Chemical Burns

< 5% of admissions to Burns Units. Typically occur in men of working age, workers in industry and
laboratories and in the building industry, wartime (eg phosphate). Usually a low %TBSA affected

Especially significant when the eyes are involved.

May be associated with GIT or respiratory problems.
Pathophysiology
1. Burn

Acids coagulates tissue protein causing coagulative necrosis. Unlike thermal burns, chemical
burns continue to cause damage until the agent is removed or neutralised.

Alkalis cause saponification followed by liquefaction necrosis. Some undergo exothermic
reaction when diluted leading to thermal damage.
2. Systemic toxicity

Electrolyte imbalances
Classification
1.
Oxidizing agents
a. White phosphorus
b. Peroxides
c. Chromates
d. Manganates
2.
Acids
a. Hydrofluoric acid
b. Sulfuric acid
c. Phenol
3.
Alkali
a. Calcium hydroxide (Cement burns)
b. Sodium hydroxide and potassium hydroxide
i. used in drain cleaners, oven cleaners
c. Sodium and calcium hypochlorite (pool solution)
d. Anhydrous ammonia
4.
Skin preparation agents
a. Providone iodine - usually occur in dependent parts of the body, such as the buttocks or
under a tourniquet, where the agent has not been allowed to dry. Irritation and long-term
pressure both appear to play roles in the pathogenesis of these injuries.
b. Alcohol-based skin cleansers such as chlorhexidine gluconate 0.5% in 70% methanol
Special situations

Elemental metals: The elemental forms of lithium, potassium, sodium, and magnesium react with
water. If these metals are thought to be on the skin of a patient, do not irrigate with water. The
metallic pieces should be removed manually with forceps and placed in a container of mineral oil.

White phosphorus: Keep the area immersed in water and manually remove any phosphorus particles
seen. Visualization under a Wood lamp may aid in detection and removal of retained phosphorus
particles. Copper sulphate irrigation used as an antidote.

Phenol: Phenol and cresols are more easily removed with polyethylene glycol or isopropyl alcohol. If
skin damage has already occurred, isopropyl alcohol may be very irritating. Polyethylene glycol
should be diluted with water to form a 50:50 ratio prior to using.
Inorganic acids
Hydroflouric acid

Used in pottery, glass, diamond and semiconductor industries
Pathophysiology

The 2 mechanisms that cause tissue damage
1. corrosive burn from the free hydrogen ions and chemical burn from tissue penetration of the
fluoride ions.
2. Fluoride ions penetrate and form insoluble salts with calcium and magnesium. Soluble salts
also are formed with other cations but dissociate rapidly. Consequently, with fluoride ions release
further tissue destruction occurs.

Fluoride anions may inhibit the Na-K-adenosine triphosphatase (ATPase) enzyme of the cell
membrane leading to potassium efflux. This ionic shift is thought to be responsible for the great
pain (often delayed) associated with hydrofluoric acid injuries because local nerve endings depleted of
calcium discharge frequently.

Dilute solutions deeply penetrate before dissociating, thus causing delayed injury and symptoms.
Burns to the fingers and nail beds may leave the overlying nails intact, and pain may be severe with
little surface abnormality. Severe burns with concentrations >50%.

Solutions of 14.5% immediately produce symptoms.

Solutions of 12% may take up to an hour to produce symptoms.

Solutions of less than 7% may take several hours before onset of symptoms, resulting in delayed
presentation, deeper penetration of the undissociated HF acid, and a more severe burn.

Concentrated solutions cause immediate pain and produce surface burns similar to those
produced by other common acids (eg, erythema, blistering, necrosis).

Pain often is disproportionate to apparent skin involvement.

As long as the active flouride is present the process will continue and systemic absorption of the
flouride will result in hypocalcaemia and hypophosphataemia - ECG abnormalities, VF and death.

The scab of the coagulative tissue necrosis may impede the acid extending deeper.

Inhalation of the gas causes pneumonitis.

Ingestion causes GIT necrosis.

Ocular lesions - ulcers, corneal loss, loss of vision, ectropion
Investigations

Check for hypocalcemia, hypomagnesemia and hyperkalemia

Monitor for QT prolongation from hypocalcemia or signs of hyperkalemia.
Management

Remove soiled clothing.

Decontaminate by irrigation with copious amounts of water.

Assess and manage life-threatening conditions as with any other cause.

Commence comprehensive monitoring for significant exposures.

With any evidence of hypocalcemia, immediately administer 10% calcium gluconate IV

Apply 2.5% calcium gluconate gel to the affected area. If the proprietary gel is not available,
constitute by dissolving 10% calcium gluconate solution in 3 times the volume of a water-soluble
lubricant (eg, KY gel). For burns to the fingers, retain gel in a latex glove.

Gel is continued to be massaged into the skin six times a day for 3−4 days.

If pain persists for more than 30 minutes after application of calcium gluconate gel, further
treatment is required. Subcutaneous injections of calcium gluconate is recommended at a dose of
0.5ml of a 10% solution per square centimeter of surface burn extending 0.5 cm beyond the margin
of involved tissue. Do not use Calcium chloride because it is an irritant and may cause tissue
damage.

Ocular burns: Generously irrigate with sterile water or saline for at least 5 minutes. Local anesthetic
may be required. If pain persists, irrigate with a 1% solution of calcium gluconate, which is made by
diluting the 10% solution in 10 times the volume of normal saline. Do not use undiluted 10% calcium
gluconate.

Digital burn - Local infiltration of digits is not recommended because of pain, disfigurement, and
potential complications. Alternative treatment methods:
1. IV regional calcium gluconate (Biers)
 10-15 mL of 10% calcium gluconate plus 5000 units of heparin diluted up to 40 mL in 5%
dextrose.
 Use a Bier ischemic arm block technique to infuse the solution intravenously.
 Release the cuff when any of the following conditions first occur: (1) pain from the digits
resolves, (2) the cuff becomes more painful than the burn, or (3) 20 minutes of ischemic
time elapses.
 Treatment can be repeated after 4 hours if needed.
2. Intra-arterial calcium gluconate:
 should be reserved for only the most severe cases of hydrofluoric acid burns
unresponsive to local therapy due to the potential damage to the arterial tree.
 probably of most value in digital burns where there is little subcutaneous space in which to
infiltrate the solution.
 Place an arterial catheter in the radial or brachial artery to perfuse the affected digits.
 Infuse a solution of 10 mL of 10% calcium gluconate in 40 mL of 5% dextrose over a 4hour period.
 Follow with further infusions repeated after 4-8 hours, if necessary.
3. Metabolic alkalosis with sodium bicarbonate may be induced to enhance renal excretion of
fluoride ions. Haemo-dialysis may be useful after excessive fluoride absorption to remove
fluoride anion and to correct abnormal serum chemistries.
Sulphuric acid

Action depends on concentration and duration of contact

The concentrated acid is very viscous and denser than water. It also generates significant heat when
diluted. These attributes make sulfuric acid an effective drain cleaner. Concentrated sulfuric acid is
hygroscopic. Thus, it produces dermal injuries by dehydration, thermal injury, and chemical
injury.

First aid - wash with copious amounts of water until the substance is completely removed; alkaline
neutralizers must NOT be used as they cause tissue destruction by means of exothermic reactions.

Results in coagulative necrosis and vascular thrombosis - dark bronze scabs.

Systemic absorption causes haemolysis, haemoglobinuria and renal failure (ATN) - this requires IV
fluid administration with bicarbonate +/- mannitol to ensure a forced diuresis.

The “cured leather” appearance of the skin makes determination of burn depth difficult - tissue
biopsies may be required.
Nitric acid

Action depends on concentration and duration of contact

First aid - wash with copious amounts of water until the substance is completely removed

Results in coagulative tissue necrosis
Phenol / Cresol

Cause coagulative necrosis due to their powerful hygroscopic nature

Deep dark scabs form

Systemic effects:
Haematuria, renal impairment
GIT haemorrhages
Liver impairment with raised transaminases
Anaemia
Dyspnoea
Hypotension

concentrated cresol can form a crust, which partly impedes its absorption, thus dilution alone can
worsen the situation and one must ensure that copious lavage removes ALL the cresol.

A similar situation arises when phenol is mixed with limited amounts of water or alcohol.
Polyethylene glycol and soapy water are recommended as solvents for phenol

Systemic deterioration may require:
IV fluids
Osmotic diuresis, dialysis
Correction of electrolyte disturbances
Antibiotics
Oxygen, assisted ventilation
Phosphorous

Usually in wars / terrorist acts

First aid - wash with copious amounts of soapy water and remove all particle.

These burns are caused by the reaction of phosphorous with oxygen and will continue to burn as long
as the phosphorous is in contact with the tissue. Therefore all the phosphorous particles must be
removed (a Wood’s lamp may be helpful).

Can cover with petroleum jelly to stop combustion.

Systemic absorption causes alterations in levels of PO4-2 and Ca+2 - ECG abnormalities, bradycardia,
arrhythmias, haemolysis, haematuria, haemoglobinuria - renal failure. Monitoring is essential.
Inorganic alkalis

Action depends on concentration and duration of contact. Produce late effects

mechanism by which these alkali injuries are caused is due to three factors:
1. saponification of fat causes fatty tissue to lose its function with increased damage due to heat
reaction.
2. extraction of water from cells causing dessication
3. bind with the proteins of the tissues to form alkaline proteinates.
Sodium hydroxide

Great destructive and penetrative ability. Produces very deep burns, tissue damage and deep ulcers
until the substance is neutralized.

First aid - wash with copious amounts of water until the substance is completely removed, or use
weak acidic solutions eg 1% acetic acid in paraffin (water increases penetration)
Calcium hydroxide (Lime)

Common after kneeling in wet cement for prolonged period - typical distribution of injury involving
the knees and lower legs

Insidious onset. Most patients comment that they notice only mild irritation initially. Cement contains
lime (calcium oxide), which will potentially penetrate clothing and react with sweat causing an
exothermic reaction.

Even when not exposed to moisture, the dry powder is very hygroscopic and may also cause a
desiccation injury. Hydrated calcium oxide becomes calcium hydroxide that causes skin damage
primarily due to the hydroxyl ion.

In lime burns, the dry lime must be brushed away before washing in order to minimize the production
of heat. If cement is not removed from the skin it continues to corrode and often painlessly
deepens necrosis under clothing.

Great destructive and penetrative ability producing very deep burns

Produce tissue damage and deep ulcers until the substance is neutralized
Overall treatment plan
On site

Remove patient from substance first priority in treatment is to ensure complete removal of the
offending agent. Thorough decontamination is key.

Prevent contaminated irrigation solution from running onto unaffected skin.

Remove soaked clothing

Wash with copious amounts of tepid water unless contra-indicated (eg sodium) - A burn center case
series found that patients who received irrigation within 10 minutes had a 5-fold decrease in fullthickness injury and a 2-fold decrease in length of hospital stay (Leonard, 1982).

Lavage has a threefold effect.
1. dilutes a chemical already in contact with the skin, washes unreacted agent from the skin and
helps correct the hygroscopic effects that some agents have on tissues.
2.
shown to reduce hospital stay
3. reduce the extent of full-thickness injury.

Any patient having 'copious lavage' is in danger of suffering induced hypothermia. Core and
peripheral temperatures should be monitored, room temperatures maintained between 31 and 33°C
and the lavage water kept as near to body temperature as possible.

Wash the eyes copiously

Identify the substance

Cover burn with moist saline swabs / Burnshield
Casualty unit

IV fluids (unless very small burn) +/- osmotic diuresis

Analgesia

Oxygen

Neutralization of the substance if the antidote is known (use pH strips to help)
Burns unit

Specialist treatment as required e.g. dialysis

Local burn wound treatment e.g. topical dressings, excision and grafting
Ocular involvement

First line treatment is treat with topical anesthetics followed by copious irrigation, induction of
cycloplegia and mydriasis as soon as possible.

Alkalis tend to cause more severe damage due to their capacity to saponify lipids, thus going deeper
into ocular structures, denaturing collagen and causing vascular thromboses

Acids tend to invoke protein precipitation and a crust, which may act as a barrier

Titanium tetrachloride (ceramics and plastics industries) can cause burns as severe as those of alkalis

Lesions caused include:
1. Corneal ulcers/opacities
2. Perforations
3. Glaucoma
4. Lacrimal obstruction
5. Ectropion/entropion

An ophthalmologist should be involved in the treatment which may include:
1. Topical steroids/antibiotics/mydriatics
2. Topical anaesthesia initially