions (OH– ). Examples of strong acids (pH < 2) include sulphuric acid (H2SO4) and hydrochloric acid (HCl), which are both corrosive and also a desiccant and a reductant respectively. Injurious alkalis usually have a pH > 11.5 and include cement. The remaining causes of chemical burns can be largely classed as organic or inorganic solutions.

Table19.1 Classes ofburning chemicals accordingtomechanism ofaction

Mechanism of action Examples

Reductants Electron donors HCl, nitric acid, alkyl mercuric

Oxidants Accepts electrons Sodium hypochlorite,

Corrosives Denature proteins on contact Phenols, cresols, lyes, H2SO4,

Protoplasmic poisons

Desiccants Dehydrate tissues H2SO4 and concentrated HCl

Vesicants Ischaemia leading to anoxic

DMSO; dimethylsulfoxide

Form esters with proteins or bind/ inhibit vital organic ions such as calcium

necrosis; forms blisters

compounds

potassium permanganate, chromic acid

HCl, sodium metals

Ester formers:formic and acetic acid, inhibitors:oxalic, hydrouoric acid

Mustard gas, DMSO, Lewisite, cantharides

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CHAPTER19 Chemical burns

Pathophysiology

Chemicals denature proteins by disrupting the weak bonds that maintain the protein’s tertiary three- dimensional structure. Acids, apart from hydrouoric acid, cause coagulation necrosis upon contact with skin, resulting in the formation of an eschar or coagulum. This limits the amount of acid that penetrates underlying tissue. However, alkalis usually produce more severe wounds as they cause liquefaction necrosis of cutaneous tissue, allowing alkalis to react with underlying fat and other tissues. Alkalis tend to manifest the true extent of injury days after initial insult. Therefore, thorough examination and evaluation for involvement of deeper tissues is warranted in cases of alkaline chemical injury. Organic solutions dissolve lipid cell membranes and thereby disrupt cell architecture while inorganic solutions damage skin by direct binding to injurious agents and salt formation with proteins.

Clinical features

The severity of the resulting burn injury is dictated by the substance responsible, its phase (air, liquid, or gas), quantity and concentration, duration of exposure and total body surface area (TBSA) burnt, subsequent management, regional skin properties and mechanism of action. Athorough history and physical examination may reveal some of these factors and are therefore warranted. Ahigh index of suspicion for concealed injury should also be maintained.

Clinical features can be general to all chemical burns or specic to par-

ticular substances or classes of substances.

General features

Skin and appendages

Mottled dry or wet skin; may develop blisters; partial and/ or full thickness burn

Gastrointestinal

Oral burns or oedema; drooling; abdominal pain; guarding; dysphagia:there is an increased likelihood of perforation and oesophageal strictures.

Ophthalmic

Decreased visual acuity; diplopia; corneal abrasion; corneal opacication: this increases risk of blindness.

Respiratory

Respiratory arrest; stridor; wheezing; dyspnoea; tachypnoea; use of accessory muscles; subcutaneous air (Haman’s crunch).

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Workup

Investigations

Full blood count; urea and electrolytes; liver function tests; blood urea nitrogen; serum creatinine; coagulation prole; urinalysis: myoglobinuria; arterial blood gas (ABG) analysis; electrocardiogram; also see Table 19.1 for specic investigations depending on the chemical involved. Suspicion of ocular injury mandates uorescein and slit-lamp examinations.

Imaging

Chest X- ray if respiratory symptoms; abdominal X- ray:supine and erect if suspected peritonitis.

WORKUP

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CHAPTER19 Chemical burns

General management principles

The principles of managing chemical burns are generally similar to thermal burns, but special considerations are to be made regarding initial management of chemical burns.

Removal ofchemical fromskin

• Remove particulate debris, brush o dry chemicals, and remove all

potentially contaminated clothing. Carers should wear protective clothing to avoid injury.

Hydrotherapy withappropriate drainage

Copious irrigation with water for duration of at least 30 minutes to 2 hours may be required. Immersion into a tub is not recommended as chemical containment exacerbates burn injury. Examine for signs of hypothermia; maintain room temperature between 28°C and 31°C and lavage water near body temperature. Caution is advised on relation to neutralizing the chemical as this may induce a biochemical reaction, thereby precipitating further injury, but specic neutralizing agents for chemical injuries do exist and are widely available especially in industry, such as Diphoterine. Diphoterine is of particular value as it is eective against a range of chemical classes, including acids and alkalis, and can be used on th skin, eyes and has been used for esophageal burns.

Correct estimation ofthe extent ofinjury

• Depth and TBSA of burn.

Identication ofsystemic toxicity

• Acid/ base imbalances should be identied early. Hydrouoric acid in

particular can cause systemic derangement including hypocalcaemia and resultant ventricular arrythmias such as Torsades de Pointes and ventricular brillation. Other biochemical derangements such as hypomagnesia and hyperkalaemia can also occur and compound the risk of death even with HF burns of <1% TBSA.

Treatment ofocular contacts

• Copious irrigation is required and an ophthalmologic consult should be

made. Fluorescein staining to assess corneal or scleral abrasions. Assess pH of the eyes. Diphoterine may also be used to irrigate eyes. pH may also be used to assess adequacy of irrigation: aim for pH 7.0–7.3.

Management ofchemical inhalation injury

• Acute airway inammation and necrosis may occur after caustic

ingestion. Consider establishing a denitive airway if the patients is in respiratory distress. All chemical inhalation burns should be reviewed early by an Anaesthetist.

Special considerations forspecic agents

Assaults using corrosive substances

• Often referred to as ‘acid attacks’ although attacks may be from caustic

(alkali) or acids.

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GENERAL MANAGEMENT PRINCIPLES

• Recent published guidelines describe the three Rs:remove (clothing),

rinse (copiously with water), and report (to emergency services).

• After rst aid management, care should be delivered at specialist burns

services.

Table19.2 Specic features and management

Substance (industrial uses)

Chromic acid (laboratory glassware cleaning, chromium plating)

Hydrouoric acid (glass etching, oil renery)

Phosphorous (water treatment plants, pesticides)

Oxalic acid (dyes, bleaches)

Nitric acid (fertilizers) Yellow- brown staining of

Features/ workup Special management points

Non- painful corrosive ulcers; may cause respiratory distress if inhaled; monitor for systemic eects as even 10% TBSA burns are often fatal; blood urea nitrogen; creatinine

Damage may appear minimal initially; can cause cardiorespiratory, neurological and gastrointestinal eects. Subungal tissues are particularly prone. Monitor Ca2+, K+, Mg2+ and ECG (long Q- T syndrome)

ECG:cardiac arrhythmias; Ca2+; PO

Limits muscle contraction; monitor urea and electrolytes, calcium ion levels; cardiopulmonary function monitoring

skin and formation of a coagulum

Irrigation ± phosphate buer solution in an industrial setting. For systemic eects, dimercaprol 4 mg/ kg IM for 2days then 2– 4 mg/ kg/ day for 7days. Dialysis lowers chromium blood levels

Treatment is in four stages:hydrotherapy with water (or hexauorine lavage); topical treatment (eg. Ca2+ gel); inltration of 0.5 mL of 10% calcium gluconate per cm2 and radial arterial infusion of 10 mL of 10% calcium gluconate and 40 mL 5% dextrose solution over 2– 4 hours, until cessation of pain

White phosphorous

ignites with oxygen;

identify and remove phosphorous particles using phosphorescence or 0.5% CuSO4, which turns particles black; important to keep the wound moist, eg. with a water- soaked gauze dressing or petroleum jelly

Irrigation and IV Ca

Irrigation then topical silver sulphadiazine. Gauze dressings or occlusive, antiseptic moist bandages are used to maintain wound moisture depending on burn depth

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CHAPTER19 Chemical burns

Subsequent care

The subsequent management of chemical burns follows similar principles to management of other burn types. Begin initial assessment and management using trauma resuscitation protocols such as ATLS or EMSB. Depending on the extent of the burn, uid resuscitation and pain management protocols are as described (electrical injuries chapter). Urine output is one of the key markers of adequate resuscitation. Once the patient is stabilized, early excision and grafting are indicated to improve outcomes if deep dermal or full thickness burns are sustained. Psychological input may be required at an early stage.

Complications

Scarring, poor wound healing, local infections, cataract formation, loss of vision.