More than 25,000 products are capable of producing chemical burns.
Exposures occur both occupationally and during use of chemicals
for activities in daily life. It is estimated that chemical burns
account for 5% to 10% of all U.S. burn center
admissions. Nonoccupational exposures may number up to 100,000 per
year, the vast majority being minor. Deaths are rare (<1% of
exposures) and usually result from caustic ingestion. In 2008, there
were 5620 reported nonfatal chemical exposures in private industry
causing days missed from work, representing about 0.6% of
all injuries. There were 130 deaths from exposure to chemicals and
chemical products reported in private industry in 2008; 4 from acids
and 3 from alkalies.1 See http://www.bls.gov/iif/oshwc/osh/case/ostb2200.pdf.
Common household chemical burns are caused by lye (drain cleaners), paint
removers (halogenated hydrocarbons), phenols (deodorizers, sanitizers,
disinfectants), sodium hypochlorite (disinfectants, bleaches), methacrylic
acid (artificial nail products), and sulfuric acid (toilet bowl cleaners).
In industries, chemicals are used for cleaning, tanning, curing, extracting,
preserving, soldering, and other functions. The most commonly used
industrial acids are tungstic, picric, sulfosalicylic, tannic, formic,
sulfuric, acetic, cresylic, trichloroacetic, chromic, hydrochloric,
and hydrofluoric. Widely used alkalis are the hydroxide salts of
sodium, potassium, ammonium, lithium, barium, and calcium. White
phosphorus used in munitions was the most common cause of chemical
burns to military personnel during times of armed conflict in the
1960s, and was reported to be used as an incendiary in Fallujah,
Iraq, in 2004 and 2005. White phosphorus also may be found in rodenticides,
pesticides, and fireworks.
The body sites most often burned by chemicals are the face, eyes,
and extremities. In general, chemical burns are smaller than thermal
burns and the mortality rate is lower. However, wound healing and
duration of hospital stay are longer. Disability and time away from
work tend to be greater than that of other occupational injuries.
The skin is a barrier and transition zone between the internal
and external environments. Although the outer stratum corneum layer
of the skin functions as an excellent barrier against many chemicals,
some penetrate it readily. Chemicals can produce burns, dermatitis,
allergic reaction, thermal injury, or systemic toxicity.
Pathophysiologically, burns produced by all chemicals are similar
because the skin has a limited variety of toxic responses.2 Toxic
reactions are described mainly on the basis of morphologic rather
than functional responses.3 Skin has protective
mechanisms and elements, including the epidermal barrier, eccrine
sweating, phagocytic cells, metabolic detoxification, immunologic
processes, and melanin pigmentation (Figure 211-0.1)
However, these protective mechanisms vary according to phenotype and
may be affected by systemic or local disease.
Skin damage by chemicals may demonstrate the classic signs of
thermal injury (erythema, blistering, or full-thickness loss). Early
on, injuries may be deceptively mild, only to be followed by extensive
skin damage and systemic toxicity. A superficial (first-degree)
burn causes capillary and arterial dilatation. Initially, this involves
only the superficial vessels, but then vascular dilatation extends
to the deeper subcutaneous vessels. Tissue hyperemia and congestion
cause itching, burning, or pain. More extensive inflammatory reactions
cause an outpouring ...