buEdgar J. Pierre, Steven E. Wolf
Nonthermal burns differ from thermal injuries in many ways, however the
results are similar, soft tissue damage. These nonthermal injuries consist of burns
from chemicals and injuries from electrical current. While thermal injury damages
tissue by the transfer of heat, chemicals and electricity damage tissue by transfer
of potential energy from chemical reactions and transfer of electrical energy respectively.
It must be pointed out that thermal injury produced by chemical reactions
and heat developed by resistance to electrical current can cause secondary
damage in these injuries.
CHEMICAL BURNS
Most chemical burns are accidental from mishandling of household cleaners,
although some of the most dramatic presentations involve industrial exposures.
In the scope of this chapter, it is impossible to address the many thousands of
agents which may be encountered, and for this reason only the most common are
reviewed here.
Thermal burns are in general short-term exposures to heat, but chemical injuries
may be of longer duration, even for hours in the absence of appropriate treatment.
The degree of tissue damage as well as the level of toxicity is determined by
the chemical nature of an agent, concentration, and the duration of skin contact.1
Chemicals cause their injury by protein destruction, with denaturation, oxidation,
formation of protein esters, or desiccation of the tissue. In the
of most household and industrial chemicals can be obtained from the
Speed is essential in the management of chemical burns. For all chemicals,
lavage with copious quantities of clean water should be done immediately after
removing all clothing. Dry powders should be brushed from the affected areas
before irrigation. Early irrigation dilutes the chemical which is already in contact
with the skin, and timeliness increases effectiveness of irrigation. For example,
10 ml of 98% sulfuric acid dissolved in 12 liters of water will decrease the pH to
5.0, a range which can still cause injury. If the chemical composition is known
(acid or base), monitoring of the spent lavage solution pH will give a good indication
of lavage effectiveness and completion. A good rule of thumb is to lavage
with 15-20 liters of tap water or more for significant chemical injuries. The lavage
site should be kept drained in order to remove the earlier, more concentrated
effluent. Care should be taken to drain away from uninjured areas to avoid further
exposure.
All patients should be monitored according to the severity of their injuries.
They may have metabolic disturbances, usually from pH abnormalities because
of exposure to strong acids or caustics. If respiratory difficulty is apparent, oxygen
therapy and mechanical ventilation must be instituted. Resuscitation should be
guided by the body surface area involved (burn formulas); however, the total fluid
needs may be dramatically different from the calculated volumes. Some of these
injuries may be more superficial than they appear, particularly in the case of acids,
and therefore will require less resuscitation volume. Injuries from bases, however,
may penetrate beyond that which is apparent on exam and therefore will require
more volume. For this reason, patients with chemical injuries should be observed
closely for signs of adequate perfusion, such as urine output. All patients with
significant chemical injuries should be monitored with indwelling bladder catheters
to accurately measure the outputs.
Operative debridement if indicated should take place as soon as a patient is
stable and resuscitated. Following adequate lavage and debridement of those
wounds treated nonoperatively, burn wounds are covered with antimicrobial agents
or skin substitutes. Once the wounds have stabilized with the indicated treatment,
they are taken care of as with any loss of soft tissue. Skin grafting or flap coverage
are performed as needed.
SPECIFIC CHEMICALS
ALKALI
Alkalies such as lime, potassium hydroxide, bleach, and sodium hydroxide are
among the most common agents involved in chemical injury. Accidental injury
frequently occurs in infants and toddlers exploring cleaning cabinets. There are
three factors involved in the mechanism of alkali burns: 1) saponification of fat
causes the loss of insulation of heat formed in the chemical reaction with tissue;
2) massive extraction of water from cells causes damage because of alkali’s hygroscopic
nature; and 3) alkalis dissolve and combine with the proteins of the tissues
to form alkaline proteinates, which are soluble and contain hydroxide ions. These
ions induce further chemical reactions, penetrating deeper into the tissue.2 Treatment
involves immediate removal of the causative agent with lavage of large volumes
of fluid, usually water. Attempts to neutralize alkali agents with weak acids
are not recommended, because the heat released by neutralization reactions induces
further injury. Particularly strong bases should be treated with lavage and
consideration of wound debridement in the operating room. Tangential removal
of affected areas is performed until the tissues removed are at a normal pH.
CEMENT
Cement (calcium oxide) burns are frequent, and they are usually work-related.
Such a burn is similar to an alkali injury, and the critical substance responsible for
the skin damage is the hydroxyl ion.3 Oftentimes, the agent has been in contact
with the skin for prolonged periods, such as underneath the boots of a cement
worker who seeks treatment hours after the exposure, or after the cement penetrates
clothing and when combined with perspiration induces an exothermic reaction.
Treatment consists of removing all clothing and irrigating the affected area
with water and soap until all the cement is removed and the effluent has a pH of
less than 8. Injuries tend to be deep because of exposure times, and surgical excision
and grafting of the resultant eschar may be required.
ACIDS
Acid injuries are treated initially like any other chemical injury, with removal
of all chemicals by disrobing the affected area and copious irrigation. Acids induce
protein breakdown by hydrolysis, which results in a hard eschar that does
not penetrate as deeply as the alkalis. These agents also induce thermal injury by
heat generation with contact of the skin, further causing soft tissue damage. Some
acids have added effects, such as calcium chelation by phosphoric and hydrofluoric
acid. Common acids causing injuries and their mechanisms of action are listed
below in Table 10.1.
Table 10.1. Common acids and their peculiarities
Acid Uses and Mechanism of Action
Acetic Acid Glacial acetic acid is the 100% form, the 5% form is
known as vinegar, typical acid burn
Chromic Acid Metal cleaner in a strong sulfuric acid solution, typical
acid burn
Dichromate Salts Corrosive agents, surgical debridement should be
entertained (lethal dose 50 mg/kg)
Hydrochloric Acid Typical acid burn, fumes can cause a pneumonitis
Muriatic Acid Commercial grade hydrochloric acid
Nitric Acid Strong acid, can form organo-nitrate compounds
Oxalic Acid Binds calcium salts, treat like a hydrofluoric acid burn
Phosphoric Acid Binds calcium salts, treat like a hydrofluoric acid burn
Sulfosalicylic Acid Typical acid burn, systemic absorption may cause renal
and hepatic toxicity
Sulfuric Acid Typical strong acid burn
Tannic Acid Typical acid burn, systemic absorption may cause renal
and hepatic toxicity
Trichloroacetic Acid Typical acid burn, systemic absorption may cause renal
and hepatic toxicity
FORMIC ACID
Formic acid injuries are relatively rare, usually involving an organic acid used
for industrial descaling and as a hay preservative.4 Electrolyte abnormalities are of
great concern for patients who have sustained extensive formic acid injuries, with
metabolic acidosis, renal failure, intravascular hemolysis, and pulmonary complications
(ARDS) common.5 Acidemia detected by a metabolic acidosis on arterial
blood gas analysis should be corrected with intravenous sodium bicarbonate. Hemodialysis
may be required when extensive absorption of formic acid has occurred.
Mannitol diuresis is required if severe hemolysis occurs after deep injury.
A formic acid wound typically has a greenish appearance, and is deeper than what
it initially appears to be; it is best treated by surgical excision.
HYDROFLUORIC ACID
Hydrofluoric acid is a toxic substance used widely in both industrial and domestic
settings, and is the strongest inorganic acid known. Management of these
burns differs from other acid burns in general. Hydrofluoric acid produces dehydration
and corrosion of tissue with free hydrogen ions. In addition, the fluoride
ion complexes with bivalent cations such as calcium and magnesium to form insoluble
salts. Systemic absorption of the fluoride ion then can induce intravascular
calcium chelation and hypocalcemia, which causes life-threatening arrhythmias.
Beyond initial copious irrigation with clean water, the burned area should be treated
immediately with copious 2.5% calcium gluconate gel. These wounds in general
are very painful because of the calcium chelation and associated potassium release.
This finding can be used to determine the effectiveness of treatment. The gel
should be changed at 15-minute intervals until the pain subsides, an indication of
removal of the active fluoride ion. If pain relief is incomplete after several applications
or symptoms recur, intradermal injections of 10% calcium gluconate
(0.5 ml/cm2 affected), and/or intra-arterial calcium gluconate into the affected
extremity may be required to alleviate symptoms. If the burn is not treated in
such a fashion, decalcification of the bone underlying the injury and extension of
the soft tissue injury may occur.
All patients with hydrofluoric acid burns should be admitted with electrical
cardiogram monitoring, with particular attention to prolongation of the QT interval.
Twenty ml of 10% calcium gluconate solution should be added to the first
liter of resuscitation fluid,6 and serum electrolytes must be closely monitored. Any
EKG changes require a rapid response by the treatment team with intravenous
calcium chloride to maintain heart function. Several grams of calcium may be
required in the end until the chemical response has run its course. Serum magnesium
and potassium also should be closely monitored and replaced. Speed is the
key to effective treatment of this chemical injury.
HYDROCARBONS
The organic solvent properties of hydrocarbons promote cell membrane dissolution
and skin necrosis. Symptoms present with erythema and blistering, and
the burns are typically superficial and heal spontaneously. If absorbed systemically,
toxicity can produce respiratory depression and eventual hepatic injury
thought to be associated with benzenes. Ignition of the hydrocarbons on the skin
induces a deep full-thickness injury.
ELECTRICAL INJURY
Three to five percent of all admitted burned patients are injured from electrical
contact. Electrical injury is unlike other burn injuries as the visible areas of
tissue necrosis represent only a small portion of the destroyed tissue. Electrical
current enters a part of the body, such as the fingers or hand, and proceeds through
tissues with the lowest resistance to current, generally the nerves, blood vessels,
and muscles. The skin has a relatively high resistance to electrical current, and is
therefore mostly spared. The current then leaves the body at a “grounded” area,
typically the foot. Heat generated by the transfer of electrical current and passage
of the current itself injures the tissues. During this exchange, the bone is a sink for
the generated heat from the surrounding muscle and serves as a source of additional
and continued thermal damage in the ensuing moments. Blood vessels transmitting
much of the electricity initially remain patent, but may proceed down a
path of progressive thrombosis as the cells either die or repair themselves. For
these reasons, most of the damaged tissue is not visible.
Injuries are divided into high and low voltage injuries. Low voltage injury is
similar to thermal injury without transmission to the deeper tissues and exhibits
zones of injury from the surface extending into the tissue.7 Most household currents
(110-220 volts) produce this type of injury, which only causes local damage.
The worst of these injuries are those involving the edge of the mouth (oral commissure)
sustained by children gnawing on household electrical cords.
The syndrome of high voltage injury consists of varying degrees of cutaneous
burn at the entry and exit sites combined with hidden destruction of deep tissue.
8,9 Oftentimes, these patients will also have cutaneous burns associated with
ignition of clothing from the discharge of electrical current. Initial evaluation may
consist of cardiopulmonary resuscitation from induced ventricular fibrillation;
thus if the initial electrocardiogram (ECG) findings are abnormal or there is a
history of cardiac arrest associated with the injury, continued cardiac monitoring
is necessary along with pharmacological treatment for any dysrhythmias.10 The
most serious derangements occur in the first 24 h after injury. If patients with
electrical injuries have no cardiac dysrhythmias on initial ECG or history of cardiac
arrest, no further monitoring is necessary.
Patients with electrical injuries are at risk for other injuries associated with
being thrown from the electrical jolt, or from falls from heights in an effort to
disengage from the electrical current. In addition, the violent tetanic muscular
contractions which result from alternating current sources may cause a variety of
fractures and dislocations.11 These patients should be assessed as would any patients
with blunt traumatic injuries. Intra-abdominal injuries with bowel disruption are
also reported with high-voltage injuries; therefore attention to this possible complication
should take place.
The key to managing patients with an electrical injury lies in the treatment of
the wound. The most significant injury is within the deep tissue, and subsequent
edema formation can cause vascular compromise to any area distal to the injury.
Assessment should include circulation to distal vascular beds, as immediate
escharotomy and fasciotomy may be required. Should the muscle compartment
be extensively injured and necrotic such that the prospects for eventual function
are dismal, early amputation may be necessary. We advocate early exploration of
affected muscle beds and debridement of devitalized tissues, with attention to the
deeper periosteous planes, as this is the area with continued damage from the
heated bones. Fasciotomies should be complete, and may require nerve decompressions,
such as carpal tunnel and Guyon’s canal releases. Tissue that has questionable
viability should be left in place, with planned re-exploration in 48 h. Many
such re-explorations may be required until the wound is completely debrided.
After the devitalized tissues are removed, closure of the wound becomes paramount.
Although skin grafts will suffice as closure for most wounds, flaps may
offer a better alternative, particularly with exposed bones and tendons. Even exposed
and superficially infected bones and tendons can be salvaged with coverage
by vascular tissue. Early involvement by reconstructive surgeons versed in the various
methods of wound closure is optimal.
Muscle damage results in release of hemochromogens (myoglobin), which are
filtered in the glomeruli and may result in obstructive nephropathy. Therefore,
vigorous hydration and infusion of intravenous sodium bicarbonate (5% continuous
infusion) and mannitol (25 gms every 6 h for adults) are indicated to
solubilize the hemochromogens and maintain urine output if significant amounts
are found in the serum. These patients also will require additional intravenous
volumes over predicted amounts based on the wound area because most of the
wound is deep, and cannot be assessed by standard physical examination. In this
situation, urine output should be maintained at 2 cc/kg/h.
DELAYED EFFECTS
Neurological deficits may occur. Serial neurological evaluations should be performed
as part of routine examination in order to detect any early or late neuropathology.
Central nervous system effects such as cortical encephalopathy, hemiplegia,
aphasia, and brain stem dysfunction injury have been reported up to 9 months
after injury,12 and others report delayed peripheral nerve lesions characterized by
demyelination with vacuolization and reactive gliosis. Another devastating long
term effect is the development of cataracts, which can be delayed for several years.
These complications may occur in up to 30% of patients with significant highvoltage
injury, and patients should be made aware of their possibility even with
the best treatment.
SUMMARY
Chemical and electrical injuries represent a challenge to the treating surgeons,
with some deviations from typical burn care as described above. The long-term
goals, however, remain the same. Namely, timely intervention to save life and limb,
followed by efforts to maximize functional and cosmetic outcome.
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