BLISTER AGENTS (VESICANTS)
SECTION I - INTRODUCTION
a. Blister agents (vesicants) are likely to be used to produce casualties and to force opposing troops to wear full protective equipment. Blister agents are used to degrade fighting efficiency rather than to kill, although exposure to such agents can be fatal. Thickened blister agents will contaminate terrain, ships, aircraft, vehicles, or equipment and present a persistent hazard. ; Vesicants include sulphur mustard (H and HD), nitrogen mustards (HN), lewisite (L) (this may be used in mixture with HD), and halogenated oximes (example, phosgene oxime (CX)). Halogenated oximes properties and effects are very different from those of the other vesicants.
b. Vesicants burn and blister the skin or any other part of the body they contact. They may act on the eyes, mucous membranes, lungs, and skin; mustards may act on blood-forming organs. They damage the respiratory tract when inhaled and cause vomiting and diarrhea when ingested.
c. Some vesicants have a faint odor; others are odorless. They often have more serious effects than is immediately apparent. Both L and CX cause immediate pain on contact. The mustards are insidious in action, with little or no pain at the time of exposure. In some cases, signs of injury may not appear for several hours.
d. Vesicants poison food and water and make other supplies dangerous to handle.
e. Vesicants can be disseminated by artillery shell, mortar shell, rocket, aircraft spray, and bomb.
f. The severity of a blister agent burn is directly related to the concentration of the agent and the duration of contact with the skin.
4-2. Self-Aid
a. Assume MOPP 4 whenever liquid or vaporized agents are known to be
present.
b. Liquid vesicants in the eyes or on the skin require immediate
decontamination procedures as outlined in appendix d.
4-3. Precautions in Receiving Casualties
a. Casualties contaminated with vesicants endanger unprotected
attendants. Individuals in contact with these casualties must be at MOPP
4, plus wear a butyl rubber apron.
b. Special precautions must be taken in receiving contaminated
casualties to prevent injury to others. Contaminated casualties are
decontaminated outside the field MTF to prevent vapor accumulation indoors.
They are kept separated from clean (uncontaminated) casualties until
decontamination is completed. Contaminated litters, blankets, and
equipment must be left outdoors. Decontamination is necessary for
equipment, vehicles, watercraft, and aircraft that have been used to
transport contaminated casualties. Appendix B
contains further information on decontamination.
c. Unhydrolyzed mustard on patients' skin surface can present a hazard
to individuals receiving or treating these patients even after several
hours. As mustard reacts with skin and subcutaneous tissue, it is
hydrolyzed; however, the destroyed tissue becomes a barrier for complete
hydrolyzation of excess mustard on the surface.
a. The protective mask protects only the face, eyes, and respiratory
tract. The mask protects against both liquid and vapor forms of vesicants.
b. Chemical protective overgarments help prevent the vesicant from
reaching the skin.
4-5. Disposition of Casualties
See section V for disposition of casualties with blister agent burns.
a. Physical Properties. Mustard is an oily liquid ranging from
colorless, when pure (neat), to dark brown when plant-run (unpurified form
when first produced). Mustard is heavier than water, but small droplets
float on water surfaces and present a special hazard in contaminated areas.
It smells like garlic or horseradish. Distilled HD, the most common form
of mustard, freezes at 57¡F (14¡C) and boils at 442¡F (228¡C). It is only
slightly soluble in water, which gradually destroys it, but undissolved
mustard may persist in water for long periods. It is most soluble in fats
and oils. It is freely soluble in acetone, carbon tetrachloride, alcohol
and liquid fuels (gasoline, kerosene, and diesel); however, these solvents
do not destroy mustard. Mustard disappears from contaminated ground or
materials through evaporation or through hydrolysis. It is rapidly
destroyed by decontaminating chemicals or by boiling in water. The primary
use of mustard is to cause delayed casualties by the liquid and vapor
effects on the skin and the eyes and by the vapor effects through the
respiratory system.
b. Persistence. The persistence of hazard from mustard vapor or liquid
depends on the degree of contamination by the liquid, type of mustard,
nature of the terrain and soil, type of munition used, and weather
conditions. Mustard may persist much longer in wooded areas than in the
open. Mustard persists two to five times longer in winter than in summer.
The hazard from the vapor is many times greater under hot conditions than
under cool conditions. Standard chemical agent detector kits should be
used to detect the presence of HD vapor in the field.
c. Cumulative Effect. Even very small repeated exposures to mustard
are cumulative in effect. For example, repeated exposures to vapors from
spilled mustard can kill or produce 100 percent disability by irritating
the lungs and causing a chronic cough and pain in the chest.
[DATA UNAVAILABLE - FORTHCOMING]
4-7. Effects of HD on the Eyes
a. Pathology, Symptoms, and Prognosis. In a single exposure, the
eyes are more susceptible to mustard than either the respiratory tract or
the skin. Figures 4-1 through 4-4 show effects of mustard on the eyes.
Conjunctivitis follows an exposure time of about 1 hour to a concentration
barely perceptible by odor. This exposure does not affect the respiratory
tract or the skin significantly. A latent period of 4 to 12 hours follows
mild exposure, after which there is lacrimation and a sensation of grit in
the eyes. The conjunctivae and the lids become red and edematous. Heavy
exposure irritates the eyes after 1 to 3 hours and produces some severe
lesions. Although temporary blindness may occur, permanent blindness is
very rare. Casualties should therefore be reassured and a positive
attitude taken. Care must be exercised to avoid transferring liquid agent
from the hands to the eyes. Mustard burns of the eyes may be divided as
follows:
(1) Mild conjunctivitis (75 percent of cases in World War I).
Recovery takes 1 to 2 weeks.
(2) Severe conjunctivitis with minimal corneal involvement (15
percent of the cases in World War I). Blepharospasm, edema of the lids,
and conjunctivae occur, as may orange-peel roughening of the cornea.
Recovery takes 2 to 5 weeks.
(3) Mild corneal involvement (10 percent of the cases in World
War I). Areas of corneal erosion stain green with fluorescein.
Superficial corneal scarring and vascularization occurs as does iritis.
Temporary relapses occur and convalescence may take 2 to 3 months.
Hospital care is indicated for casualties of this type.
(4) Severe corneal involvement (about 0.1 percent of mustard
casualties in World War I). Ischemic necrosis of conjunctivae may be seen.
Dense corneal opacification with deep ulceration and vascularization
occurs. Convalescence may take several months. Patients may be
predisposed to late relapses.
b. Treatment.
(1) Self-aid.
(a) The risk of leaving liquid vesicant in the eyes
is much greater than the risk from exposure of the eyes to vesicant vapors
during the short period of decontamination. Decontamination must,
therefore, be done despite the presence of vapor.
(b) Speed in decontaminating the eyes is absolutely
essential. This self-aid procedure is very effective for mustard within
the first few seconds after exposure but is of less value after 2 minutes.
Decontamination is done the same as for other vesicants (app D).
(2) Treatment of mustard conjunctivitis.
(a) Mild lesions require little treatment. Although the
lesions may become infected, a steroid antibiotic eye ointment, such as
dexamethasone sodium phosphate-neomycin ophthalmic ointment, can be
applied. Ophthalmic ointments, such as 5 percent boric acid ointment, will
provide lubrication and minimal antibacterial effects. The application of
sterile petroleum jelly between the eyelids will provide addi-
tional lubrication and prevent sealing of the eyelids.
(b) More severe injuries will cause enough edema of
the lids, photophobia, and blepharospasm to obstruct vision. This
obstruction of vision alarms patients. To allay their fears, the lids may
be gently forced open to assure them that they are not blind.
(c) The pain is controlled best by systemic narcotic
analgesics. Patients with severe photophobia and blepharospasm should have
one drop of atropine sulfate solution (1 percent) instilled in the eye
three times a day. To prevent infection, a few drops of 15 percent
solution of sodium sulfacetamide should be instilled every 4 hours. Other
antibacterial ophthalmic preparations may be substituted for sodium
sulfacetamide.
(d) The eye must not be bandaged or the lids allowed
to stick together. Sealing of the lids may be prevented as described in a
above. The accumulation of secretions in the conjunctival sac or pressure
on the eye predisposes to corneal ulceration. To prevent complications,
the patient should be treated by an ophthalmologist as soon as possible.
When possible, the patient should be kept in a darkened room, given dark
sunglasses, or given an eyeshade to help his photophobia.
[DATA UNAVAILABLE - FORTHCOMING]
Figure 4-3. Casualty showing eye effects of mustard vapor.
Figure 4-4. Casualty showing effects of mustard conjunctivitis.
c. Classification of Eye Lesions. See paragraph 4-29b.
4-8. Effects of HD on the Skin
a. Pathology. The severity of the lesions and the rapidity with which
they develop are greatly influenced by weather conditions as well as by the
degree of exposure. Hot, humid weather strikingly increases the action of
mustard. Even under temperate conditions, the warm, moist skin of the
perineum, external genitalia, axillae, antecubital fossae, and neck are
particularly susceptible.
(1) Latent period. Exposure is followed by a latent period
which varies with the degree of exposure. It may be as short as an hour
after liquid contamination, when the weather is hot and humid, or as long
as several days after mild vapor exposures. With most vapor exposures in
temperate weather, the latent period is usually 6 to 12 hours.
(2) Erythema. Erythema gradually appears (2 to 48 hours postexposure)
and becomes brighter, resembling sunburn (figs 4-5 and 4-6). Slight edema
of the skin may occur. In severe burns, the edema may limit motion of the
limb. Itching is common and may be intense. As the erythema fades, areas
of increased pigmentation are left (this sequence is reminiscent of that
seen in sunburn).
(3) Vesication. Except with mild vapor burns, erythema is followed by
vesication (figs 4-7, 4-8, 4-9, and 4-10). This is caused by progressive
development of liquefaction necrosis of the cells in the lower layers of
the epidermis. Exudation of tissue fluid into the spaces so formed results
in an intraepidermal vesicle. Clinically, multiple pinpoint lesions may
arise within the erythematous skin; these enlarge and coalesce to form the
typical blister (which is unusually large, domed, thin-walled, yellowish,
and may be surrounded by erythema). The blister is filled with a clear or
slightly yellow liquid that tends to coagulate. The blister fluid does not
contain mustard and is not a vesicant. Liquid contamination of the skin
usually results in a ring of vesicles surrounding a gray-white area of skin
which, although necrotic, does not vesicate. As noted in paragraph 4-3c
above, unhydrolyzed vesicant on contaminated patients may pose a hazard to
other individuals coming in contact with them.
Figure 4-5. Noncasualty with erythema.
(5) Healing. Since the damage to the corium is relatively
superficial, healing occurs with little scar tissue formation, except in
more extensive or infected burns where scarring is more severe.
(6) Pigmentation. Mustard burns usually are followed by a persistent
brown pigmentation except at the site of actual vesication, where there may
be a temporary depigmentation due to exfoliation of the pigmented layers of
the skin (figs 4-11 and 4-12).
(7) Hypersensitivity. Repeated burns may lead to hypersensitivity of
the skin to mustard.
b. Symptoms and Prognosis.
(1) An outstanding characteristic of the action of mustard is
its insidiousness. Exposures to mustard are not accompanied by immediate
symptoms, nor do any local manifestations occur until erythema develops.
At this time there may be itching and mild burning. This pruritus may last
several days and persist after healing. The blisters may be painful.
Figure 4-6. Casualty with generalized erythema and systemic intoxication.
Figure 4-7. Casualty with severe vestication.
(3) Moderate contamination of mustard skin lesions with saprophytic
bacteria, which causes no appreciable inflammatory reaction, does not seem
to delay the healing of mustard burns. Active infection, with inflammation
and purulent exudation, may increase the severity of the lesions and delay
healing greatly (fig 4-14).
c. Diagnosis of Skin Lesions Due to Mustard. Similar skin burns are
produced by mustard and the nitrogen mustards. Mustard burns are also
similar in appearance to those caused by arsenical vesicants.
Differentiation of mustard lesions from those produced by arsenicals is
based upon:
(1) History of exposure to mustard.
(2) Absence of pain or discomfort at time of contamination (L is
irritating and immediately painful).
(3) A zone of erythema surrounding blisters (not predominant
with arsenicals). It should be remembered that vesicular lesions, much
like mild mustard burns, may be produced in sensitive individuals by a
variety of substances, notably plant poisons such as poison ivy or poison
oak. However, the skin lesions of plant contact are on exposed skin and
linear in configuration. The earliest affected areas of skin from mustard
are the skin folds, groin, and inner aspects of the extremities.
d. Decontamination of Casualties. Casualties who have experienced
liquid mustard contamination of the skin or clothing will seldom be
received by the medical service in time to prevent subsequent blistering.
Nevertheless, if erythema has not appeared, known or likely contaminated
skin areas should be decontaminated as described in appendix d. Cut away
and discard hair contaminated with liquid mustard. Decontaminate the
exposed scalp with the M291 Skin Decontaminating Kit. If short of these
substances, use 0.5 percent aqueous chlorine solution for decontamination
of skin and hair. Wash off the decontaminating solutions promptly (within
3 or 4 minutes) to prevent additional skin injury, taking
care that none of the solutions wash into the eyes. If erythema of the
skin has appeared, soap and water
is the best decontaminant. Contaminated clothing should be removed
promptly from casualties outside the treatment facility to prevent more
severe burns and to lessen the vapor hazard to patients and attendants.
e. Treatment of Mustard Erythema. Mustard erythema in mild cases
requires no treatment. If an annoying itch is present, considerable relief
may be obtained with topical steroid creams or sprays. Severe erythema
around the genitalia may become quite painful and associated weeping and
maceration may ensue. Often, treatment with exposure of the area is
desirable and care must be taken so that secondary infection of tissue does
not occur.
f. Treatment of Mustard Blisters.
(1) Once blisters have broken, it is best to remove its ragged
roof to decrease the possibility of secondary infection. Cleanse the area
with tap water or saline, then apply sterile petrolatum gauze when the
areas are small. Dressings should be changed and the wound inspected every
3 to 4 days. Small blisters on the face are opened and best left
uncovered. Large blisters may best be treated by open methods. Apply
about one-eighth of an inch thick layer of 10 percent mafenide acetate or
silver sulfadiazine burn cream to the blisters as a topical antibiotic
agent. Figure 4-15 shows a casualty with widespread vesication caused by
mustard burns.
(2) If the dressing sticks to the wound, care will be necessary
to avoid pulling off the top of the blister. It is good practice to trim
the edges of adherent gauze, leave it in place, and put a fresh dressing
over it. If the wound needs to be examined, the dressing may be soaked off
with sterile saline.
g. Treatment of Denuded Areas.
(1) Contamination of mustard burns with saprophytic bacteria is
common and unless careful wound care is given, serious infection may
result. If there is no inflammatory reaction, the treatment is the same as
for uncontaminated burns. Figure 4-16 shows burns produced by the reaction
of mustard vapor with sweat.
(2) Wounds which become infected must be treated with appropriate
antibiotics after adequate cultures have been obtained. The medical
officer must evaluate the infection and make the appropriate decision
regarding further care.
h. Specific Antibacterial Therapy. Routine wound inspection aids in
the early detection and institution of appropriate therapy for any
complicating bacterial infections. Appropriate antibacterial drugs may be
given either locally or systemically, as indicated. The early use of an
appropriate topical antibacterial agent (such as mafenide acetate or silver
sulfadiazine cream) may prevent a bacterial infection.
4-9. Effects of HD on the Respiratory Tract
a. Pathology.
(1) Inhalation of mustard vapor causes damage primarily to the
laryngeal and tracheobronchial mucosa. The lesion develops slowly after
exposure. A single exposure to a small amount of mustard vapor ordinarily
does not produce significant injury. Repeated or chronic exposure to low
concentrations of mustard vapor may lead to progressive pulmonary fibrosis,
chronic bronchitis, and bronchiectasis. Moderate exposures result in
hyperemia of the respiratory mucous membrane and necrosis of the lining
epithelium. With severe exposures, the necrotizing action is accompanied
by exudation resulting in a diphtheritic-like pseudomembrane, which may
form a cast of the tracheobronchial tree.
(2) In the more severe cases, the pulmonary parenchyma shows
congestion, mild patchy edema, and focal atelectasis. Altogether, these
changes may be insufficient to cause hypoxia and they are frequently
complicated by bacterial infection of the lungs, which results in
suppurative bronchitis and bronchopneumonia. The latter is responsible for
almost all deaths following vapor exposures. The early mortality from
mustard among American troops in World War I (slightly more than 2 percent)
was due almost entirely to such pulmonary complications following
inhalation of vapor.
b. Symptoms and Prognosis. Respiratory tract lesions develop slowly
and do not reach maximal severity for several days. Symptoms begin with
hoarseness, which may progress to loss of voice. A cough (worse at night)
appears early and later becomes productive. Fever, dyspnea, rhonchi, and
moist rales may develop. The incidence of bronchopneumonia is high.
Convalescence is slow; the cough may persist a month or longer. Milder
symptoms, like hoarseness, last only 1 or 2 weeks.
c. Treatment of Respiratory Tract Injury Due to Mustard. Mild
respiratory tract injury, with hoarseness and sore throat only, usually
requires no treatment. Cough may be relieved by codeine-containing cough
syrups. Laryngitis and tracheitis may be treated symptomatically with
steam or sterile cool mist inhalations. If more severe respiratory tract
injury is suspected, hospitalization may be advisable. If a bacterial
pneumonia occurs, isolation of the specific organisms with their antibiotic
sensitivities should be performed, then antibiotic therapy can be limited
to the specific agents.
4-10. Systemic and Gastrointestinal Effects of HD
a. Pathology.
(1) Ingestion of mustard produces vacuoles and nuclear swelling
of the epithelial cells of the gastrointestinal tract, with eventual
necrosis and desquamation with hemorrhage. Absorption of the mustard from
the intestinal lumen results in damage to the blood-forming organs
mentioned in (2) below.
(2) With lesser skin or respiratory exposures to mustard, no apparent
systemic lesions develop. However, with amounts approaching a lethal dose,
injury to the hematopoietic tissues (bone marrow, lymph nodes, and spleen)
may result. Such hematopoietic damage is reflected in the peripheral blood
by leukopenia, thrombocytopenia, and anemia. Lymphoid tissue is involved
also, with consequent lymphocytopenia.
b. Symptoms.
(1) Ingestion of food or water contaminated by liquid mustard produces
nausea and vomiting, pain, diarrhea, and prostration. Mustard vapor does
not significantly contaminate food or water.
(2) Exposure of only the skin to mustard may cause systemic symptoms
such as malaise, vomiting, and fever, coming on about the time of onset of
the erythema. With severe exposures, particularly by extensive liquid
contamination of the skin, these symptoms may be so marked as to result in
prostration. Exceptional cases of severe systemic mustard poisoning may
also present central nervous symptoms (such as cerebral depression) and
parasympathomimetic effects (such as bradycardia and cardiac
irregularities). (In animals, cerebral excitation and salivation have been
observed, as well as bloody diarrhea with excessive loss of fluid and
electrolytes.) Hemoconcentration and hypovolemic shock may occur. It must
be emphasized that severe systemic effects only occur when sufficient agent
has been absorbed systemically. Lesser mustard exposures do not cause
severe systemic effects.
c. Prognosis.
(1) With mild to moderate field exposures to mustard vapor, it
is not anticipated that deaths will occur from the systemic effects of the
absorbed mustard. However, death may occur from prolonged exposures to
high concentrations of mustard vapor or, in instances of extensive liquid
contamination of the skin, where decontamination is neglected or unduly
delayed. The occurrence of shock or pronounced leukopenia in these cases
may be regarded as grave prognostic signs. Bone marrow failure is the most
frequent cause of late deaths.
Figure 4-15. Casualty with widespread vesication.
d. Self-Protection. Never drink water which has been subjected to
chemical attack until it has been certified as fit to drink by the Medical
Department. Never eat foods which have been exposed to liquid vesicants,
unless in sealed cans or aluminum-laminated pouches (meal, ready to eat
(MRE) pouches), until examined by U.S. Army veterinary personnel and
certified as safe to eat. Refer to FM 3-5, FM 8-10-7, and TB MED 577 for
additional information.
e. Treatment of Systemic Mustard Poisoning.
(1) In the treatment of systemic symptoms, atropine subcutaneously
(0.4 to 0.8 mg; NOT the 2 mg automatic injector) may prove useful in
reducing the gastrointestinal activity. General discomfort and
restlessness may be treated with sedatives but may also be a manifestation
of hypovolemic shock from severe systemic injury. In the exceptional cases
of severe systemic poisoning with vomiting and diarrhea, leukopenia,
hemoconcentration, and shock, every effort should be made to maintain an
adequate nutritional status and to replace the loss of fluid and
electrolytes. There may be a need to monitor the white blood count,
hemoglobin, and platelets in severe systemic poisoning. If the white blood
count decreases significantly, isolation and appropriate antibiotics may be
necessary. It has been suggested by some authorities that sodium
thiosulfate will prevent or reduce damage from mustard, provided that it can be given IV within 20
minutes of exposure. Its efficacy is very doubtful if given later.
(2) Injury due to the ingestion of liquid mustard in food or water may
require morphine and atropine for relief of pain and shock therapy for
collapse.
The HNs are oily, colorless, pale yellow liquids, sparingly soluble in
water but freely soluble in organic solvents. Some have a faint fishy
odor, while others are odorless. Their volatility varies with the
particular compound. All are persistent but not equally so. The most
likely to be seen are HN1 and HN3. Nitrogen mustard (HN1) is more volatile
and less persistent than HD but only one-fifth as vesicant to the skin as
mustard. Nitrogen mustard (HN3) is less volatile and more persistent and
about equal to HD in its vesicant effects. Nitrogen mustards are less
readily hydrolyzed than Hd. All their hydrolytic products, except the
final ones, are toxic.
4-12. Effects of HN on the Eyes
a. Pathology and Symptoms. In single exposures, HN irritates the
eye in doses which do not significantly damage the skin or respiratory
tract. This irritation appears sooner than that from Hd. Mild or moderate
exposure causes light smarting and lacrimation within 20 minutes.
Thereafter, symptoms may wax and wane until they become persistent about 2
1/2 hours later and reach the maximum in 8 to 10 hours. After more severe
exposure, symptoms begin immediately and progress for 24 hours or longer.
Mild exposure produces erythema and edema of the palpebral and bulbar
conjunctivae and superficial, steamy haziness of the cornea. Irritation,
lacrimation, deep eye pain, miosis, and photophobia are usually present.
After more severe exposure, these symptoms are followed by spotty
hemorrhagic discolorations of the iris. The corneal epithelium shows a
roughened, lusterless surface, with areas of punctate staining demonstrable
by instilling fluorescein. Severe exposure may cause the corneal
epithelium to exfoliate. Slit lamp examinations will reveal clouding and
edema of the corneal substance extending deep below the Bowman's membrane.
Local necrosis of the cornea may rupture the globe.
b. Prognosis. The prognosis in contamination of the eye with any
liquid HN is serious unless the agent is removed by immediate
decontamination. Mild injury progresses to complete recovery in about 2
weeks; severe injury requires 9 to 12 weeks or longer. The cornea heals by
vascularization, and scarring may be expected in severe cases. The iris is
frequently left discolored and atrophied.
c. Treatment. The treatment is the same as for HD conjunctivitis (para
4-7b(2) ). In general, the lesions and symptoms are more severe, requiring
intensive and early treatment. Spasms of the ciliary and orbicular muscles
may require frequent instillation of atropine for relief of pain.
[DATA UNAVAILABLE - FORTHCOMING]
4-13. Effects of HN on the Skin
a. Pathology and Symptoms. In mild vapor exposures, there may be no
skin lesions. After severe vapor exposure or after exposure to liquid HN,
erythema may appear earlier than in HD contamination. There may be
irritation and itching as with Hd. Later, blisters may appear in the
erythematous areas. The skin lesions are similar to those caused by Hd.
b. Prognosis. Prognosis is similar to that of HD burns (para 4-8b).
c. Treatment. If early decontamination has not been done, late
decontamination should be performed even if erythema is already present and
no liquid HN is visible on the skin. The rate of absorption of liquid HN
through the skin is slower than that of Hd. Therefore, to prevent systemic
toxicity, decontamination should be done as early as possible (within 2 or
3 hours after exposure even if it increases the severity of the local
reaction).
4-14. Effects of HN on the Respiratory Tract
a. Pathology. The lesions caused by HN are similar to those caused
by Hd. The lesions decrease in severity down the respiratory tract from
the point of entry. In the nose, larynx, and trachea, there may be
swelling, erythema, and necrosis of the mucosa, followed by sloughing and
fibrinous exudation. Small multiple ulcerations are commonly seen in the
pharynx and tonsillar areas. Laryngeal edema and necrosis may lead to
respiratory obstruction. In severe cases, the damage may extend to the
bronchioli and alveoli. Although pulmonary edema usually is not massive,
secondary pulmonary infection is common.
b. Symptoms. The symptoms are the same as those due to HD; namely,
delay in appearance, irritation of the nose and throat, hoarseness
progressing to loss of voice, and a persistent cough. Fever, dyspnea,
rhonchi, and moist rales may develop. Chemical pneumonitis may appear
after the first 24 hours.
c. Prognosis. Mild inflammation of the trachea is likely to result in a persistent cough.
Low-grade fever may persist a week or longer. The prognosis is grave if there is severe
respiratory tract involvement. Late deaths due to pneumonia may occur.
d. Treatment. The treatment of respiratory tract involvement is the
same as for HD (para 4-9c).
4-15. Effects of HN on the Gastrointestinal Tract
Following oral administration or systemic absorption, HN injures the
intestinal tract. The ingestion of 2 to 6 mg of HN causes nausea and
vomiting.
a. Pathology. The most specific effects of HN are on the hematopoietic
and lymphoid tissues. These effects follow absorption from the intact
skin, respiratory or gastrointestinal tract. In bone marrow, the
degenerative changes can be detected within 12 hours and may progress to
severe aplasia. The thymus, spleen, and lymph nodes involute rapidly, with
necrosis and phagocytosis of their lymphocytes. This injury is
demonstrable in the blood as a transient leukocytosis of a few hours
duration, followed by severe lymphopenia, granulocytopenia,
thrombocytopenia, and a moderate anemia. The blood picture may show little
change other than lymphopenia for 5 to 10 days after exposure, when the
white count may fall to 500 cells per cubic millimeter (mm3) or lower. The
various HNs differ in their ability to produce these changes.
b. Diagnosis. Diagnosis is based upon a history of exposure, a faint
fishy odor on the skin and clothing, and the signs and symptoms described
in paragraph 4-15 and a above.
c. Prognosis. Severe leukopenia, thrombocytopenia, and a hemorrhagic
diathesis are grave manifestations.
d. Treatment. Frequent white blood cell and hematocrit determinations
and examination of peripheral blood smears are necessary to institute
proper treatment if anemia and thrombocytopenia occur. Severe vomiting and
diarrhea may necessitate IV supplementation with balanced salt solutions or
volume expanders. Sedatives, opiates, and atropine are to be used
judiciously. The probability of infection with severe leukopenia may be
significant and isolation of the patient to protect against infection is
appropriate. If infection does occur, it should be vigorously treated with
antibiotics.
a. These agents are organic dichloroarsines. The main ones are
phenyldichloroarsine (PD) and chlorovinyldichloroarsine (L).
Ethyldichloroarsine and methyldichloroarsine have also been used.
b. All arsenical vesicants are colorless to brown liquids, soluble
in most organic solvents but poorly soluble in water. In general, they are
more volatile than mustard and have fruity to geranium-like odors. They
react rapidly with water to yield the corresponding solid arsenoxides, with
concurrent loss of volatility and most of their vesicant properties. As
liquids they gradually penetrate rubber and most impermeable fabrics.
c. They are much more dangerous as liquids than as vapors. The liquids
will cause severe burns of the eyes and skin, while field concentrations of
the vapors are unlikely to cause permanent significant injuries. Immediate
decontamination is required to remove the liquid agents in time to prevent
severe burns, but decontamination is not required for vapor exposure unless
pain is experienced. When inhaled, the vapors cause sneezing and may
produce irritation of the upper respiratory tract. More significant
respiratory injury is unlikely from ordinary field concentrations of vapor.
4-18. Effects of Arsenical Vesicants on the Eyes
a. Pathology, Symptoms, and Prognosis. Arsenical vesicants cause
severe damage to the eye. On contact, pain and blepharospasm occur
instantly. Edema of the conjunctivae and lids follows rapidly and closes
the eye within an hour. Inflammation of the iris usually is evident by
this time. After a few hours, the edema of the lids begins to subside,
while haziness of the cornea develops and iritis increases. The corneal
injury, which varies with the severity of the exposure, may heal without
residuals, induce pannus formation, or progress to massive necrosis. The
iritis may subside without permanent impairment of vision if the exposure
was mild. After heavy exposure, hypopyon may ensue, terminating in
necrosis, depigmentation of the iris, and synechia formation. Arsenical
vesicants instantly produce a gray scarring of the cornea, like an acid
burn, at the point of contact. Necrosis and sloughing of both bulbar and
palpebral conjunctivae may follow very heavy exposure. All injured eyes
are susceptible to secondary infection. Mild conjunctivitis due to
arsenical vesicants heals in a few days without specific treatment. Severe
exposure may cause permanent injury or blindness.
b. Treatment. Treatment is largely symptomatic. In severe cases,
the systemic use of morphine may be necessary for control of pain. When
the conjunctival edema subsides enough to permit ophthalmic examination,
the cornea should be stained with fluorescein to detect erosions, and the
iris should be examined for iritis. Atropine sulfate ointment should be
instilled to obtain and maintain good mydriasis in all cases with corneal
erosions, iritis, cyclitis, or with marked photophobia or miosis. Sodium
sulfacetamide solution may be used to combat infection after the first 24
hours. Sterile petrolatum applied to the lid margins will help prevent
their sticking together. Irrigations of the eye should be sparing,
employing only isotonic or slightly hypertonic solutions (example, 1
percent sodium chloride). Occlusive dressings or pressure on the globe
must be avoided.
4-19. Effects of Arsenical Vesicants on the Skin
a. Pathology. Liquid arsenical vesicants produce more severe lesions
of the skin than liquid mustard. Contamination of the skin is followed
shortly by erythema, then by vesication which tends to cover the entire
area of erythema. The surrounding halo of erythema is less noticeable than
with mustard blisters, although the two are often indistinguishable.
Microscopically, the blister roof is slightly thicker than the mustard
blister roof, consisting of almost the complete thickness of the epidermis
and showing more complete coagulation necrosis and less disintegrative
necrosis than that of the mustard blister. The yellowish blister fluid is
slightly more opaque than that of the mustard blister and, microscopically,
contains more inflammatory cells. It contains a trace of arsenic but is
nontoxic and nonvesicant. Within the corium and subcutaneous tissue, there
is deeper injury to the connective tissue and muscle, greater vascular
damage, and more severe inflammatory reaction than is exhibited in mustard
burns. In large, deep, arsenical vesicant burns, there may be considerable
necrosis of tissue, gangrene, and slough.
b. Symptoms. Stinging pain is felt usually in 10 to 20 seconds after
contact with liquid arsenical vesicants. The pain increases in severity
with penetration and in a few minutes becomes a deep, aching pain. Pain on
contact with liquid arsenical vesicants usually gives sufficient warning so
that decontamination may be begun promptly and deep burns avoided in
conscious victims. After about 5 minutes of contact, there appears a gray
area of dead epithelium resembling that seen in corrosive burns. Erythema
is like that caused by mustard but is accompanied by more pain. Itching
and irritation persist for only about 24 hours whether or not a blister
develops. Blisters are often well developed in 12 hours and are painful at
first, in contrast to the relatively painless mustard blister. After 48 to
72 hours, the pain lessens.
c. Prognosis. The erythema of arsenical vesicants usually recedes
more rapidly than the erythema of mustard and with less pigmentation.
Small blisters heal in about the same time as those due to mustard. Large
lesions may involve deep injuries which heal slowly and require skin
grafts. After repeated burns, sensitization to arsenical vesicants occurs,
as with mustard.
d. Treatment.
(1) Dimercaprol (British anti-lewisite (BAL)) ointment should be
tried on contaminations of the skin which are seen before actual vesication
has begun. Any protective ointment already on the skin must be removed
before application of the BAL ointment because it destroys the latter.
British anti-lewisite ointment is spread on the skin in a thin film, rubbed
in with the fingers, allowed to remain at least 5 minutes, and later washed
off with water. Occasionally, BAL ointment causes stinging, itching, or
urticarial wheals. This condition lasts only an hour or so and should not
cause alarm. Mild dermatitis may occur if BAL ointment is frequently
applied on the same area of skin. Because of its dermatitis properties,
BAL should not be used as a protective (barrier) ointment on unaffected
skin.
(2) Some blistering is inevitable in most arsenical vesicant
cases which come to the Medical Services. The treatment of the erythema,
blisters, and denuded areas is identical with that for similar mustard
lesions. A severe third degree burn involving a large surface area is
similar to a thermal injury and must be managed by IV resuscitation to
correct potential hypovolemic shock. Morphine and splinting of the
affected parts may be necessary to relieve pain. Hospitalization is
indicated when the involved body surface area is greater than 20 percent.
Hospitalization may be indicated when the involved area is less than 20
percent but the depth of the skin involvement appears to be significant.
The wound is debrided and treated with 10 percent mafenide acetate burn
cream, or silver sulfadiazine topical burn cream.
4-20. Effects of Arsenical Vesicants on the Respiratory Tract
a. Symptoms. The vapors of arsenical vesicants are so irritating to
the respiratory tract that conscious casualties will immediately put on a
mask to avoid the vapor. No severe respiratory injuries are likely to
occur except among the wounded who cannot put on masks and the careless who
are caught without masks. The respiratory lesions are similar to those
produced by mustard except that, in the most severe cases, pulmonary edema
may be accompanied by pleural effusion.
b. Prognosis. The prognosis is unknown because there have been no
known human cases of poisoning by vapors of arsenical vesicants.
Extrapolating from animal experiments, the prognosis probably is similar to
that for respiratory injury by mustard.
c. Treatment. The treatment is a combination of that for mustard
respiratory injury (para 4-9c) and that for the systemic effects of
arsenical vesicants (para 4-21c).
4-21. Systemic Effects of Arsenical Vesicants
a. Pathology and Symptoms. Liquid arsenical vesicants on the skin,
as well as inhaled vapor, are absorbed and may cause systemic poisoning. A
manifestation of this is a change in capillary permeability, which permits
loss of sufficient fluid from the bloodstream to cause hemoconcentration,
shock, and death. In nonfatal cases, hemolysis of erythrocytes has
occurred with a resultant hemolytic anemia. The excretion of oxidized
products into the bile by the liver produces focal necrosis of that organ,
necrosis of the mucosa of the biliary passages with peribiliary
hemorrhages, and some injury of the intestinal mucosa. (Acute systemic
poisoning from large skin burns causes pulmonary edema, diarrhea,
restlessness, weakness, subnormal temperature, and low blood pressure in
animals (hypovolemic shock)).
b. Prognosis. Burns severe enough to cause shock and systemic
poisoning are life-threatening. Even if the patient survives the acute
effects, the prognosis must be guarded for several weeks.
c. Treatment.
(1) Indications for treatment. The indications for systemic
treatment, following exposure to arsenical vesicants by any route, are:
(a) A cough with dyspnea and frothy sputum, which may be
blood tinged, and other signs of pulmonary edema.
(b) A skin burn the size of the palm of the hand, or larger, caused
by a liquid arsenical vesicant which was not decontaminated within the
first 15 minutes.
(c) Skin contamination by an arsenical vesicant covering
5 percent (about 1 square foot) or more of the body surface, in which there
is evidence of immediate skin damage (gray or dead-white blanching of the
skin), or in which erythema develops over the area within 30 minutes.
(2) Types of treatment. The following two types of treatment
may be used:
(a) Local neutralization on and within the skin by a
liberal application of BAL ointment. The affected skin is to be left
covered with a layer of ointment. Remove any other protective ointment
before treatment with BAL ointment.
(b) Intramuscular injection of BAL in oil (10 percent).
(3) Dose of BAL in oil.
(a) An immediate IM injection of BAL in oil (10 percent)
is given deep into the muscles of the buttocks. Take every precaution
against injecting into a blood vessel. Dosage must be adjusted to the
estimated weight of the patient (0.5 ml per 25 pounds, up to a maximum of
4.0 ml) as follows:
(b) Intramuscular injection of BAL in oil should be
repeated at different sites in the buttocks at 4, 8, and 12 hours after the
initial injection, for a total of four equal doses.
(c) If pulmonary symptoms or other evidence of severe
arsenical poisoning are present, the interval between the first and the
second dose may be shortened to 2 hours. In severe cases, subsequent half
doses should be given at the rate of one injection per day for 3 to 4 days.
(d) In toxic patients, liberal fluids by mouth (or IV if
necessary) and high-vitamin, high-protein, high-carbohydrate diets are
indicated. If shock is present, the usual supportive measures (such as IV
administration of electrolyte solutions, blood transfusions, or other
vascular volume expanders) are indicated.
(4) Symptoms caused by BAL in oil. Symptoms caused by BAL in
oil appear 15 to 30 minutes after injection and last about 30 minutes.
Unless unduly severe or prolonged, they do not contraindicate the full
course of treatment. The symptoms may include:
4-22. Mixtures of Blister Agents
Arsenical vesicants such as L or PD are often mixed with mustard. These
mixtures do not produce more severe lesions than either agent alone, but
tend to confuse and make diagnosis difficult.
a. Phosgene oxime (CX) (chemical name dichloroformoxime) is an example
of the class of chemical agents called urticants (or nettle gases). These
agents are primarily irritants to skin and mucous membranes, but they
differ from mustard by producing an immediate sensation of pain. This pain
may vary from a mild prickling to a feeling resembling that caused by a
severe bee sting.
b. Phosgene oxime has a disagreeable, penetrating odor. It may appear
as a liquid or as a colorless, low-melting point (crystalline) solid,
readily soluble in water. Phosgene oxime has an appreciable vapor
pressure. A powerful irritant, it is especially effective as a liquid.
4-24. Symptoms and Course of Lesions of Phosgene Oxime
Phosgene oxime is violently irritating to the mucous membranes of the eyes
and nose. Even very low concentrations of it can cause lacrimation. Any
exposure to liquid or vapor which produces pain will also produce skin
necrosis at the site of contact. Within 30 seconds, the area of contact
becomes blanched and is surrounded by an erythematous ring. This is
followed by the appearance of a wheal within the next half hour. At about
24 hours, the original blanched area acquires a brown pigmentation. At 1
week, an eschar forms in the pigmented area; and at about 3 weeks, the
eschar generally sloughs. Itching may be present throughout the course of
healing. Some 20 percent of those exposed to CX may be expected to show
healing delayed beyond 2 months.
4-25. Protection from Phosgene Oxime
A properly-fitting protective mask protects the respiratory system. The
field protective mask, hood, and chemical protective overgarment protect
the body.
Because of the rapid reaction of CX with tissue, decontamination will not
be entirely effective after pain has been produced. Use the M291 Skin
Decontaminating Kit for skin decontamination. If the M291 kit is not
available, flush the contaminated area as rapidly as possible with copious
amounts of water to remove any CX which has not yet reacted with tissue.
4-27. Treatment for Phosgene Oxime Injury
Treat as any other ulcerated necrotic skin lesion with due consideration of
other supportive measures, as indicated.
a. Applicability. This information should be used as guidance by
medical personnel confronted with casualties produced by blister agents.
It assists medical personnel in the forward area in the disposition, rather
than the treatment, of casualties. Therapy for blister agent burns is
given in Sections II through IV.
b. Locations of Burns in World War I Allied Troops. During 1917-1918,
many Allied troops with mustard burns were evacuated needlessly from the
front lines. The analysis below shows the locations of mustard burns among
6,980 cases from World War I. (The incidence of permanent blindness among
the eye cases was low.)
d. Types of Blister Agent Burns.
(1) Two broad types of blister agent patients will not offer a
problem in disposition.
(a) The first type consists of those who have sustained
burns too minor to impair military effectiveness significantly. These
individuals will be classed as noncasualties and returned to their units as
soon as possible with or without treatment.
(b) The second type consists of the totally disabled who
are incapable of either offensive or defensive activity regardless of the
urgency of the military situations. These individuals will be classed as
casualties, promptly treated, and evacuated. Examples are injuries causing
total disability and blindness, vesication of extensive areas of the trunk,
or vesication of an entire limb.
(2) The intermediate types are partially disabled individuals
who can perform only certain kinds of military duties but not others. The
disposition of such cases is likely to constitute the main problem. This
section is confined to typical injuries within this group. In disposing of
these cases, the medical officer will be influenced not only by the
severity of the lesions, but also by the military situation, plus the
general physical and mental condition of the individual and his military
occupational skill.
e. Differentiation Among Injuries According to Agent. For simplicity,
no effort is made here to differentiate between the several blister agents
that may be used by an enemy. While there are differences between the
typical mustard and arsenical vesicant lesions, it is not recommended that
the medical officer in the field try to dispose of such cases separately.
The diagnostic features of the various blister agent lesions and the
therapy peculiar to each are described in Sections II through IV.
(3) Treatment of infected mustard burns of the eye. Secondary
infection is a serious complication and increases the amount of permanent
scarring of the cornea. If infection develops, initial treatment should be
carried out with several drops of a 15 percent solution of sodium
sulfacetamide every 2 hours. After appropriate cultures, specific
antibacterial preparations may be applied. Irrigation should be gentle and
employed only to remove accumulated exudate. Pain is controlled as
described in (2) (c) above. Patients with secondary infection or other
complications should be referred to an ophthalmologist. Local anesthetics
should not be used.
(4) Resorption. If the blister does not rupture, resorption
takes place in about a week. The roof forms a crust beneath which
reepidermization takes place. However, because of their thinness and
tenseness, the blisters are fragile and usually break. If the roof becomes
ragged, the burn may be considered an open wound. Once the blister has
broken, it is best to remove its ragged roof to decrease the possibility of
secondary infection.
(2) Mustard erythema heals at about the
same rate as sunburn of like severity. Areas of multiple pinpoint
vesication usually heal, with desquamation, in 1 to 2 weeks. Healing times
for mustard blisters vary widely with both severity and anatomical
location. In general, blisters of the face heal in 1 to 2 weeks. Blisters
located in other areas may take slightly longer to heal; but if protected from infection,
they will heal in 2 to 4 weeks. If cutaneous injury results in full-thickness coagulation
necrosis, skin grafting may ultimately be necessary. However, a mustard
burn of the skin is usually limited to the epidermis and does not require grafting
(fig 4-13).
(2) Severe injury from ingestion of mustard is rare.
Location of burns
Percent
Eyes
86
Respiratory
75
Scrotum
42
Face
27
Anus
24
Legs
11
Buttocks
10
Hands
4
Feet
1.5
c. World War II Experience. The effects of blister agent burns on
the ability of troops to carry out usual military duties were investigated
during World War II. In the United States, Canada, Great Britain, and
Australia, volunteers ranging from recruits to troops with combat
experience were exposed to blister agents. The degree of disability was
evaluated on assault courses, route marches, or in simulated combat
exercises lasting several days. These observations defined the limitations
of casualty production according to type of lesion and are the basis for
this guidance. It should not be considered an adequate substitute for
clinical observations of blister agent burns in the orientation of medical
personnel.