Chemical Burn, Etiology, Types and Management.pptx

Department of Plastic, Reconstructive and Aesthetic Surgery
Chemical Burn
Dr Junaid Khurshid
MBBS, MS, MCh, DrNB, MNAMS
Fellowship Aesthetic Surgery
Fellowship Oncoplastic and Reconstructive Microsurgery

EPIDEMOLOGY
• 2nd
to thermal burn in burn hospital admission
• Represent 10% burns but 30% burn related deaths
• Majority Men
• MC Chemical Acid Related
• Setting Industrial MC
• Children tend to suffer chemical injuries in the
home; whereas, adults suffer chemical injuries in
the workplace.

Etiology
Chemical burns are the result of exposures to a
variety of substances commonly found in the home,
workplace, and surrounding environment.
The burn may be obvious, for example, from a direct
spill or other exposure, or more covert, especially in
children

Common causes of chemical burns
• Acids: Sulfuric, nitric, hydrofluoric, hydrochloric,
acetic acid, formic, phosphoric, phenols, and
chloroacetic acid
• Bases: Sodium and potassium hydroxide, calcium
hydroxide, sodium and calcium hypochlorite,
ammonia, phosphates, silicated, sodium
carbonate, lithium hydride

• Oxidants: Bleaches like chlorites used in the home,
peroxides, chromates, magnates
• Miscellaneous: White phosphorus, metals, hair
coloring agents, airbag injuries
• Vesicants : like mustard gas

Pathophysiology
• Chemical burns cause damage as a result of irritant
properties, acidity/alkalinity, concentration, form,
amount of contact, the length of exposure, and
location of contact.
• Contact with a mucosal surface such as the eye is
likely to cause earlier and more extensive damage
than contact with intact skin.
• After inadvertent or intentional ingestion, there will
be prompt contact with the mucosal surface and
both direct and absorptive toxicity.

Toxicokinetics
• After exposure to an alkaline agent, the -OH moiety
causes injury due to liquefaction necrosis which
leads to often irreversible changes in the protein
matrix.
• Additionally, there is vascular damage that can
create a local or systemic effect.

• Acidic agents cause coagulation necrosis which
leads to cytotoxicity. Additionally, there are mucosal
or skin changes which may prevent further toxicity
and limit absorption.
• Overall, alkaline agents are more toxic than acidic
agents, due to the irreversible changes in protein
and tissue damage.

History and Physical Examination
• The most common findings represent structural
changes to the tissue directly affected, for example,
the eye, oral mucosa, skin, esophagus, and lower
intestinal system, especially the stomach and
pylorus, respiratory system, among others.

• In children, ingestion is generally the most
worrisome event, because of changes, both short-
term and long-term, often leading to extensive
tissue death.
• Eye exposure, either acid or alkali, represents a
significant acute injury. Copious irrigation is
necessary, and measuring pH is appropriate,
although rarely informative.

Evaluation
• Direct examination of external exposure sites is
mandatory.
• In case of ingestion, endoscopic evaluation is
necessary.
• In the instance of Hydrofluoric (HF) acid exposure
monitoring of serum calcium and magnesium levels
is critical to prevent chelation with the fluoride ion
and cytotoxicity.
• With most other topical exposures, observation and
serial monitoring of changes are sufficient.

• Any gastrointestinal (GI) exposure must be seen by
an experienced endoscopist who may need to
perform serial evaluations to document healing.
• Likewise, eye injuries must be examined by an
experienced ophthalmologist who will follow-up
with the patient sequentially and guide additional
therapy.

• With ingestions, especially when concerned about
systemic absorption, laboratory evaluation
(complete blood count [CBC], platelets, electrolytes,
calcium, magnesium, arterial/venous blood gas,
liver and kidney studies, lactic acid level, and,
occasionally, coagulation studies) may be indicated

Radiographic studies
• An upright chest film, may help to determine if
there is the presence of free air, which is suggestive
of a perforation.
• Non-contrast CT may be used if there is concern
about mediastinal free air, resulting from a
perforation after exposure.
• Previously, a radio-opaque contrast was used, but
this should be avoided in suspected perforation.

Treatment / Management
• Copious irrigation of affected external areas is
mandated.
• Endoscopic examination best explores internal
injuries after ingestion.
• If there is concern about ingestion of disc or other
flat batteries, radiographic assessment is mandated.
It would be unusual that CT scanning would be
needed, and MRI studies are interdicted.
• Ultrasonography in experienced hands may provide
answers as to location as well.

Note
• It is not appropriate to introduce emetic agents or
"neutralizing" agents into the treatment regimen
after ingestion. There is high concern about
aspiration, increased tissue damage with retching,
and a strong possibility of exacerbating a bad
situation.
• There is no current recommendation of systemic
medications such as steroids, antibiotics, or
prophylactic renal/hepatic therapies.

1 Hydrofluoric acid (HF)
• One of the strongest inorganic acids, is
used mainly for industrial purposes
(eg, glass etching, metal cleaning,
electronics manufacturing).
• May be found in home rust removers.
• Exposure usually is unintentional and
often is due to inadequate use of
protective measures

HF Injury Management
• Can be treated with copious irrigation and
application of a calcium gluconate gel.
• When applied, the treating clinician should use
barrier protection.
• In some circumstances, intradermal or intraarterial
injections of calcium (gluconate strongly preferred)
have been used.
• Relief of pain is a good marker of efficacy of
treatment. Monitoring of calcium and magnesium
levels is important.

Contd.
• Oral ingestion, often in the context of suicidal
behavior, is likely to be fatal and may be treated
with lavage. Monitoring of heart rhythms and
electrolytes, including calcium and magnesium, is
necessary. Lavage may be helpful, especially if
calcium salts are used.

ROLE OF SURGERY
• The majority of HF burns (which are minor and low
concentration) are not lethal, but simply painful,
and the role of surgery is to debride blisters or to
excise eschar, thereby allowing application and
adequate penetration of topical agents.
• At the opposite extreme, there are cases in the
literature in which immediate surgery was reported
as crucial and lifesaving

Contd.
• In these infrequent, severe cases, such as a 5%
total body surface area burn with >50%
concentration HF in a patient who develops cardiac
arrhythmias, conservative methods alone, such as
infiltration, may be futile because the patient is in
need of aggressive resuscitation and consideration
for immediate surgical debridement.

NAIL INJURIES
• HF readily passes through and around the nail plate
causing severe damage to the delicate subungual
tissues.
• Involvement of the nail bed poses a unique challenge
in calcium gel delivery and removal of the fingernail is
often required. One should not hesitate to remove the
nail if severe pain is present.
• This requires local block or sedation and the finger
pads can be injected at the same time

White Phosphorus
• Used in weapons as hand grenades and bombs
• On contact with skin it begins to burn until it is
oxidised or starved of oxygen by immersing in water
• Causes tissue injury by oxidising adjacent tissue,
protein denaturation and thermal injury.
• Charactarestic yellow color and garlic-like odor.
Smoke may be released from the burn site from the
continued burning of white phosphorus or the
formation of phosphoric acid.

Military Use
• Well known for its use in military warfare, white
phosphorus burns displaying an illuminous yellow
flame producing a thick white smoke that serves as
a smokescreen, interferes with infrared cameras
and weapon tracking devices.
• For military personnel, materials as white
phosphorus present a high risk for burns from
incendiary shells and detonators and such injuries
warrant the expertise of experienced military burn
surgeon.

Management
• Use of copper sulfate in the treatment of white
phosphorus has evolved over the past century
primarily for the identification of phosphorus
particles. When in contact with copper sulfate, the
phosphorus turns black for easy identification and
subsequent removal

Contd.
• As white phosphorus become liquid at 44 °C, it is
critical that the use of warm water is avoided and as
reported in our case, saline soaked gauze/pads
were used to cover the wound.
• Use of saline soaked gauze for wound coverage
facilitates oxygen depletion to any remaining
phosphorus particles.
• The primary goal is to stop the burning process and
immediately remove any contaminated clothing and
shoes

Mustard Gas
• Sulfur mustards act as vesicants and alkylating
agents. They have been used as chemical warfare
since 1917 during the first world war
• Sulfur mustard gas (dichlorodiethylsulfide) is the
prototypical vesicant alkylating agent used in the
fabrication of chemical weapons.
• It was first used by the Germans during World War I
(1917) causing over 125,000 casualties. It was then
used in World War II and during the Iran- Iraq war
(1980-1988)

• Due to its low volatility, in open areas with little
wind, mustard gas can persist in the air for more
than a week, especially in temperate climates.
• Battlefield air concentrations during World War I,
for example, approached 19-33 mg/mm3. At such
concentrations, exposure for several minutes can
potentially lead to skin and eye injury. Longer
exposures (30-60 minutes) can result in severe
respiratory injury, systemic poisoning, or even
death.

Mechanism of action
• Sulfur mustard rapidly alkylates the purine bases (adenine &
guanine) of DNA which triggers the activation of
endonucleases for depurination (excision) of the alkylated
bases, leaving apurinic sites where DNA breaks readily occur.
• This creates a considerable need for DNA repair, activating
poly-(ADP ribose) polymerase enzymes that rapidly deplete
NAD+.
• Depletion of NAD+, which typically occurs within an hour of
exposure and is highest after four hours, inhibits glycolysis,
leading to the release of multiple proteases that ultimately
result in tissue necrosis.

• Tissue necrosis occurs in the affected system,
namely in the skin (producing vesication of the
epidermis), in the hematological system (leading to
pancytopenia), in the respiratory system (causing
respiratory failure), and in the gastrointestinal
system (leading to mucositis).
• Death may occur, and mortality rates in the Iran-
Iraq War were reported to be as high as 3-4%.Death
was attributed to respiratory failure or bone
marrow suppression.

• Regular clothing does not afford adequate
protection. Specialized military protective garments
are needed; these have a layer of charcoal to
absorb the penetrating sulfur mustard and provide
approximately six hours of protection after
exposure.
• Patients presenting with signs and symptoms of
upper airway obstruction (i.e. stridor) require
immediate endotracheal intubation or, in the
presence of severe upper airway edema,
treacheotomy.

• Once the skin is exposed, rapid removal of the SM
substance is crucial as it becomes irreversibly fixed
in the tissues within minutes.
• Mustard scavengers, antioxidants, NAD+
precursors, polymerase inhibitors, and
corticosteroids have all shown value in animal
models; however, currently there is no accepted
antidote for the treatment of SM gas exposure in
humans.

Management
• Increased survival and fewer pathological organ
effects were noted after administration of
parenteral doses of sodium tiosulfate (3000mg/kg),
vitamin E (20mg/kg), or dexamethasone (8mg/kg)
within 15 minutes of exposure.
• The combination of all three was the most effective.
• Thiosulfate acts as a mustard scavenger, vitamin E
as an antioxidant, and corticosteroids act by
inhibiting lipooxygenase activity thereby decreasing
the synthesis of prostaglandins and leukotrienes. 1

Disc Battery
• Disc batteries have the potential to leak alkali and
cause local, generally esophageal, burns. This is
typically seen in children and will require
endoscopic management and radiographic tracking
of location.
• Early removal is strongly recommended.
• If the battery has passed the pylorus, watchful
waiting, and inspection of stool for passage is
appropriate.

Remember
• A BB can fuse to the mucosa rapidly, leading to
difficult removal that may require rigid
esophagoscopy.
• Identification of a gastric foreign body does not
preclude esophageal injury.
• BBs can transiently lodge in the esophagus and cause
severe erosion and ongoing injury.
• Even after passage of the battery to the stomach,
necrosis of the esophagus and surrounding tissues is
an ongoing process that can lead to fistulization and
associated severe outcomes.

• Despite a reassuring esophagram and clinical
stability 5 days after ingestion, devastating
hemorrhage from esophageal erosion secondary to
BBI can unexpectedly occur weeks out from the
initial ingestion.
• Because of the high arterial pressure from AEF,
Blakemore tubes may not be able to control or
stabilize bleeding.

• As mucosal injury occurs with even short exposure
to BBs, every effort should be made to expedite
removal when possible.
• MRI is a useful tool for post–battery-ingestion
evaluation of the extension of injury beyond the
esophagus and may help guide treatment
decisions.

• A total BB exposure time of just 2.5 hours was
associated with contained esophageal perforation,
giving credence to the growing concern for
potential morbidity associated with any BB
exposure to the esophageal mucosa.
• As with other type of esophageal foreign bodies,
children with a history of tracheo-esophageal fistula
(TEF) have an increased risk of impaction.

In otherwise healthy toddlers with acute onset
of severe hematemesis, a high index of
suspicion for battery ingestion should be
maintained.

Cement burns
• Insidious onset.
• Most patients notice only mild irritation .
• Cement contains lime (calcium oxide), which will
potentially penetrate clothing and react with sweat
causing an exothermic reaction.
• 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 hydroxyl
ion.

• Cement burn injuries are not confined to
construction workers.
• Occasionally, sports players receive superficial burns
following contact with the calcium oxide used to
mark out touchlines on football or rugby fields.

Mechanism
• Dry cement contains calcium oxide, which is not
particularly dangerous.
• When water is added to cement, calcium hydroxide
is formed, which is extremely alkaline with a pH of
12 to 13.
• Wet cement can produce alkaline (caustic) skin
burns which progress and get worse without more
exposure.
• A worker may have wet concrete on his or her skin
for hours without feeling any discomfort; however,
the cement is damaging the skin microscopically.

Clinical Profile
• Cement burns frequently produce discoloration of
the skin, gradually changing to a deep purple-blue
color, eventually progressing to painful burns,
ulcerations and, in the worst cases, amputation.
• Some patients report red inflamed skin near the
affected area followed by severe blistering.
• Cement burns can also lead to allergic dermatitis.

• Cement burns to the knees usually occur after
kneeling in wet cement while spreading it. Because
the hands are usually washed before they have
been in prolonged contact with cement, burns to
the hands are rare. Like most burns, those caused
by cement start with localised erythema, odema,
and blistering and heat in the areas of contact
(Sherman and Larkin 2005). Partial burns can reach
full thickness if the alkali is not fully washed away.
The initial sequela of cement burns is raised,

6 Severe Airbag Related Ocular Alkali Injury
• Airbag restraints have saved many lives since their
mandatory incorporation into automobiles.
• However potentially devastating ocular implication
of airbag deployment — airbag related alkali
keratitis
• Stress the importance of prompt ocular irrigation
following airbag deployment.

Mechanism
• Airbags are made of woven nylon, which are explosively
deployed upon automobile impact, inflating within 50 msec.
• In addition to inflation-related thermal and blunt trauma,
eye injury can occur as a result of alkaline burn due to the
chemical components of the inflation reaction.
• In order to create rapid inflation within the airbag, a solid
propellant, sodium azide, is ignited and converted to
hydrocarbon gases, rapidly expanding the volume of the
airbag.

• This conversion creates byproduct sodium
hydroxide, sodium bicarbonate, and metallic oxides
in a fine powder form.
• The airbag is deflated within two seconds of
inflation though side exhaust ports.
• Small amounts of sodium hydroxide powder can
escape through the woven nylon meshwork,
creating the potential for direct exposure of sodium
hydroxide powder onto the cornea, conjunctiva,
and in the cul de sac of the lids, particularly
inferiorly due to Bell's reflex.

Photographs of right eye after airbag-related alkali burn at 1 week (a), 2 months (b), 4
months (c), and 6 months (d) after the initial MVA with airbag deployment. Note severe
limbal ischemia at 1 week (a) leading to severe conjunctivalization of the cornea at later
time points

Management
• Immediate occular irrigation for patients involved
in airbag deployment MVAs,emergency
departments are often preoccupied with more
pressing issues
• Oversight in the treatment of the patient's ocular
injuries results in significant vision loss, and
disability.

• Immediate irrigation for no less than 15 minutes
with no less than 1 liter of eye rinsing solution, such
as buffers (Cedorroths, etc) or amphoteres (Previn,
etc), or lactated Ringer's or normal saline if the
above are not available, is recommended for the
prevention of serious ocular alkali burns.
• Irrigation must be continued until pH testing is
normalized.
• Awareness in the emergency medicine and first
responder community should be raised in order to
avoid disabling complications

NEWS
• (CNN)A series of acid attacks in London left five men
injured over a 70-minute period . One victim is
considered to have life-changing facial injuries.
• Acid attacks are on the rise in the British capital,
with police reporting an increase in yearly filed
incidents to 454 in 2016 from 261 in 2015. They
have been connected to robberies and gang
violence.

Background
• Acid assault burns are a particularly vicious form of
attack where the motive is not to kill but to cause
permanent disfigurement.
• The priority of the acute care is to limit the damage
while the priority of the reconstructive care is to
restore as much as possible the patient to optimum
form and function.

• A recent review indicates that there are reports of
such assaults that have occurred in many parts of
the world but there appears to be a rising incidence
in the developing countries where medical
resources are limited.
• Bangladesh has the highest reported incidence,
among developing countries.

8 OCULAR BURN
• Chemical burns represent potentially blinding
ocular injuries and constitute a true ocular
emergency requiring immediate assessment and
initiation of treatment. The majority of victims are
young and exposure occurs at home, work place
and in association with criminal assaults.

• Alkali injuries occur more frequently than acid
injuries. Chemical injuries of the eye produce
extensive damage to the ocular surface epithelium,
cornea, anterior segment and limbal stem cells
resulting in permanent unilateral or bilateral visual
impairment. Emergency management if appropriate
may be single most important factor in determining
visual outcome.

Etiological Factors
• Recent studies put the incidence of ocular burns of
the eye at 7.7-18% of all ocular traumas. The
majorly of victims are young and exposure occurs at
home, work and in association with criminal
assaults. Alkali injuries occur more frequently than
acidic injuries.

Effects of Ocular surface burn

Initial evaluation and immediate treatment
• Patients suffering from a chemical injury often
present to the emergency. Once history of chemical
exposure is obtained chemical should be identified
if possible, but this should but delay treatment.
Immediate treatment should include copious
irrigation prior to ophthalmic evaluation irrigation
with isotonic saline or lactate ringer solution should
be performed and sometimes irrigating volumes up
to 20 L or more is required to change pH to
physiological levels (pH testing should be done.

• Once copious irrigation is achieved and pH is
neutralized, the ocular examination should proceed
with attention is being paid to fornices, visual
acuity, IOP, perilimbal blanching. In pediatric cases,
if the examination is not possible under topical
anesthesia it should be done under general
anesthesia

Major treatment goals
(a) reestablishment and maintenance of an intact and
healthy corneal epithelium
(b) control of the balance between collagen synthesis
and collagenolysis and
(c) minimizing the adverse sequelae that often follow
a chemical injury

Acute phase treatment
• Broad spectrum topical antibiotic
• Cycloplegic
• Antiglaucoma therapy..

Modalities to promote reepithelization
• Tear substitutes: Preservative free tear substitutes
can ameliorate persistent epitheliopathy, reduce the
risk of recurrent erosions and accelerate visual
rehabilitation
• Bandage soft contact lens: Hydrophilic high oxygen
permeability lenses should be preferred. They
promote epithelial migration, helps in the basement
membrane regeneration and enhances epithelial
stromal adhesion

Investigational drugs
• Retinoic acid - Has shown promise in treatment of
ocular surface disorders associated with goblet cell
dysfunction
• Epidermal growth factor and fibronectin - Has a
favorable effect on promoting epitheliazation.

Drugs that support repair and minimizing ulceration
• Ascorbate: Ascorbate is an essential water soluble
vitamin that is a cofactor in rate limiting step of
collagen formation.
• Supplementation of ascorbate by restoring depleted
aqueous ascorbate levels reduces the incidence of
corneal thinning and ulceration.
• Oral ascorbate (2 g/day) and topical 10% solution
formulated in artificial tears are effective

• Collagenase inhibitors: Collagenase inhibitors
promote wound healing by inhibiting collagenolytic
activity and thus preventing stromal ulceration.
Several collagenase inhibitors including cysteine,
acetylcysteine, sodium ethylenediamine tetra acetic
acid (EDTA), calcium EDTA, penicillamine and citrate
have been reported to be efficacious.

Drugs to control inflammation
• An intact epithelium should have already been
achieved by this time. If it has not been, then
aggressive therapy is instituted by use of lubricants,
punctual plugs, punctual occlusion with cautery,
bandage contact lens, tarsorrhaphy. If epithelium is
not intact, corticosteroids dosage is tapered and
discontinued by 14th
day after injury. Ascorbate and
citrate are continued, antiglaucoma therapy is
continued as required. Antibiotics are maintained
and examination for the formation of symblepharon
continued.

Late reparative phase treatment
• The patient whose injured eye has not achieved an
intact epithelium by the 21st
day is at significant risk
of permanent vision loss.
• Along with continued medical treatment, surgical
modalities are the mainstay of treatment in this
state of ocular burn.
• The various strategies include conjunctival/tenons
advancement, tissue adhesives, therapeutic
penetrating keratoplasty, amniotic membrane
transplantation.

Rehabilitative phase
• After the eye has stabilized, limbal stem cell
transplantation has shown remarkable promise in
rehabilitating ocular chemical injuries that have
resisted treatment.
• Limbal stem cell can be donated from the patient
uninjured fellow eye, a blood relative or a post
mortem globe. All have shown promise in
reestablishing a healthy ocular surface prior to
further reconstructive surgery. Once a healthy
surface is achieved, penetrating keratoplasty or
keratoprosthesis may be considered.

Conclusion
• Patient coming with chemical ocular injury need a
through and immediate evaluation and intensive
treatment.
• Advances in understanding of the pathophysiology
of the injury have led to improvement in treatment
such as use of topical ascorbate and citrate,

• Surgical treatment such as Amniotic membrane
transplantation, stem cell transplantation,
penetrating keratoplasty and ultimately
keratoprosthesis placement if necessary.
• The goal of treatment is restoration of the normal
ocular surface anatomy and lid position, control of
glaucoma and restoration of corneal clarity.

Prognosis
• The prognosis depends on the type of chemical and
extent of the injury.
• Most small lesions heal well, but larger wounds
often do not heal and can develop into scars.
• Hydrofluoric acid burns have typically been
associated with loss of digits.
• Chemical injuries to the eye are the most serious,
resulting in severe scarring and permanent loss of
vision.

Complications
• The most common complications are pain and
scarring.
• Vision loss occurs when the eye is injured.
• Most patients require multiple doctor visits, and
many patients require skin grafts to alleviate the
scars.

Postoperative and Rehabilitation Care
• Except for first degree burns, all other burns require
some type of follow-up.
• Skin burns need to be evaluated every 2-4 days until
there are signs of healing.
• Patients with eye burns need to be seen in 24
hours.
• For those who suffer a burn to the esophagus,
endoscopy has to be repeated in 14-21 days to
ensure that there is no stricture formation.

Consultations
• Besides a general surgeon or a burn specialist, other
consultants involved in the care of these patients
include an ophthalmologist, ENT surgeon,
Gastroenterologist and a pediatrician.

Other Issues
• Chemical burns have the potential to impair short
and long-term health and, especially when the eye
or esophagus are involved, severely alter the
individual's well-being.
• The clinician must be vigilant to monitor even minor
appearing burns, especially with HF acid, as what
initially appears to be minor may have serious side
effects.

Enhancing Healthcare Team Outcomes
• Because burns can occur on almost any part of the
body, specific guidelines in the management of each
organ system are lacking.
• There still remain several gaps in the early
management of chemical burns. What solution to
rinse the skin or the eye and when to debride are
two issues that continue to be debated.

Outcomes
The outcomes following a chemical burn
depend on
• Chemical
• Extent of burn
• Comorbidity of the patient
• Time to intervention.

Acknowledgements
• Our Teachers
• Patients for giving
consent
Thank you

Chemical Burn, Etiology, Types and Management.pptx

More Related Content

Similar to Chemical Burn, Etiology, Types and Management.pptx

More from Dr. Junaid Khurshid

Recently uploaded

Chemical Burn, Etiology, Types and Management.pptx