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 Plastic Surgery for Chemical Burns

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Plastic Surgery for Chemical Burns

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injuries are commonly encountered following exposure to acids and
alkali, including hydrofluoric acid (HF), formic acid, anhydrous
ammonia, cement, and phenol. Other specific chemical agents that cause
chemical burns include white phosphorus, elemental metals, nitrates,
hydrocarbons, and tar. Since World War II, the number of
chemicals developed, produced, and used in the United States has
increased dramatically. More than 65,000 chemicals are available on the
market, and an estimated 60,000 new chemicals are produced each year.
Unfortunately, the potential deleterious effects on human health of many
of these chemicals are unknown. The Superfund Amendments and
Reauthorization Act (SARA) contains extensive provisions for emergency
planning and the rights of communities to be informed of toxic chemical
releases.[1] In
addition to individualized state health departments, the following 5
national sources provide information regarding death and injuries caused
by chemical releases: National Response Center (NRC), Department of
Transportation (DOT), Hazardous Materials Information System (HMIS),
Acute Hazardous Events (AHE) Database, and American Poison Control
Centers Association.[2] Health
departments from 5 states (Colorado, Iowa, Michigan, New Hampshire, and
Wisconsin) evaluated 3,125 emergency chemical-release events involving
4,034 hazardous substances that occurred from 1990-1992. Of these
events, 77% involved stationary facilities and 23% were
transportation-related. In 88% of events, a single chemical was
released. The most commonly released hazardous substances were volatile
organic compounds (18%), herbicides (15%), acids (14%), and ammonia
(11%). These events resulted in 1,446 injuries and 11 deaths.
Respiratory irritation (37%) and eye irritation (23%) were the most
commonly reported symptoms. Chemical exposures also can occur at home or
as the result of an attack. Many common products once believed
to be innocuous (eg, cement, gasoline) are now regarded as potentially
hazardous and as the cause of serious injury and illness. Exposure to
these agents can be reduced significantly through educational programs,
cautionary labeling of toxic products, and appropriate use of protective
clothing. When poison control centers identify new products that
are toxic to skin, information is added to the regional poison
information system to ensure that injured patients are given the benefit
of new data. Concomitantly, this information is shared with the
manufacturer and Consumer Product Safety Commission (CPSC) to recognize
and address the problem nationally. For example, numerous cases of
serious permanent injury and, occasionally, death caused by exposure to
sulfuric acid drain cleaners have been recorded by the CPSC. As a result
of this alarming problem, the CPSC currently proposes banning the sale
of this product to consumers. For excellent patient education resources, visit eMedicine's Burns Center. Also, see eMedicine's patient education articles Chemical Burns and Thermal (Heat or Fire) Burns.
Next Section: Pathophysiology


chemical agents damage the skin by producing a chemical reaction rather
than hyperthermic injury. Although some chemicals produce considerable
heat as the result of an exothermic reaction when they come into contact
with water, their ability to produce direct chemical changes on the
skin accounts for most significant injury. Specific chemical changes
depend on the agent, including acids, alkalis, corrosives, oxidizing and
reducing agents, desiccants and vesicants, and protoplasmic poisons.
The concentration of toxic agent and duration of its contact primarily
determine the degree of skin destruction. When the skin is exposed to
toxic chemicals, its keratinous covering is destroyed, and underlying
dermal tissues are exposed to continuous necrotizing action. Both
inorganic and organic acids denature the proteins of the skin,
resulting in a coagulum, the color of which depends on the acid
involved. Nitric acid burns result in a yellow eschar, whereas sulfuric
acid eschar is black or brown. Burns caused by hydrochloric acid or
phenol tend to range from white to grayish-brown. Following the initial
exposure, cellular dehydration and further protein
denaturation/coagulation occur. This dehydrative effect results in the
characteristic dry surface of acid burns. The method(s) of
neutralization used in the treatment of acid burns depend on the nature
of the acid. Alkali burns are those caused by lime (cement),
ammonia, and caustics (sodium hydroxide, potassium hydroxide). Alkali
dissolves protein and collagen, resulting in alkaline complexes of these
molecules. Cellular dehydration (as in acid burns) and saponification
of fatty tissue also occurs. Whereas acid burns are characterized as
"dry" burns, with little fluid loss or edema, alkali burns present with
marked edema and extensive fluid loss. Neutralization of alkali exposure
is accomplished by first irrigating the burned site with a large amount
of water to dilute any unreacted alkali remaining on the wound surface.
This protects the wound from further damage caused by heat released
during the neutralization reaction. After skin contact, absorption of some agents may cause systemic toxicity. Dichromate poisoning produces liver failure, acute tubular necrosis, and death. Oxalic acid and HF injuries may result in hypocalcemia.
Tannic and phosphorous burns may be followed by nephrotoxicity.
Absorption of phenol may be associated with CNS depression and
hypotension. Inhalation injury may result from exposure to toxic fumes,
particularly when the exposure occurs within a closed space.
Next Section: Pathophysiology

Community Preparedness and HAZMAT Response

materials (HAZMAT) are substances that may injure life and damage
environment if improperly handled. These substances can be encountered
in the home, in urban (industrial) areas, in rural (agricultural) areas,
or anywhere involving the release of hazardous material. HAZMAT
accidents are particularly dangerous for responding personnel, who are
in danger of exposure from the time of arrival on the scene until
containment of the accident. The surrounding community also is commonly
endangered. The Superfund Amendment and Reauthorization Act (SARA)
mandates community preparedness for dealing with HAZMAT accidents.[1] Before
a community develops its plans for responding to HAZMAT accidents, it
needs to determine what types of materials are likely to be involved. For
those exposed to potentially dangerous chemicals at home, it is best to
remove the chemical from the anatomic site by irrigation with copious
amounts of water. A friend or relative must then telephone the regional
poison control center certified by the American Association of Poison
Control Centers.[3, 4] If
the chemical is judged dangerous, make arrangements to transfer the
exposed person to the nearest emergency department (ED) for definitive
care. Notify the ED as soon as possible after the accident to allow
staff to prepare to receive the patient.
Identify and assess hazardous environment

and members of the HAZMAT response team (usually firefighters) must
work together to identify toxic chemicals and assess hazardous
environments. Placards, shipping papers, United Nations chemical
identification numbers, and markings on shipping containers help
identify hazardous agents. In some cases, members of the HAZMAT team may
have to use chemical analysis to identify the agent. The presence of
carbon monoxide, cyanide, hydrogen sulfide, oxygen, and combustible
gases can be detected using different instruments. Colorimetric
detector tubes can approximate the concentrations of chemicals in the
air. Alpha, beta, and gamma radiation detectors can record radioactive
contamination. Contacting the 24-hour hotline of Chemtrec (Chemical
Manufacturers Association, Washington, DC, 1-800-424-9300) can provide
helpful information regarding identification and management of HAZMAT.
At the scene of the incident, members of the HAZMAT team should wear a
self-contained breathing apparatus (SCBA) and protective apparel.
Contingency plan

contingency plan for HAZMAT management can be divided into 2 parts:
initiation of the site plan and evacuation. Initiation of the site plan
begins after identifying HAZMAT and assessing the surrounding
environment. Once HAZMAT is identified, determine health risks to the
environment. A command post away from the exposure site is essential to a
large incident involving HAZMAT, because it allows paramedics, HAZMAT
team members, firefighters, police, representatives from state and local
government, and manufacturer and shipper to coordinate activities.
Coping with HAZMAT incidents

coping with HAZMAT incidents, 2 distinct goals must be achieved
concomitantly. First, HAZMAT must be contained, fire and explosions must
be extinguished, and the site eventually must be cleaned. Second, those
exposed to HAZMAT must be treated. The first priority in the care of
people exposed to HAZMAT is decontamination, which is initiated by
removing the victim's clothes and isolating them in plastic bags. Liquid
chemicals are washed off the victim's body with water, whereas dry
chemicals are first brushed off, followed by copious water irrigation
delivered under low pressures. Priority of decontamination should
progress from cleansing of contaminated wounds to eyes, mucous
membranes, skin, and hair. While performing decontamination,
conduct a primary and secondary survey of the patient to detect
life-threatening injuries and take appropriate steps to stabilize the
patient's condition (eg, administer oxygen to dyspneic patients).
Ideally, patients should be thoroughly decontaminated before arrival in
the ED. Hospital personnel involved in decontamination should
wear chemical-resistant clothing with built-in hood and boots, at least 2
layers of gloves, protective eyewear, and some form of respiratory
protection. The minimum level of respiratory protection for hospital
personnel during decontamination has not been established.
Next Section: Pathophysiology
Acids and Alkali

Chemical Burns

Chemical burns continue to destroy tissue until the causative agent is inactivated or removed.[5] For
example, when hydrotherapy is initiated within 1 minute after skin
contact with either an acid or alkali, severity of the skin injury is
far less than when treatment is delayed for 3 minutes. Early treatment
is followed by a return of skin pH to normal. When contact time exceeds 1
hour, the pH level of a sodium hydroxide (NaOH) burn cannot be
reversed. Similarly, brief washing of a hydrochloric acid (HCl) burn
more than 15 minutes after exposure does not significantly alter acidity
of damaged skin. Because contact time is a critical determinant
of the severity of injury for skin exposed to a toxic liquid chemical,
an exposed person or a witness to the injury must initiate hydrotherapy
immediately. When workers' clothes are soaked with such agents, valuable
time is lost if their clothing is removed before copious washing
commences. Gentle irrigation with a large volume of water under low
pressure for a long time dilutes the toxic agent and washes it out of
the skin. During hydrotherapy, the rescuer should remove the patient's
clothes and wear powder-free, latex-free, emergency medical examination
gloves to prevent hand contact with the chemical(s).Emergency
medical technicians, paramedics, firefighters, and emergency department
(ED) personnel must wear latex-free emergency medical examination gloves
to avoid eliciting an allergic reaction in the latex-sensitized
patient.[6] Most
emergency medical technicians, paramedics, and firefighters are now
wearing powder-free emergency medical examination gloves that comply
with the stringent codes and standards established by the National Fire
Protection Association (NFPA), while very few hospital ED personnel have
been provided with NFPA-approved gloves.Four well-defined goals
assist emergency medical services, fire departments, and hospitals in
the selection and purchase of emergency medical examination gloves.
First, the purchasing department must understand the stringent
regulations for such gloves outlined by the NFPA. This design and
performance standard was devised by the NFPA to address protective
clothing for emergency medical operations. The requirements were
described by the NFPA in 1999, in Standard on Protective Clothing for Emergency Medical Operations, 1997 edition. The revised 2003 edition can be viewed here.
Design requirements emphasize that at least 5 different sizes of gloves
must be available. Performance requirements include liquid-tight
integrity, biopenetration resistance, puncture resistance, soluble latex
protein content, dexterity, and ultimate elongation and tensile
strength.Second, the purchasing department must be familiar with
the 2 certification organizations that certify that emergency medical
examination gloves comply with the stringent NFPA design and performance
requirements reviewed in the 2003 edition. Recommendations have been
made to the NFPA committee to revise the 2003 edition to contain more
information on the design and performance requirements for emergency
medical examination gloves. Familiarity with these certification
organizations allows the purchasing agents of fire departments,
ambulance services, and hospital EDs to select the best powder-free
emergency medical examination gloves for their health care workers.Third,
purchasing agents must have information about the certified
manufacturers of emergency medical examination gloves that can assist
purchasing organizations in the glove selection process.Finally,
the exemplary efforts of FirstLine LLC (Buellton, Ca) in providing
comprehensive information about the performance and specification of a
wide range of emergency medical examination gloves should be emphasized.
The fit of the glove as well as its textured finish are key
considerations in the selection of emergency medical examination gloves.
Note that the uniform fit of the Intercept Elite nitrile emergency
medical examination glove extends beyond the wrist crease. Remember that
the finger tips of these nitrile gloves have a finish that enhances the
dexterity of the emergency medical health care worker. Hydrotherapy

exposure to strong alkali, prolonged hydrotherapy is especially
important to limit severity of injury. In experimental animals, the pH
level of chemically burned skin does not approach normal concentration
unless more than 1 hour of continuous irrigation has been maintained,
and it often does not return to normal for 12 hours despite
hydrotherapy. This differs from HCl skin burns, in which the pH level
usually returns to normal within 2 hours after initiating hydrotherapy. The
mechanism by which NaOH maintains an alkaline pH level despite
treatment is related to byproducts of its chemical reaction to skin.
Alkalis combine with proteins or fats in tissue to form soluble protein
complexes or soaps. These complexes permit passage of hydroxyl ions deep
into the tissue, limiting their contact with water diluent on the skin
surface. Conversely, acids do not form complexes, and their free
hydrogen ions are easily neutralized. Regardless of causative
agent, continue hydrotherapy once the patient arrives in the ED. If the
chemical is localized in the patient's hand, immerse the injured part in
a sink under flowing tap water. For other anatomic sites, place them
supine in a hydrotherapy tank in which the temperature of the water can
be regulated. Continue hydrotherapy treatment for 2-3 hours for acid
burns and for at least 12 hours for strong alkali burns. When the
patient's clothing comes in contact with solid chemical (eg, lye),
remove contaminated clothing before instituting hydrotherapy. Remove all
visible solid particles from the patient's skin during copious
irrigation with water. Deliver water to the wound at the lowest possible
pressure, because high-pressure irrigation (shower) may disperse liquid
or solid chemical into the patient's or rescuer's eyes. Water Is the Agent of Choice

is the agent of choice for decontaminating acid and alkali skin burns.
Deleterious effects of attempting to neutralize acid and alkali burns
were first noted in experimental animals in 1927.[7] In
every instance, animals with alkali or acid burns that were washed with
water survived longer than animals treated with chemical neutralizers.
The additional trauma of the heat generated by the neutralization
reaction superimposed on the already existing burn accounts for the
striking difference between the results of these 2 treatment methods.
The same effect may occur when certain chemicals contact water, yet
large volumes of water tend to limit this exothermic reaction. Surgeons
are beginning to question the belief that neutralization of an alkaline
burn of the skin with acid does, indeed, increase tissue damage due to
the exothermic nature of acid-based reactions.[8] In
experimental studies in animals, surgeons demonstrated that topical
treatment of alkaline burns with a weak acid such as 5% acetic acid (ie,
household vinegar) resulted in rapid tissue neutralization and
reduction of tissue injury in comparison to water irrigation alone. The
observed benefits of treating alkaline burns with 5% acetic acid in the
rat model are significant and require clinical testing. Treating Acid and Alkali Eye Injuries

Acid and alkali injuries involving the eye are among the most disastrous of chemical burns.[9] Regardless
of the nature of chemical involved, the primary goal is to immediately
institute copious irrigation. At the scene of the injury, the exposed
person should submerge his or her eyes in a container of tap water and
continuously open and close them. In the absence of a container, hold
face and eyes beneath a faucet and continuously irrigate with water. If
possible, maintain irrigation during transport to hospital. In
the ED, subject the eye to immediate hydrotherapy. This is most easily
accomplished using a low-flow stream of 0.9% NaCl from intravenous (IV)
tubing. The patient's response to chemical spillage into the eye can
frustrate emergency treatment: responses include severe blepharospasm,
tearing, and forceful rubbing of the eye. Topical anesthetic agents
help limit pain and improve patient cooperation. Lid retractors may be
necessary to evert eyelids and ensure adequate evaluation and irrigation
of conjunctival sac. First, remove any foreign material or solid
chemical. Continue irrigation until the pH level of the conjunctival sac
returns to its physiologic level (pH 7.4). Monitor the pH level of the
conjunctival sac with a Ninhydrin reagent strip. Compare the pH levels
of the affected and unaffected eye. After irrigation, stain eyes
with fluorescein to detect corneal injury. Then perform slit-lamp
examination of the eye with corneal injury to determine the extent of
damage to the anterior segment of the eye and anterior third of the
vitreous chamber. Initial slit-lamp examination of alkali burn often
reveals corneal erosion, swelling of the corneal epithelium, and
clouding of the anterior chamber. Treat all eyes that demonstrate
corneal abrasion with a broad-spectrum antibiotic emollient instilled in
the conjunctival sac (eg, chloramphenicol, gentamicin). Ophthalmologic
consultation and close follow-up care are warranted in all significant
exposures, and hospitalization for continuous irrigation occasionally
may be required. (For more information, see eMedicine Ophthalmology
article Burns, Chemical.)
Measure intraocular pressure serially to detect pressure increases.
Occasionally treat the injured eye with long-acting cycloplegic,
mydriatic, and carbonic anhydrase inhibitor for 2 weeks or until pain
disappears. This treatment decreases the potential for pupillary
constriction, increased intraocular pressure, and early glaucoma. Encourage mobility of the globe to avoid development of conjunctival adhesions (symblepharon). Ocular
chemical injury remains one of the most difficult ocular emergencies.
The prognosis for a burned eye depends not only on the severity of the
injury, but also on the rapidity and mode of treatment. Recently,
amniotic membrane patching (AMP) has been demonstrated to be useful
toward achieving a desirable outcome for acute ocular chemical burns.
The human placenta was obtained shortly after elective caesarean
delivery from a donor mother. Human immunodeficiency virus, hepatitis virus type B, hepatitis virus type C, and syphilis
were serologically excluded. Temporary AMP with modifications in suture
placement was performed in patients inflicted with acute chemical
injury. Clinical results suggest that immediate AMP is quite useful for
managing moderately severe acute ocular chemical injury by facilitating
rapid epithelialization and pain relief and by securing ocular surface
Effects of Alkali Burns

Alkali substances are
the most toxic chemicals, and anhydrous ammonia appears to be the worst
offender. Even alkali burns that seem mild can result in devastating
injury, because alkalis tend to react with the lipid in corneal
epithelial cells to form soluble soap that penetrates corneal stroma.
Alkali moves rapidly through the stroma and endothelial cells to enter
the anterior chamber. Anhydrous ammonia can penetrate the anterior
chamber in less than 1 minute. Alkali usually kills each tissue
layer of the anterior segment of the eye that it contacts. This results
in occlusive vasculitis around the corneoscleral limbus, which makes
repair of these tissues difficult. As the tissues of the anterior
segment of the eye degenerate, perforation follows with the development
of endophthalmitis and loss of the eye. If perforation can be prevented,
recovery of sight may be possible through eventual corneal
transplantation. Recent experimental studies conclude that destruction
of corneal stroma can be minimized by drug therapy (eg,
N-acetylcysteine, steroids). However, drug therapy has limited
therapeutic usefulness because of the need for frequent applications,
significant number of clinical failures, and potential adverse effects.
Management of Ingested Alkali

esophagitis has been a long-lasting problem, especially in
olive-producing areas. In recent years, household lye products have come
into routine use and have unfortunately been associated with increased
frequency of caustic esophagitis induced by accidental ingestion.
Frequently, the concentration of the ingested agent is unknown because
of the absence of manufacturers' labels on the containers. The victims
are usually children in families of low socioeconomic status. The
ingestion of lye can cause serious injury to the esophagus, frequently
causing corrosive esophagitis
and the even more serious complication of esophageal strictures.
Esophageal burns vary in burn location, burn length, burn severity,
admission time after ingestion, and complications. Consequently, the
management of these injuries has been a challenge to pediatric surgeons
and the gastroenterologist.Atabeck et al outlined a strategy for treating caustic burns.[10] If
strictures formed, they were treated at 2-3 week intervals by antegrade
dilatation via a rigid esophagoscope with the patient under general
anesthesia. A nasogastric tube was placed into the stomach to allow
feeding and to prevent complete luminal obstruction. (Click here to view eMedicine’s illustrated guide to nasogastric tube placement.)In
cases of severe burns and when difficulty was encountered with
antegrade dilatation, a gastrostomy was performed with a trans-stricture
string, followed by antegrade string-guided dilation of the stricture.
Initial dilation was performed with a dilator 1-2 sizes smaller than the
estimated diameter of the stricture. In general, the patients were only
dilatated 2-3 French (F) sizes larger than the first dilator that met
resistance per dilation session. Patients with recalcitrant esophageal
strictures were entered into their esophageal stenting treatment
program.In cases that did not respond to 3 consecutive dilations,
gastrostomy and esophageal stenting were performed.
Polytetrafluoroethylene (PTFE) intraluminal stenting was used to treat
serious cases. The esophageal stent was inserted 12 weeks after caustic
ingestion. The length and caliber of the esophageal stricture was
determined by esophagoscopy. PTFE esophageal stent was custom-made for
each patient. The length of the strictured segment of the esophagus was
measured; the stent was made 2 cm longer so that the stent would overlap
1 cm beyond the stricture on each end when correctly positioned. Both
ends of the stent were secured to a 4F ureteral catheter with zero
polypropylene. The proximal part of the ureteral catheter was fixed to
the nose, while the distal part was fixed to the gastrostomy tube.If gastroesophageal reflux
was diagnosed with 24-hour pH monitoring before or during the stenting
period, a Collis gastroplasty was performed. During the stenting period,
the patients underwent barium esophagogram every 2 months. No
esophagoscopy was performed in this period. The esophageal stenting
program was terminated after 9-14 months of stenting. All patients were
swallowing fluids and semisolid foods easily. The most severe
complication was esophageal perforation.Ingestion of caustic
agents often causes severe corrosive gastritis, in which ulceration is
most extensive in the antrum. Early perforation with peritonitis and
late cicatricial stenosis with thickening of the gastric wall are the
most important complications of corrosive gastritis. Kamijo et al
reported the case of a patient in whom high-resolution images of the
gastric wall were obtained by endoscopic ultrasonography (EUS).[11] This
visualization documented severe corrosive gastritis and helped to
predict the development of antral stenosis, which ultimately required
surgical intervention. The patient was subsequently treated with a
laparoscopic gastrectomy.
Effects of Acid Burns

tolerate acid burns better because like other living tissue, they have
significant acid-buffering capacity. Tear film, the proteins present in
tears, and conjunctival epithelial cells rapidly neutralize acid.
Consequently, acid typically causes epithelial and basement membrane
damage, yet rarely damages deep endothelial cells. Acid burns that
injure the periphery of the cornea and conjunctiva often heal
uneventfully, leaving a clear corneal epithelium. In contrast, acid
burns of the central part of the cornea may lead to corneal ulcer
formation with neovascularization and scarring, requiring later
Hydrofluoric Acid

During 1985 and 1986,
the American Association of Poison Control Centers Data Collection
System received 2367 reports of human exposures to hydrofluoric acid
(HF).[12, 13] Four
fatalities occurred, three from ingestion and one as a result of dermal
exposure. Significant local and systemic toxicity can result from
exposure of eye, skin, or lung to HF.HF is one of the strongest
inorganic acids. Its use is mainly industrial, involving glass etching,
metal cleaning, electronic industries, and biochemical laboratories.
However, it can also be found in households as a component of rust
removers and aluminum-cleaning products. Because of these numerous
applications, there is a large risk for accidental human exposure to HF.
In the United States, more than 1000 incidents of accidental exposures
to HF are reported annually. The risk and potential toxicity associated
with such exposure are often underestimated by persons handling this
liquid in households, laboratories, and industrial plants. Significant
local and systemic toxicity can result from exposures of the eyes, skin,
or lungs to HF.Inhalation of HF vapor is rare and usually
involves explosions that produce fumes or high concentrations of liquid
HF (>50%) that soak the clothing of the upper body. Patient outcomes
vary considerably depending on concentration and duration of exposure to
HF. Inhalation and skin exposure to 70% HF has caused pulmonary edema
and death within 2 hours.Pulmonary injuries that are not evident
until several days after exposure also can occur. The patient has no
respiratory symptoms and a normal chest radiograph initially, yet
massive purulent tracheobronchitis that is refractory to treatment may
develop. Respiratory symptoms may persist for months after inhalation of
HF fumes. Sustained irritation of the larynx and pharynx with
fibrinous, granulating deposits on thickened vocal cords may cause
persistent cough and hoarseness
.Management of exposure to HF

Management of inhalation exposure involves removing the patient from the source, then decontaminating clothes and skin.[14, 15] If
respiratory symptoms are present, monitor the patient with pulse
oximetry, administer humidified oxygen using a nonrebreathing reservoir
bag mask system, and evaluate him or her for laryngeal edema,
pneumonitis, pulmonary edema, pulmonary hemorrhage, and systemic
toxicity. Treatment of HF inhalation injury is primarily
symptomatic. Administration of 2.5-3% calcium gluconate solution by
nebulizer as therapy for inhalation of HF has been suggested but not
tested. Admit asymptomatic patients with possible HF inhalation for
observation. Eye exposure to HF vapors produces more extensive
damage than that of other acids at similar concentration. The extent of
damage by HF depends on its concentration. Exposure of rabbits to 0.5%
HF causes mild initial conjunctival ischemia that resolves in 10 days;
8% HF causes severe initial ischemia that is still noted after 65 days.
Corneal opacification and necrosis occur after exposure to 20% HF.
Irrigation therapy for HF

immediate and copious irrigation of the exposed eyes at the scene of
exposure and continue for at least 30 minutes during transport to the
ED, where an ophthalmologic examination can be performed promptly. Local
ophthalmic anesthetic drops enhance patient comfort and cooperation
during irrigation and evaluation. In experimental animals, single
irrigations with 1 L of water, isotonic saline, or magnesium chloride
are the only treatments that are therapeutically beneficial without
causing toxicity. Benefits include decreased epithelial loss and reduced
corneal inflammation. Repeated irrigations over time have no
therapeutic merit and are associated with an increased occurrence of
corneal ulceration. Patients with significant ocular exposure to HF
should be seen emergently by an ophthalmologist.
HF skin exposures

large number of personnel in industry and research handle concentrated
solutions of HF. Relatively dilute solutions of HF (0.6-12%) are
available to the public in the form of rust removal and aluminum
cleaning products. During handling of containers holding HF, inadvertent
contamination of unprotected fingers and hands often occurs, resulting
in chemical burn injury. HF skin burns have certain distinct
characteristics. First, exposure causes progressive tissue
destruction associated with intense pain that can be delayed in onset
for hours and can persist for days if untreated. Skin at the site of
contact develops a tough, coagulated appearance. Untreated sites
progress to indurated, whitish, and blistered vesicles that contain
caseous, necrotic tissue. In exposure of the digits, HF has a
predilection for subungual tissue. Severe untreated burns may progress
to full-thickness burns and may even result in loss of digits.
Treatment of HF skin exposure

treatment of HF skin exposure is immediate irrigation with copious
amounts of water or a saturated solution of sodium bicarbonate for at
least 15-30 minutes. Most exposures to dilute solutions of HF respond
favorably to immediate irrigation. Severe pain or any pain that persists
after irrigation denotes a more severe burn that requires
detoxification of fluoride ion by promoting the formation of an
insoluble calcium salt. Remove all blisters first because
necrotic tissue may harbor fluoride ions. Then detoxify fluoride ion
through topical treatment, local infiltrative therapy, or intra-arterial
infusion of calcium. Calcium gluconate (2.5%) gel is the preferred
topical agent. Because skin is impermeable to calcium, topical treatment
is effective only for mild, superficial burns. Because this gel is not
stocked in most hospital pharmacies, it must be formulated by mixing 3.5
g of calcium gluconate powder in 150 mL of water-soluble lubricant (eg,
K-Y Jelly). An occlusive cover (eg, latex glove) should secure the gel.
Infiltrative therapy for HF burns

Infiltrative therapy
is necessary to adequately treat deep and painful HF burns. Calcium
gluconate is the agent of choice and can be administered either by
direct infiltration or intra-arterial injection.

  • Direct
    infiltration: A commonly used technique involves injecting 10% calcium
    gluconate subcutaneously through a 30-gauge needle at a maximum dose of
    0.5 mL/cm2 of skin. Using 5% calcium gluconate made by
    diluting the aforementioned solution with an equal amount of isotonic
    saline recently has been shown to reduce irritation of tissues and
    decrease subsequent scarring. Hospitalize patients receiving this
    treatment for observation and toxicologic consultation.
its wide acceptance, the infiltration technique has notable
disadvantages, especially when treating digits. A regional nerve block
is recommended because injections may be very painful. Removal of the nail
to expose the nail bed is required if subungual tissue is involved.
Vascular compromise can occur if excessive fluid is injected into skin
exposure sites, and unbound calcium ions have a direct toxic effect on
tissue. Despite these disadvantages, intra-arterial infusion of calcium
is gaining popularity.

  • Intra-arterial
    injection: Place an intraarterial catheter in the appropriate vascular
    supply close to the site of HF exposure (eg, radial, ulnar, brachial,
    carotid artery). A variety of dilute solutions of calcium salts have
    been infused over 4 hours, including the following: (1) 10-mL solution
    of 10% calcium gluconate or calcium chloride mixed in 40-50 mL of D5W,
    repeated if pain returns within 4 hours; (2) 10-mL solution of 20%
    calcium gluconate in 40 mL of normal saline for radial or ulnar artery
    infusion; and (3) 20 mL of 20% calcium gluconate in 80 mL of normal
    saline for brachial artery infusion, repeated at 12-hour intervals if
    needed. If more than 6 hours have elapsed since the time of HF exposure,
    tissue necrosis cannot be prevented, even though pain relief can occur
    up to 24 hours after exposure.
  • The
    intra-arterial infusion technique also has potential disadvantages. The
    procedure may induce arterial spasm or thrombosis, resulting in
    significant skin loss. It is also more costly because it requires
    hospitalization for use of the infusion pump and monitoring of serum
    calcium if repeated infusions are used.
HF action

binds calcium and magnesium with strong affinity. Systemic fluoride
toxicity, including dysrhythmias and hypocalcemia, can occur from
ingestion, inhalation, or dermal exposure to HF. Consequently, all
patients with significant HF exposure should be hospitalized and
monitored for cardiac dysrhythmias and electrolyte status for 24-48
hours. Hypocalcemia
can occur after significant exposures to HF and should be corrected
with 10% calcium gluconate administered intravenously. If left
untreated, a burn caused by 7 mL of 99% HF can theoretically bind all
available calcium in a 70-kg man. Prolonged QT interval on
electrocardiogram is a reliable indicator of hypocalcemia. Formic Acid

Formic acid is a caustic organic acid used in industry and agriculture.[16, 17, 18] It
causes cutaneous injury by coagulation necrosis. Systemic toxicity
occurs after absorption and manifests as acidosis, hemolysis, and
hemoglobinuria. Hemolysis is the result of the direct effect of formic
acid on red blood cells. Institute copious wound lavage immediately.
Treat acidosis with sodium bicarbonate. Mannitol may be used to expand
plasma volume and promote osmotic diuresis in patients with hemolysis.
Exchange transfusions and hemodialysis may be needed in patients with
severe formic acid poisoning.
Anhydrous Ammonia

Ammonia is used in the manufacture of explosives, petroleum, cyanide, plastic, and synthetic fibers.[19] In
addition, it is widely used as a cleaning agent and as a coolant in
refrigerator units. As an agricultural fertilizer, ammonia is ideal
because of its high nitrogen content (82%). Sudden release of
liquid ammonia can cause injury through two different mechanisms. It has
an extremely low temperature (-33°C) and freezes any tissue it
contacts. Ammonia vapors readily dissolve in the moisture of skin, eyes,
oropharynx, and lungs to form hydroxyl ions, which cause chemical burns
through liquefaction necrosis. The severity of injury directly relates
to the concentration and duration of exposure to ammonia.
Irrigation for anhydrous ammonia injury

consists of prompt irrigation of eyes and skin with water and
management of inhalation injury. If necessary, secure the airway by
nasal or oral intubation. Use a large diameter tube to prevent distal
airway obstruction from sloughing of mucosa. After intubation, manage
lower airway injury with positive end expiratory pressure (PEEP)
Cement burns are alkali burns.[20] When
dry cement is combined with water, hydrolysis occurs. Resulting mixture
is essentially a solution of slated lime saturated in water with an
initial pH of 10-12. As hydrolysis continues, the pH level may continue
to rise to 12 or 14, which is comparable to that of sodium, potassium
hydroxide, or lye. In addition, contact dermatitis from chromate (a
trace element) has been reported.
Treatment of cement burns

best treatment of cement burns is immediate copious irrigation until
the substance is completely gone, a practice performed by experienced
workers who habitually wash off cement throughout the day. Prominent
warning labels on packages containing cement products direct the user to
wear protective gloves when using the product in either its wet or dry
state. Cement burns of the lower extremities respond well to
immediate copious irrigation followed by coverage with a medicated
bandage (eg, Gelocast Unna boot) that allows patient to ambulate.
Phenol and its Derivatives

are used industrially as starting materials for many organic polymers
and plastics. They are used widely in agricultural, cosmetic, and
medical fields. Because of their antiseptic properties (first
appreciated by Lister), they are used commonly in many commercially
available germicidal solutions. A number of phenol derivatives (eg,
hexylresorcinol, resorcinol) are more bactericidal than phenol itself.
Chemical peels

Plastic surgeons use dilute solutions of phenol for chemical facial peels.[21] Phenol
(which is usually mixed with water, soap, and croton oil for this
application) can produce a partial-thickness burn of predictable depth
in a controlled manner. It has been the standard for many years for new
technologies in skin resurfacing to remove both coarse and fine
wrinkles, irregular facial pigmentation, and actinic keratoses. The
concentration of phenol is kept sufficiently low to reduce the
occurrence of systemic complications. Interestingly, higher
concentrations of phenol result in a shallower burn depth. A higher
concentration of phenol results in increased coagulation of the keratin
in the skin, thus forming a barrier to further penetration. Histologic
studies have demonstrated that 100% concentrations of phenol produce
35-50% less penetration than a 50% phenol solution. The physician
performing phenol chemical peels should be concerned about the
possibility of rapid phenol absorption. When phenol is applied to more
than 50% of the facial surface in less than 30 minutes, a high incidence
of cardiac arrhythmias is reported. When the application time over the
same area was increased to 60 minutes, arrhythmias were avoided. Because
of the complication of cardiac arrhythmias, all patients undergoing
phenol peeling should be monitored electrocardiographically and have an
intravenous line in place. Following application of the phenol
solution, the skin is covered with an occlusive dressing that consists
either of multiple layers of waterproof tape or petroleum jelly to
prevent evaporation of the phenol, allowing for increased penetration
and burn depth. The peeled skin is maintained by daily cleansing and
consequent reapplication of ointment, which keeps the surface moist and
prevents desiccation. If this protocol is followed, healing is completed
within 5-7 days. Phenol is an aromatic acidic alcohol.[22] This
compound and its derivatives are highly reactive, corrosive, contact
poisons that damage cells by denaturing and precipitating cellular
proteins. Their characteristic odor usually signals their presence.
After phenol penetrates dermis, it produces necrosis of papillary
dermis. This necrotic tissue may temporarily delay its absorption. When
skin comes in contact with phenol, institute treatment immediately.
Irrigate exposed area with large volumes of water delivered under low
pressure. Dilute solutions of phenol are more rapidly absorbed through
skin than concentrated ones, thus avoid gentle swabbing of surface of
skin with sponges soaked in water. Because phenol may become trapped in
the victim's hair or beard, remove any hair that has come into contact
with the chemical agent as soon as possible.
Symptoms of exposure

animal studies, exposure to as little as 0.625 mg/kg of phenol causes
death. In humans, absorbed phenol causes profound CNS depression,
resulting in coma and death from respiratory failure. Marked hypotension
may occur as a result of central vasomotor depression in addition to a
direct effect on the myocardium and small blood vessels. Phenol also is a
powerful antipyretic that produces a fall in body temperature.
Metabolic acidosis may result from shock as well as from the direct
effect of acidic phenol. A number of substituted phenols (eg,
resorcinol, picric acid) have systemic actions distinct from that of
phenol. Stimulation of CNS is commonly encountered after absorption of
resorcinol. Picric acid hemolyzes RBCs and causes acute hemorrhagic
glomerulonephritis and acute liver injury.
Treatment of phenol exposure

studies indicate that water alone is effective in reducing the severity
of burns and preventing death in animals with skin exposed to phenol
and its derivatives. The most effective treatment is undiluted 200-400
molecular weight polyethylene glycol (PEG) or isopropanol. This material
should be stocked in hospitals located near areas of phenol use. Often,
it can be located in the chemical section of hospital pharmacies. A
quick wipe of the skin with PEG solution reduces mortality and burn
severity in experimental animals. These solutions can be used in phenol
burns of the face because they are not irritating to eyes. Decontaminate
with water until the PEG solution is obtained. Use large amounts of
water because small amounts are detrimental, enhancing dermal absorption
of phenol. Remove phenol in a well-ventilated room to avoid exposing
hospital personnel to high concentrations of phenol fumes. Treatment
of systemic symptoms is purely symptomatic. Respiratory depression may
require ventilatory support. Treat hypotension with isotonic crystalloid
fluid and pressor agents as needed. Metabolic acidosis may require
treatment with sodium bicarbonate. Alkalinization also prevents the
precipitation of hemoglobin in urine that occurs with hemolysis.
Administering mannitol intravenously, which causes osmotic diuresis, can
enhance hemochromogen excretion in urine. Anticonvulsants may be
required to treat seizures resulting from CNS stimulation.
Next Section: Pathophysiology

White Phosphorus

phosphorus is a yellow, waxy, translucent solid element that burns in
air unless preserved in oil. When it ignites spontaneously in air, it is
oxidized to phosphorous pentoxide, which forms metaphosphoric and
orthophosphoric acids with addition of water. Phosphorus can
ignite spontaneously in air at temperatures higher than 34°C; this has
encouraged its use as an incendiary agent in military weapons and
fireworks. After explosion of phosphorous munition, flaming droplets may
become embedded beneath skin, where they oxidize adjacent tissue unless
removed. In nonmilitary industry, white phosphorus is used in the
manufacture of insecticides, rodent poisons, and fertilizers.
Tissue injury

injury from exposure to white phosphorous appears to be caused
primarily by heat production, rather than by liberation of inorganic
acids or cellular dehydration by hygroscopic phosphorous pentoxide. The
ultimate result of this thermal injury is often a painful partial or
full-thickness burn.
Prehospital care

Prehospital care
should include immediate removal of contaminated clothing followed by
submersion of phosphorus-contacted skin in cool water. Avoid warm water
because white phosphorous becomes liquid at 44° C. Remove phosphorus
particles from victim's skin and submerge in water. Cover burned skin
with towels soaked in cool water during transport to the ED.
Treatment of white phosphorus burns

the patient's arrival in the ED, wash burned skin with a suspension of
5% sodium bicarbonate and 3% copper sulfate in 1% hydroxyethyl
cellulose.[23, 24] (This
mixture must be made by hospital pharmacies.) Phosphorus particles
become coated with black cupric phosphide, allowing for easy
identification. Copper sulfate also decreases the rate of oxidation of
phosphorus particles, limiting their damage to underlying tissue. Since
blackened particles can still elicit tissue injury, they should be
removed. If absorbed systemically, copper sulfate is toxic.
Absorption of copper sulfate can be minimized by surface-active agent in
the aforementioned suspension, as well as by sodium lauryl sulfate.
Before the advent of these agents, prolonged treatment of phosphorus
burns with copper sulfate solutions led to systemic copper poisoning,
which manifests as vomiting, diarrhea, hemolysis, oliguria, hematuria,
hepatic necrosis, and cardiopulmonary collapse. After subjecting burned
skin to a suspension of copper sulfate for 30 minutes, thoroughly wash
the antidote from the skin. Washing limits the development of systemic
copper toxicity. An alternative approach is to use a Wood lamp to
identify phosphorus particles because they fluoresce under ultraviolet
light. Metabolic derangements have been identified in white
phosphorous burns. Postburn serum electrolyte changes consist of
depression of serum calcium and elevation of serum phosphorus. Also
identified are postburn ECG abnormalities, including prolongation of QT
interval, bradycardia, and ST-T wave changes. These ECG changes may
explain early sudden death occasionally seen in patients with apparently
inconsequential white phosphorous burns. After hydrotherapy and
treatment with appropriate antidote, definitively manage skin burns in
the hospital intensive care unit setting as with any other burn wound.
Elemental Metals

metals (sodium, potassium) are harmless unless activated by water,
which causes an exothermic reaction with the release of heat and
generation of hydrogen gas and hydroxide.[25] Evolved
heat is sufficient to ignite hydrogen gas, which results in even
greater heat and causes additional thermal burns. Furthermore, formation
of hydroxide compound may result in significant chemical injury to
tissue. Reaction occurs more rapidly with elemental potassium than with
sodium. These deleterious effects of potassium have been attributed to
trace amounts of potassium superoxide released on exposure to room air.
Therefore, water lavage is dangerous in these circumstances. In
the prehospital setting, use only a class D fire extinguisher
(containing sodium chloride, sodium carbonate, or graphite base) or sand
to suppress flames. When the fire is extinguished, metal is covered by
oil (eg, mineral oil, cooking oil) to isolate metal from water.
Transport the patient to the ED for wound debridement and cleansing.
Remove small pieces of metal from the skin. Place sodium fragments in
isopropyl alcohol containing no more than 2% water; insert potassium
particles into tert butyl alcohol for safe deposit.
Next Section: Pathophysiology

Toxic methemoglobinemia is a well-recognized hazard of ingestion of nitrates and nitrites.[26] Occasionally,
severe methemoglobinemia has been reported in patients sustaining burn
injury from molten sodium and potassium nitrates. In these patients,
methemoglobinemia is caused by absorption of nitrates through burned
skin. Diagnosis of methemoglobinemia should be sought in a
cyanotic patient who is unresponsive to oxygen therapy and whose blood
appears chocolate brown. Methemoglobin levels lower than 20-30% usually
are asymptomatic and require no treatment. Levels higher than 30%, with
or without symptoms, should be treated with high-flow oxygen and
intravenous methylene blue administered slowly at dose of 1-2 mg/kg body
weight. Exchange transfusions also may benefit severe cases by rapidly
decreasing circulating methemoglobin concentration.
Next Section: Pathophysiology


Cutaneous injury from immersion in gasoline and other hydrocarbons may occur in individuals involved in motor vehicle accidents.[27] Solvent
properties of hydrocarbons cause cell membrane injury and dissolution
of lipids, resulting in skin necrosis. Although full-thickness injuries
can occur, most injuries are partial thickness. Once gasoline
damages the protective skin barrier, hydrocarbons are absorbed. This
produces systemic toxicity leading to neurologic, pulmonary,
cardiovascular, GI, and hepatic injuries. Treatment of individuals
exposed to gasoline includes immediate removal from site of exposure,
removal of all clothing, copious irrigation, and transfer to the ED
while continuing copious irrigation. Management in the ED consists of
wound care of burn injuries and a search for evidence of systemic
Next Section: Pathophysiology


Burns from hot tar are a challenging clinical problem.[28, 29] Hot
liquified tar that contacts skin transfers heat to cause burn injury.
Tar then cools and solidifies on the skin surface, making removal
difficult. Hot tar includes two distinct groups of materials: coal tar
pitches and petroleum-derived asphalts. Both products are heated to
maintain liquid form. Paving roads requires tar temperatures from
275-300°F, while roofing demands higher tar temperatures of 450-500°F.
Deeper burn injuries are associated with burns from roofing asphalt.
Mechanisms of injury include cauldron explosion, falling from buildings,
trucks rolling over, pipe explosion, spillage from buckets, and
industrial accidents. Prehospital treatment

When hot tar
contacts skin, it rapidly cools, solidifies, and becomes enmeshed in the
hair. It is important to facilitate this cooling process by adding cold
water to the tar at the scene of the accident. Cooling tar with cold
water limits the amount of tissue damage and prevents the spread of tar.
Tar should be continually washed with water until it has cooled and
hardened. After cooling, dry skin with towels to prevent systemic
hypothermia. Do not remove adherent tar at the scene of the
accident. In the ED, definitive care of tar burn injury involves early
removal of tar, because it occludes injured skin and encourages
bacterial growth. This can convert a partial-thickness burn to a
full-thickness burn. Tar adheres to skin because it is enmeshed in the
hair, not because of a direct bond between epidermis and tar. Treatment to remove tar

used to remove tar ideally should have close structural affinity to
tar. Asphalts are susceptible to both aromatic (eg, naphthalene) and
aliphatic (eg, hexade) hydrocarbon solvents, while coal tars are only
susceptible to aromatic hydrocarbons. The cleansing capacity of these
solvents is enhanced by prolonged contact with tar. Broad-spectrum
antibiotic ointments such as bacitracin (400 U/g), polymyxin B (5000
U/g), and neomycin (5 mg/g) may be added to lower the incidence of
infection. Remove antimicrobial petrolatum ointments and reapply every
hour until all tar is removed. The process of tar removal usually takes
12-48 hours. Antibiotic ointment has been used successfully to remove
even tar layered over corneas and conjunctivas. An alternative to
petrolatum ointments is surface-active agents, such as polyoxyethylene
sorbitan (Tween 80) and polysorbate (De-Solv-It). These are more water
soluble and more easily removed from skin with water than petrolatum
ointments. These surface-active agents are an effective, safe, and
inexpensive means of removing tar from skin. NISA baby oil, sunflower
oil, and butter also have been used to remove adherent tar from skin,
taking from 30-90 minutes for complete removal. Sunflower oil has proven
effective and safe in removing tar without inflicting further skin
Next Section: Pathophysiology

Scientific Basis for the Selection of Medical Gloves

surgery, the surgeon should wear sterile surgical gloves without
cornstarch. In 2008, 13 health professionals filed a citizen’s petition
with the Food and Drug Administration (FDA) to ban cornstarch powder on
all medical gloves.[30] Cornstarch
has been documented as promoting wound infection and causing serious
peritoneal adhesions and granulomatous peritonitis, and it is a well
documented vector of the latex allergy epidemic.The FDA allows
1.5% of surgical gloves to have holes. These holes allow the
transmission of blood with deadly viral infections between the patient
and the surgeon. Consequently, the Biogel double-glove hole indication
system should be used to detect the location and presence of holes in
the gloves, allowing the surgeon to change the gloves when a hole is
detected.[31] After
surgery has begun, one of the major causes of glove holes is surgical
needle penetration, which can be detected by the double-glove hole
indication system.In collaboration with Dr. Robert Zura of Duke
Medical Center, the authors have developed a poster entitled: A
Demonstration of How the Biogel Patented Puncture Indication System
Works When Immersed in Water or Saline.Poster for the Biogel puncture indication system. This
poster can be framed and placed in the operating room as a guide to the
appropriate use of the double-hole indication system during surgery.
Copies of the poster can be obtained by contacting Mr. Milt Hinsch at
Next Section: Pathophysiology

Acid Survivors Foundation

violence (ie, when acid is thrown in someone's face) is a particularly
vicious and damaging form of violence. In Bangladesh, the overwhelming
majority of victims are women; many of them are younger than 18 years.
The victims are attacked for many reasons. In some cases, a young girl
or woman has objected to the sexual advances of a young male, or she or
her parents have rejected a proposal of marriage. Recently, acid attacks
on children, older women, and men have been reported. These attacks are
usually the result of family and land disputes. Dowry demands are a
desire for revenge.As pointed out previously, nitric or sulfuric
acid has a catastrophic effect on human flesh. It causes severe damage
to the skin and even blindness. Since 1999, the Acid Survivors Foundation
has been working on acid violence issues in Bangladesh. Acid Survivors
Foundation works as a coordinating agency that works with doctors,
public prosecutors, and police. Acid Survivors Foundation has acquired
national and international recognition. In 2005, the Executive Director
received the 4th Humans Rights Award of Amnesty International
Germany. This organization is expanding its initiative to serve victims
throughout the world.[32]

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