Biomedical Engineering Reference
In-Depth Information
severe corneal damage with possible perforation of
the cornea and loss of the eye can occur. Eye loss
also results from panophthalmitis.
During World War I, mild conjunctivitis
accounted for 75% of eye injuries, with recovery
in one to two weeks. Moderate conjunctivitis
with minimal corneal involvement, blepharospasm,
edema of the lids and conjunctivae, and orange-
peel roughening of the cornea accounted for 15%
of the cases, with recovery in four to six weeks.
Severe corneal involvement accounted for 10% of
the cases. Those with permanent corneal damage
accounted for less than 1% of cases. About 0.1%
of these severe casualties would meet the criteria
for legal blindness today.
epistaxis, sinus pain or irritation, and irritation or
soreness of the pharynx. The damage begins in the
upper airways and descends to the lower airways in
a dose-dependent manner. Lower airway involve-
ment causes dyspnea and an increasingly severe
cough with increased quantities of sputum. Usually
the terminal airways and alveoli are unaffected
only as a terminal event. Pulmonary edema is not
usually present unless the damage is very severe,
and then usually it is hemorrhagic.
Necrosis of the airway mucosa with resulting
inflammation can cause pseudomembrane
formation. Local airway obstruction due to psue-
domembrane detachment may lead to obstruction
of lower airways. The cause of death in mustard
poisoning is commonly respiratory failure.
Mechanical obstruction by pseudomembranes and
agent-induced laryngospasm are the most common
causes of death in the first 24 hours. Deaths occur-
ring from the third to the sixth day after exposure
result from secondary bacterial pneumonia caused
by bacterial invasion of denuded respiratory
mucosa and necrotic debris. Agent-induced bone
marrow suppression is a contributory factor in
later, septic deaths from pneumonia.
6.4.4.2 Skin
Erythema is the mildest and earliest form of skin
injury after exposure to mustard. It begins to appear
in 2-48 hours after vapor exposure and resem-
bles sunburn and is associated with pruritus or a
burning, stinging pain. The skin sites most sensi-
tive are the warm, moist locations with thinner skin
such as the perineum, external genitalia, axillae,
antecubital fossae, and neck. Within the erythema-
tous areas, small vesicles can develop which may
later coalesce to form bullae. The typical bulla, or
blister, is large, dome-shaped, thin-walled, translu-
cent, yellowish, and surrounded by erythema. The
blister fluid is clear, at first thin and straw-colored,
but later yellowish and tending to coagulate. The
fluid does not contain mustard and is not a vesicant.
At extremely high doses such as those from
liquid exposure, lesions may develop a central zone
of coagulation necrosis with blister formation at
the periphery. These lesions take longer to heal
and are more prone to secondary infection than
the uncomplicated lesions seen at lower exposure
levels.
6.4.4.4 Gastrointestinal (GI) tract
The mucosa of the GI tract is very susceptible to
mustard damage, either from systemic absorption
or ingestion of the agent. Even exposure to a small
amount, will often cause nausea, with or without
vomiting, lasting 24 hours or less. Diarrhea has
been reported; constipation is equally common.
Diarrhea and vomiting beginning days after a high-
dose exposure imply a poor prognosis.
6.4.4.5 Central nervous system (CNS)
The CNS effects of mustard remain poorly defined.
Animal work demonstrated that mustards (partic-
ularly the nitrogen mustards) are convulsants, and
there are several human case reports describing
victims who were exposed to very large amounts
and had neurological effects (obtundation, ataxia,
convulsions) within several hours after exposure
just prior to death. Reports from World War I and
Iran described people exposed to small amounts
6.4.4.3 Airways
The primary airway lesion from mustard is necrosis
of the mucosa with later damage to the muscula-
ture of the airways if exposure is large. The earliest
effects involve the nose, sinuses, and pharynx.
There may be irritation or burning of the nares,
