Toxicol Rev 2003; 22 (2): 111-118

REVIEW ARTICLE 1176-2551/03/0002-0111/$30.00/0

Sulphur Mustard Injuries of the Skin

Pathophysiology and Management

Paul Rice
Biomedical Sciences Department, Dstl Porton Down, Salisbury, UK

Contents
Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111
1. History of the Use of Sulphur Mustard in War . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112
2. Chemical and Physical Properties of Sulphur Mustard . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112
3. Histopathology of Vesicant-Injured Skin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113
4. Sulphur Mustard Injury in Human Skin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113
4.1 Gross Pathology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113
4.2 Microscopy and Ultrastructural Observations of Human Vesicant Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 114
4.2.1 General Observations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 114
4.2.2 Microscopic Observations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 114
4.2.3 Ultrastructural Observations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 114
5. Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115
5.1 Current Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115
5.2 Post-Exposure Surgical Intervention . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115
5.2.1 Dermabrasion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 116
5.2.2 Laser Debridement (‘Lasablation’) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 116
6. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 116

Abstract Sulphur mustard is a vesicant (blistering agent), which produces chemical burns with widespread blistering. It
was used extensively as a chemical warfare agent in the First World War, and has allegedly been employed in a
number of conflicts since then, most recently by Iraq against Iran (1984–1987). The potential further use of
mustard in military conflicts and by terrorists remains a significant threat that if realised in practice would result
in a large number of casualties with severely incapacitating, partial thickness burns. Such injuries clearly present
a huge potential wound care problem.
The development and healing of mustard-induced cutaneous injuries has not only been observed in human
casualties, but has been studied recently at the microscopic and ultrastructural levels in several animal models.
Vesication generally begins on the second day after exposure, and may progress for up to 2 weeks. Wound
healing is considerably slower than for a comparable thermal burn, and patients often require extended hospital
treatment. The current management strategy is essentially symptomatic and supportive. Recently, two tech-
niques for removing damaged tissue and improving wound healing have been investigated. Mechanical
dermabrasion and laser debridement (‘lasablation’) both produced an increased rate of wound healing in animal
models, and may be of benefit in a clinical context.

Sulphur mustard is a powerful vesicant (blistering agent) in 1984–1987, treated in various European medical centres, attest to
humans and the descriptions of the casualties from the Gulf War of the problems of management of both percutaneous and systemic
112
sulphur mustard injuries.[1-4] In addition to their association with
large, pendulous, fluid-filled blisters, the skin injuries differ in
many other respects from thermal burns with which they are often
compared (see figure 1). For example, the healing time is consider-
ably longer than for comparable thermal injury and varies from
species to species.[5] Despite the obvious clinical importance of
such lesions, the biochemical basis of vesication in human skin
remains largely undefined.[6]
Research to further elucidate the molecular mechanisms under-
lying vesication has been hampered by the lack of an appropriate
animal model. In general, fur-bearing mammals do not produce
blisters on challenge with either sulphur mustard liquid or vapour.
This species variation in cutaneous response has long been known
and several theories, none of which has yet been universally
accepted, have been proposed to explain such differences.[7,8] The
reasons for differences in the healing time remain equally elu-
sive.[9]
1. History of the Use of Sulphur Mustard in War
Sulphur mustard or ‘mustard gas’ is perhaps the most familiar
member of the heterogeneous group of chemicals that are referred
to as chemical warfare agents. The term ‘king of the battle gases’,
thought to have been coined by Foulkes in his commentaries on
the use of chemical warfare agents in the First World War,[10]
remains a relatively accurate and well-deserved description today.
The exact date of the first chemical synthesis of sulphur mus-
tard is still disputed, but various dates between 1820 and 1854
have been quoted by a number of authors. In 1860, Guthrie[11]
reported the synthesis of sulphur mustard and noted some of its
vesicant properties; this was followed by a report in 1886 detailing
Fig. 1. Panels (a) and (b) show Iranian casualties with large, fluid-filled
blisters, the characteristic acute manifestation of sulphur mustard exposure
of the skin. Panels (c) and (d) show a large sulphur mustard burn.
Rice
the synthesis of pure sulphur mustard.[12] A long period then
followed until the outbreak of the First World War, during which
time little or no practical use for the compound was proposed.
Although the British had successfully synthesised sulphur mustard
by 1916, there were no plans to develop it as a chemical weapon.
Germany, however, had recognised its potential military signifi-
cance and, following initial development by Fritz Haber and
industrial scale development by Lommel and Steinkopf,[13]
sulphur mustard was first deployed against the French troops at
Ypres, Belgium, on 12 July 1917.[14]
During the first 3 weeks of its use, the British Army sustained
more than 14 000 casualties, of whom approximately 500 subse-
quently died.[15] By the end of the war, sulphur mustard was being
used extensively by both sides and the overall casualty figure had
risen to 400 000 according to some authorities; the British alone
reported in excess of 140 000 casualties.[10] Despite these appall-
ingly high figures, the mortality rate did not exceed 2–3%;[16] the
much higher figure of 13–14% reported following the Bari Har-
bour incident in 1943 is now thought to be atypical of sulphur
mustard exposure and may have been compounded by fatalities as
a result of direct blast injury.[17]
Since the use of sulphur mustard in the First World War, there
have been several allegations of its use around the world in
numerous conflicts. Italian forces were reported to have used
sulphur mustard against Abyssinian (Ethiopian) troops in 1936
and it was used, probably on several occasions, by the Japanese in
China between 1937 and 1941.[18] Some evidence to support its
use by Poland against Germany in 1939 and by Egypt against the
Yemen in 1963–7 has also been reported.[18] Much more recently,
well-founded allegations of the use of mustard by Iraq against lran
(1984–7) were made and largely substantiated by independent
specialists acting on behalf of the United Nations Secretary Gener-
al.[19-21] During the period of the Iran-Iraq conflict, numerous
Iranian casualties whose injuries were compatible with exposure
to sulphur mustard arrived for hospital treatment in several West-
ern European countries.[1-4,22]
2. Chemical and Physical Properties of
Sulphur Mustard
The name ‘mustard’ was given to the compound by soldiers
during the First World War, apparently because of the smell
perceived during gas attacks. Since that time, the odour has been
variously described as similar to that of garlic, mustard, horserad-
ish and leeks. Sulphur mustard itself should not be confused with
mustard oil;[23,24] the latter is allyl isothiocyanate and, interesting-
ly, is also a powerful vesicant. Mustard is often referred to by the
Toxicol Rev 2003; 22 (2)
Sulphur Mustard Injuries of the Skin 113

letter ‘H’; it has also be denoted as ‘HS’ (representing H un Stoff
or ‘German stuff’), ‘HD’ to imply distilled mustard, or ‘LOST’
believed to be a derivation of LOmmel and STeinkopf, the two
German chemists responsible for its industrial-scale production.
The compound is also referred to as Yperite, particularly by the
French, in view of its initial use at Ypres.
Sulphur mustard is an oily, colourless to brown liquid at room
temperature and has the chemical name bis-(2-chloroethyl)sul-
phide; the chemical synonyms include 2,2′-dichlorodiethylsul-
phide, β,β′-dichloroethylsulphide, 1-chloro-2-(2-chloroethylthio)-
ethane and 1,1′-thiobis(2-chloroethane). Its physicochemical
properties are summarised in table I.
The vapour given off by a quantity of sulphur mustard has
considerable penetrating ability; it rapidly passes through clothing
to affect the underlying skin. Vapour will also penetrate sub-
stances such as wood and leather, albeit not as rapidly as cloth.
Materials such as metal, glass and glazed ceramics are generally
impervious; paint on metallic surfaces may, however, absorb
mustard vapour and act as a potential source of a vapour hazard in
the immediate vicinity.
3. Histopathology of Vesicant-Injured Skin
The gross and microscopic descriptions of human skin injured
by vesicant agents, and sulphur mustard in particular, have not
altered in detail since the original descriptions by Warthin and
Weller in 1919[26] and Cullumbine in 1947.[27] Application of the
relatively new techniques of enzyme histochemistry, molecular
biology and immunohistochemistry to the study of the pathogene-
sis and resolution of mustard injury have only just begun. Com-
pared with the research into the aetiology of similar human blister-
ing diseases, such as epidermolysis bullosa[28,29]and lichen planus
pemphigoides,[30,31] the elucidation of the molecular pathology of
vesicant-induced blistering is in its early stages.[32]
Since the early descriptions of human casualties, there have
been numerous studies of vesication in experimental animals, the
hope being the discovery of a model system in which the develop-
ment and healing of mustard-induced cutaneous injury could be
studied. Recently, three animal models have been proposed that
have renewed optimism in finding appropriate methods to study
the interaction between mustard and the skin.
Papirmeister et al.[9] have described well-formed blisters in
human skin grafted to athymic nude mice, whilst Mershon et al.[33]
have produced microblisters in the skin of euthymic hairless
guinea-pigs. The latter model responds in very similar ways to
sulphur mustard challenge in domestic pigs, a model recently
exploited by Mitcheltree et al.,[34] Lindsay and Rice,[32] and Brown
and Rice[35] (figure 2). These three models are currently the only
ones available.
4. Sulphur Mustard Injury in Human Skin

Table I. Physicochemical properties of sulphur mustard[25]

4.1 Gross Pathology
Parameter Description/comments
Chemical structure S.(CH2.CH2.Cl)2
Perhaps the best gross descriptions of human skin lesions are
Molecular weight = 159
those of casualties from the First World War.[5,26,27] More recently,
Boiling point 215–217°C
the author has had the opportunity to observe the gross lesions and
Melting point 14.4°C (for distilled mustard)
microscopy of several Iranian casualties injured during the recent
Specific gravity 1.27
conflict in the Middle East (unpublished observations). The ap-
Vapour pressure pearances of such injuries may be summarised as follows:
temperature (°C) pressure (mm Hg)
• The lesion is a chemical burn with appearances unlike those
0 0.025 seen in thermal, electrical or corrosive (acid/alkali) burns.
14 0.070 There is little or no thrombosis of vessels, but a great degree of
30 0.090 moistness of the affected area. The coagulated appearance of
40 0.450 thermal injuries is not a feature of vesicant injury.[36,37]
Solubility Sparingly soluble in water • The skin at first is pale but then becomes erythematous within a
0.68 g/L, half life = 5 min few hours of exposure. Vesication is not usually seen until the
In weak solutions, hydrolysed to second day and progresses, thereafter, for several more days.
thiodiglycol [S.(CH2.CH2.OH)2]
• Scab formation begins within 7 days once the early blisters
Stability Stable under normal conditions. begin to degenerate. The skin may be made to vesicate in areas
Destroyed by strong oxidising agents
of erythema by slight trauma, e.g. on rubbing, and this phenom-
Toxicol Rev 2003; 22 (2)
114
a differences between animal and human skin with respect to vesica-
E
E
D
D
b accurately reproduce the findings previously described. The model
R has also allowed lesions to be studied at the ultrastructural level in
R
F
F
Fig. 2. (a) The early stages in the development of a sulphur mustard
vapour injury in the Yucatan miniature pig at 24 hours post-exposure. The
cells comprising the epidermis (E) already show advanced degeneration,
nuclear pyknosis and focal cytoplasmic vacuolation. The individual colla-
gen bundles of the dermis (D) are forced apart by the accumulation of
oedema fluid. Note the heavy acute inflammatory cell infiltrate throughout
the dermis and the epidermis is focally separating from the underlying
papillary dermis (arrows). (b) The fully developed microblister at 72 hours
post-exposure. The roof (R) of the blister is composed of intact but degen-
erate epidermal cells and the floor (F) of degenerate papillary dermal
collagen and thrombosed, necrotic papillary dermal capillaries. The blister
cavity contains strands of cytoplasmic debris, red cells and occasional
acute inflammatory cells (arrows). Harris’ Haematoxylin & Eosin x200.
enon is known as Nikolsky’s sign. It does not imply the
persistence of active vesicant.[38]
• Four to six days after exposure, necrosis is complete and
separation of necrotic slough begins. The accompanying oede-
ma and erythema may persist.
• By 16–20 days, separation of slough is complete and re-epithe-
lialisation has begun. Healing may take 3–8 weeks post-expo-
sure to be complete and the casualty is often left with depig-
mented areas surrounded by zones of hyperpigmentation.
Based on these descriptions, it is possible to discern two strik-
ing differences between the lesions seen in animals and those
observed in humans. First, the production of grossly visible blis-
ters occurs regularly in humans but not in animals. These blisters
may enlarge by coalescence and may appear several days after the
removal of the casualty from the affected environment. Secondly,
the healing time in humans is considerably longer than that seen in
animals.[5,39] Several attempts have been made to explain the
Rice
tion, and these have been alluded to previously.[7,8]
4.2 Microscopy and Ultrastructural Observations of
Human Vesicant Injuries
Although microscopic descriptions of First World War vesicant
agent-induced lesions exist, more recently Papirmeister et al.[40]
have described a model (full-thickness human neonatal foreskin
grafted to congenitally athymic nude mice) that appears to very
an attempt to reveal additional information about the exact histo-
genesis of vesicant-induced cutaneous injuries.
4.2.1 General Observations
The observations made from this model suggest that the severi-
ty of cutaneous injury appears to depend on the degree of alkyla-
tion occurring in the skin.[39] Several dose regimens of liquid
sulphur mustard were used, based on data derived from earlier
studies by Renshaw:[41] 20 μg/cm–2 = mild injury; 60–120 μg/
cm–2 = moderate injury; 635 μg/cm–2 = severe injury. At these
doses, no systemic effects were noted as the maximum dose only
represented approximately 25% of the percutaneous dose which is
lethal to 50% of exposed animals (LD50).
4.2.2 Microscopic Observations
The microscopic observations can be summarised as follows:
• There were minimal changes at 4 hours, consistent with the
known latency for sulphur mustard cutaneous injuries. By 7
hours there was evidence of vacuolation of basal keratinocytes
which had progressed to focal necrosis accompanied by con-
gestion and oedema of the dermis by 12 hours.
• Widespread, multifocal necrosis of the epidermis accompanied
by early acute inflammation was noted at 24 hours. By 48
hours, full-thickness necrosis had obliterated all normal cellular
features, and there was a striking polymorph infiltrate at the
base of the graft.
• Animals of the high-dose group showed dermo-epidermal sepa-
ration at 24 hours with the formation of a subepidermal blister
at 48 hours. The only deviation from true human injury was the
impression of almost complete re-epithelialisation of ulcerated
lesions by 6 days post-exposure.
4.2.3 Ultrastructural Observations
The use of the electron microscope confirmed and extended the
observations outlined in section 4.2.2 and affirmed that the devel-
opment of the injury was both dose and time dependant. A definite
sequence of morphological changes was described:
Toxicol Rev 2003; 22 (2)
Sulphur Mustard Injuries of the Skin
• Condensation of heterochromatin and loss of euchromatin.
• Blebbing of the nuclear membrane with the formation of per-
inuclear vacuoles.
• Swelling of the endoplasmic reticulum and disintegration of
polysomes.
• Loss of the integrity of the cell membrane.
• Leakage of organelles into the extracellular space.
• Disruption of the anchoring filaments of the hemidesmosomes.
The authors concluded that sulphur mustard injury to human
skin commences at the level of the basal keratinocyte and thus
confirmed the original theories of McAdams.[8] They also drew
some parallels with thermal injury, which is also thought to act by
disrupting the basal epidermal layer.[27] These ultrastructural ob-
servations and the belief that blistering results from dermo-epider-
mal separation at the level of the epidermal basement membrane
have now been confirmed by immunohistochemical studies.[32]
5. Management
There is no specific therapy for sulphur mustard poisoning; the
sole aim of management in such cases is to maintain vital organ
systems and alleviate symptoms. Skin burns can be severe and
may involve extensive areas of the body surface. The naturally
moist areas of the body such as the genitalia, perineal regions,
groins, lower back and axillae often prove to be the most severely
affected areas and crops of fresh blisters may appear at any time up
to 2 weeks after exposure. The burns themselves tend to be
superficial and will heal slowly without active treatment. How-
ever, experience in the clinical management of several Iranian
casualties from the Iran-Iraq War (1984–1987) demonstrated that
those with severe burns required weeks of hospital care followed
by lengthy convalescence and that, despite the superficial nature of
the burn, it is all too easy to underestimate the period of care for
such patients.
5.1 Current Management
The current strategy for the management of sulphur mustard
cutaneous injury is essentially that for a similar degree of thermal
burn;[42] however, it is always important to bear in mind that the
signs and symptoms of injury will not be evident for several hours
after exposure. The overall management can be summarised as
follows:
• For areas of erythema and minor blistering, bland lotions such
as calamine are useful.
1 The use of tradenames is for product identification purposes only and does not imply endorsement.
115
• Topical bacteriostatic agents, such as 1% silver sulphadiazine
(Flamazine™1) cream, were used on Iranian casualties to re-
duce the incidence of secondary infection once the blisters had
ruptured.
• Moderately severe pain and itching are common problems once
blisters have developed and may be managed by the use of mild
analgesics, antihistamines and small doses of diazepam. Occa-
sionally, some cases experience severe pain and these may
require narcotic analgesics such as morphine. Newman-Tay-
lor[22] reported that carbamazapine proved valuable in alleviat-
ing pain in one patient and that its use allowed the withdrawal
of narcotic analgesics.
• Dilute topical corticosteroids have proved beneficial in reliev-
ing irritation and reducing the attendant oedema at exposed
sites; the use in human casualties appeared to have little or no
effect on the subsequent rate of healing of the lesions, so
confirming the earlier observations made by Vögt et al.[43]
• Fluid replacement is calculated in the same way as for a thermal
burn although unlike a thermal burn, large amounts of fluid loss
will only occur once the blisters have formed, rather than in the
first 24 hours.
• Although the time to healing may be long, the evidence sug-
gests that the eventual scar is softer and more pliable than that
seen in thermal injuries. Wound contracture does not appear to
be a major problem in this context despite the predilection for
the naturally moist areas such as the axillae and groin.
• Numerous other drugs and regimens, including bathing in fresh
human breast milk, have been suggested,[44] but there is no
evidence that these have any therapeutic value in established
cases.
5.2 Post-Exposure Surgical Intervention
Based on our previous experiences with Iranian casualties and
the literature,[4,5,39] it was recognised that large, full-thickness
burns heal very slowly and may ultimately require skin grafting to
achieve epithelial coverage of the ulcerated site. The success of
grafting, assessed either by an improvement in the healing time or
by the survival of the graft, will be determined by the efficiency of
the tangential excision in cutting back to healthy tissue not show-
ing sulphur mustard-induced damage. To ensure that excision is
complete, both the depth and lateral extent of alkylation in the skin
would need to be determined.
Toxicol Rev 2003; 22 (2)
116
100 Untreated
Emery cloth
80 Sanding disc
Grinding stone
Healing (%)
60
40
20
0 technology within the medical and surgical spheres, we have
0 1 3 performed (and reported) studies that have examined the role of
Time post-dermabrasion (wks)
Fig. 3. Comparative rates of epithelial healing for three different methods of
dermabrasion of established mustard vapour burns in pigs.[50]
Histological examination of sulphur mustard-induced skin inju-
ries in an established pig model[35,45] has shown that the delayed
rate of healing may be due, in part, to two distinct mechanisms:
• Alkylation of epidermal cells extends beyond the immediate
region of exposure; although cells in this area may not ulti-
mately die, the level of alkylation may be sufficient to delay or
even prevent cell replication. Re-epithelialisation of ulcerated
lesions relies partly on the replication of cells from the undam-
aged epidermis at the edge of the lesion and partly from intact
hair shafts in the base.[4]
• In addition to achieving effective epidermal regeneration, re-
epithelialisation itself is dependent on the presence of an appro-
priate substrate on which regeneration can occur.[46,47] The
papillary dermis and basement membrane are vital in this
respect and not only provide a structural scaffold for the epider-
mis but also act as signals for the subsequent differentiation of
the overlying epidermis.[48] Immunohistochemical staining of
the papillary dermis in pigs has shown that the collagen at this
site is altered by exposure to sulphur mustard, and in this
altered state, it may no longer function normally.[32]
5.2.1 Dermabrasion
Over the last few years, a number of wound healing studies
have been undertaken in the author’s laboratory that have been
directed towards establishing a more normal rate of wound healing
by removing alkylated and sublethally injured epidermis and
superficial papillary dermis. Rather than resorting to formal surgi-
cal excision, the technique of dermabrasion has been employed.
This consists of simply scrubbing the wound surface under general
anaesthesia with a sterile abrasive surface until punctate bleeding
from the deeper, viable tissues is achieved. Currently, the tech-
nique is used in cases of severe facial acne and is well recognised
in the management of deep dermal thermal burns.[49]
Studies using a rotating abrasive surface on a hand-held electric
drill to achieve superficial dermabrasion of established small,
Rice
circular mustard vapour burns in our porcine model have shown
that the healing time of such injuries can be reduced from 12
weeks to 3–4 weeks[50] (figure 3).
5.2.2 Laser Debridement (‘Lasablation’)
Following these initially encouraging results obtained through
mechanical dermabrasion, and the more recent advances in laser
surgical lasers to achieve enhancement of the healing rate of both
sulphur mustard and Lewisite burns through vaporising the necrot-
ic burn surface.
The studies employed both erbium:yttrium aluminium garnet
(YAG) and pulsed CO2 surgical lasers[51] to resurface established
vesicant burns under general anaesthesia at between 3 and 4 days
post-exposure. Sulphur mustard burns treated by pulsed CO2 laser
debridement showed a 3-fold increase in healing rate compared
with controls (untreated) at 2 weeks post-exposure (p = 0.061)
[figure 4]. This increase was achieved with only partial removal of
necrotic tissue and may be due to disruption of the eschar–wound
bed interface either allowing earlier migration of regenerating
epidermis or facilitation of phagocytosis of dead tissue as a result
of a reduction in the eschar volume.[51] Similar results were
achieved with Lewisite vapour-induced burns, with a 4-fold in-
crease in healing rate at 1 week post-surgery.[52]
6. Conclusions
Mustard gas was developed as a chemical warfare agent more
than 80 years ago. Despite intensive study, little advance in
methods recommended for the management of skin burns has been
made. Based on a number of relatively simple studies and careful,
* p = 0.061
Control
Lasablation
*
100
80
*
Healing (%)
60
40
20
0
1 2 3
Time (wks)
Fig. 4. Healing rates of control and laser ablated sulphur mustard burn
lesions in the large white pig.[51]
Toxicol Rev 2003; 22 (2)
Sulphur Mustard Injuries of the Skin
meticulous observation of the way blister agent burns develop and
subsequently heal, a post-exposure strategy has been formulated
that appears to overcome some of the clinical problems associated
with this type of injury.
The techniques of mechanical dermabrasion and ‘lasablation’
represent notable advances in the management of chemical agent
burns. In addition to their use in a military context, it seems likely
that such procedures would similarly benefit the management of
civilian chemical and thermal injuries to the skin. The clinical
value of such an approach will not be confirmed unless and until
sulphur mustard is used again. Despite significant progress under
the terms of the Chemical Weapons Convention, such use cannot
be ruled out.
Acknowledgements
No sources of funding were used to assist in the preparation of this
manuscript. The author has no conflicts of interest that are directly relevant to
the content of this manuscript.
© British Crown copyright 2003/Dstl – published with the permission of
the Controller of Her Majesty’s Stationery Office.
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Dstl Porton Down, Salisbury, Wiltshire, SP4 OJQ, UK.
Toxicol Rev 2003; 22 (2)