Transcript Skin lesions are among the most common late complications of SM

The first use of SM as chemical warfare was on
July 12, 1917, in a field near Ypres, Belgium,
where during 10 days of attack more than one
million mustard shells were fired at Allied
troops by Germans. Thereafter, it was
responsible for more than 80% of all
documented chemical casualties.
After WWI, a widespread campaign to ban
chemical warfare was mounted and the
Geneva Protocol was promulgated in 1925.
However, the Italian campaign in Ethiopia
(1935 – 1936), Italian troops used mustard
gas on a large scale against unprotected
native forces.
Despite the production of large quantities of
chemical warfare munitions, SM was not
used in combat during the Second World
War (WWII). In December 1943, however,
an Allied ship carrying large quantities of
mustard gas exploded in the harbor of Bari,
Italy, dispersing the agent and causing more
than 600 casualties.
The greatest use of SM recently, however, has
been by the Iraqi army against Iranian soldiers and
even against its own Kurdish population between
1983 and 1988.3 In one particularly distressing
event, some 5,000 Kurdish civilians were killed in
the Iranian-occupied village of Halabja in 1988.
Several CWAs, including SM and sarin, were
identified in this massacre.
• Chemical weapons are categorized as
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nerve agents,
blood agents,
vesicant/blistering agents,
lachrymatory agents,
incapacitating agents,
cytotoxic proteins, and
choking/pulmonary agents
it has been used in 12
conflicts including Iraq against Iran war (1980–
1988)
• SM is an oily, colorless to
brown liquid at room
temperature, which its smell
resembles garlic or fish.
• It has considerable penetrating ability
and rapidly passes through clothing to
affect the underlying skin.
Although SM reacts with RNA, proteins, and
phospholipids, the consensus has been
made that it is DNA alkylation, which plays
an important role in delayed healing.
The major alkylating site of nucleic acids
in mammalian origin is the nitrogen
residue of guanine
• Current studies have shown that
basal keratinocytes are more
sensitive, leading to detachment of
these cells from their basement
membrane adherence zones and
blister formation
• In warm weather, SM evaporates
and produces eye and respiratory
lesions first, whereas in cold
weather liquid SM produces skin
lesions first, particularly in skin
areas in close contact with clothes
(such as axilla and groin)
• Erythema and edema with pruritus
and burning appear at the site of
skin contact with SM after 2–24
hours.
This latency period as well as the severity of lesions depends on
concentration and
form of SM (liquid or vapor),
mode of exposure,
environmental temperature and humidity,
anatomical location,
skin pH
moisture,
friction and occlusion,
the extent of use of protective equipment (mask, clothing),
and probably the individual
• Bullous lesions usually occur on warm and
moist areas such as genitalia, axilla, and
areas where tight clothing is worn . Later
erosions and ulcers develop at the site of
skin blisters, which are usually very painful.
These lesions tend to heal in a few weeks,
more slowly than thermal burns of similar
extent.
• Hyperpigmentation, hypopigmentation, or
scarring may remain.
• The exact mechanism of blister
formation by SM is unknown, but
histopathologic examination of
lesions showed subepidermal
blister with mild dermal and
epidermal necrosis
• Skin lesions are among the most
common late complications of SM
exposure. Khateri et al. found lung
lesions in 42.5%, skin lesions in
39.3%, and eye lesions in 24.5% of
34,000 individuals 13–20 years after
exposure to SM in Iran
• Another study on 372 civilians in
Sardasht, Iran, 20 years after exposure
to SM found skin lesions in 75.5%,
mental disorders in 62.7%, respiratory
diseases in 42.5%, and ophthalmic
lesions in 19.6%, which were
significantly more common than a
matched unexposed control group
(55.5, 43.8, 39.5, and 7.1%, respectively).
• The most common subjective
symptoms of the victims in this study
were cutaneous (94.7%), respiratory
(93.5%), mental (69.2%), and ophthalmic
symptoms (52.0%), which were also
significantly more common than the
control group
• Several studies have reported the
delayed consequences of SM exposure
in Iran .
• A few of these studies which included a
control group, confirmed that pruritus,
xerosis, pigmentation disorders, scars,
and cherry angiomas are considerably
more common in patients exposed to SM
• Hyperpig~ is a common delayed finding .
• The proinflammatory cytokines and mediators
induced by SM can activate MC and produce
hyperpigm.
• Hydropic changes in epidermal basal layer can
also cause pigmentary incontinence in the dermis.
• Other possible mechanisms of hyperpigmentation
include depletion of glutathione leading to increase
in tyrosinase activity, increased melanogenesis,
and upregulation of Melanocyte Stimulating
Hormone (MSH) centrally from hypothalamus
• The melanin content of skin in SM-exposed
patients was significantly higher than a normal
control group, but was not different from a control
group consisting of patients with chronic
dermatitis.
• This finding emphasizes on the role of chronic
inflammation, pruritus, and excoriation in the
pathogenesis of hyperpigmentation.
• On the other hand, higher concentrations of SM
can destroy melanocytes and cause
hypopigmentation. Although Fekri et al. reported
higher prevalence of
in SM-exposed
patients compared to a control group, later studies
did not confirm this finding
• SM scar is the hallmark of delayed skin lesions
induced by SM Typical SM scar develops at the site
of previous blisters and consists of skin atrophy,
vascular changes (telangiectasia and cherry
angioma), hyperpigmentation and hypopigmentation
(usually with salt and pepper appearance), hair loss,
and islands of normalappearing skin with irregular
borders. Hypertrophic scar and keloids are rarely
reported.
• These scars are usually located on face, neck,
axilla, groin, and external genitalia. Thin skin,
moisture, friction, and abundance of hair follicles
aggravate skin damage by SM in these areas
• Skin cancers consisting of 5 cases of BCC
and 1 case each of SCC, Bowen disease,
dermatofibrosarcoma protuberans, and MF
were observed in 800 SM-exposed individuals
in a recent report ,
• Though none of the previous reports found
any increase in skin cancers. Currently more
than 20 years have passed since the
exposure to SM, and longer duration of time
may be required for skin cancers to develop.
It is crucial to follow SM-exposed individuals
closely and carefully for a prolonged time to
detect any skin cancers.
Protection is more important
• Treatment of mustard exposure is
based on symptoms. Because the
effects of mustards typically are
delayed, people with complaints
immediately after exposure may
have an additional injury
• For those with signs of upper
airway obstruction, must be
treat by using a tube in the
person's throat or perform
surgery to open the airway
• Decontamination: Immediate
decontamination within 2 minutes
of exposure is the most important
intervention for people who have
skin exposure to mustard, because it rapidly
becomes fixed to tissues, and its effects are
irreversible.
• Even if an exposure takes place and a person
shows no obvious sign and symptoms,
decontamination is still urgent
•Remove clothing immediately and
wash the skin with soap and water.
•Eye exposure requires immediate
washing out with a large amount of
saline or water.
• Mustard-induced burns are especially
painful. Doctors will use strong pain
relievers. Adequate burn care is
essential, because skin lesions heal
slowly and are prone to infection.
Severe burns may require removal of
dead tissue, irrigation, and placement
of antibiotics, such as silversulfadiazin,
directly on the burned area
 Although no antidotes currently are available to
treat mustard toxicity, several agents are under
investigation.
Antidotes
Management of Choronic lesions
• As prolonged extensive use of corticosteroids
may cause adverse effects, including skin
atrophy, striae and telangiectasia, other topical
antipruritic treatmentsare usually preferred.
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• Pimecrolimus and Tacrolimus have
also considerable anti inflammatory
effect, but should be used longer
than corticosteroids to achieve the
same results.
• Oral antihistamines can be used for severe or
refractory to topical treatment pruritus. H1 blocker
antihistamines have better results and are divided into
two generations:
• 1- first generation or classic antihistamines with
sedative and anticholinergic effects including
hydroxizine, diphenhydramine, chlorpheniramine, and
cyproheptadine;
• 2- second generation antihistamines with less sedative
adverse effects including cetirizine, loratadine, and
fexofenadine.
• The most effective treatment in our
experience is 10 mg loratadine in the
morning and 10–25 mg hydroxizine at
night.
• Or Loratadin+Doxepin 10-20 mg at night
for whose that have no medicin for
mood disorders(drug interaction)