FACIAL NERVE PALSY AFTER ACUTE EXPOSURE TO DICHLOROMETHANE

1
FACIAL NERVE PALSY AFTER ACUTE EXPOSURE TO
DICHLOROMETHANE

• RUBEN M. JACUBOVICH, MD, MOccH1, MICHAL
  ZILBERBERG, MOccH1, DAN LANDAU MD2, YARON BAR
  DAYAN, MD MHA1,3,
• LIAV GOLDSTEIN MD MHA1
• Surgeon General Headquarters IAF, 2) Surgeon
  General Headquarters, IDF MC 3) Department of
  health system management, the faculty of health
  sciences, Ben Gurion University, Beer Sheva,
  Israel
• Correspondence Dr. Yaron Bar-Dayan, Deputy
  Surgeon General, IAF. Address 16 Dolev St. Neve
  Savyon, Or Yehuda, Israel, Phone [phone],
  E-mail bardayan_at_netvision.net.il

Discussion In the case presented, a worker
engaged in paint stripping with a solvent
containing DCM, in an enclosed space without
adequate body protection, developed facial nerve
palsy, and possibly a mild impairment of the
motor branch of the trigeminal nerve. Carboxyhemog
lobin levels were found in the normal range 24
hours after the exposure. The delay was due to
the late development of facial nerve palsy and
referral to the hospital. The half-life of
carboxyhemoglobin is about 13 hours (18), which
may explain the low levels found in this case.
Moreover, even after accidental DCM fatality,
carboxyhemoglobin blood levels were low despite
lethal levels of dichloromethane in the blood
(9). Rioux and Myers reported two workers who
were found unconscious in a semienclosed area
with a high level of DCM fumes, with initial
presenting Carboxyhemoglobin levels of only 5 and
7 (5). A compilation of data from case reports
in the literature, show that symptoms like
nausea, light-headedness, dizziness, headaches,
correlate with air DCM levels of 1000-5000 ppm,
thus, the high probability of a significant
exposure in our case. This level is far greater
than the ambient exposure standard of 50 ppm
recommended by the American Conference of
Governmental Industrial Hygienists as the
Threshold limit value (TLV). The primary target
organ of DCM is the central nervous system
(1,7,10). Both the direct neurologic effects of
DCM and carbon monoxide toxicity appear to
contribute to the adverse effects of DCM
exposure. During acute and intense exposures to
DCM, which usually occur in poorly ventilated
areas, the direct solvent-narcotic effect may
play a greater initial role in central nervous
system depression (7, 8, 10, 12, 19). Clinical
peripheral nervous system toxicity of DCM was not
described heretofore. Nevertheless, there are
conflicting reports regarding the possible effect
of DCM on the peripheral nervous system. Workers
chronically exposed to DCM reported excess
neurological symptoms compared with a non-exposed
referent group, including numbness and tingling
in the hands and feet. No evidence, however, of
slowed motor nerve conduction velocity in either
the ulnar or median nerves was found (20). The
effects of organic solvents on the myelin sheath
of peripheral nerve tissue, was studied under
specified experimental conditions. This study
demonstrated that DCM produced complete
disorganization of the myelin structure within a
few hours after exposure, indicating possible
peripheral nerve toxicity (21). Experimental
neurotoxicologic evaluation of exposure to high
DCM concentrations in rats, revealed no evidence
of peripheral nerve pathology (22) whereas
another study revealed a decrease in sciatic
motor conduction velocity after intraperitoneal
administration of DCM in rats (23,24). Peripheral
neuropathy has been reported following carbon
monoxide intoxication (25,26,27, 28,29,30). A
clinical study of peripheral neuropathy in carbon
monoxide intoxication showed involvement of the
lower extremities (28,30), upper extremities
(26), cranial nerves with deafness development
(29). Bilateral facial palsy was described in a 3
year old girl, after severe CO intoxication
(26). The facial weakness cleared and after four
months it was no longer noticeable (26). Facial
nerve palsy following acute DCM exposure has not
been described in the literature. We cannot rule
out the possibility of idiopathic facial palsy.
Nevertheless the temporal correlation with an
acute DCM exposure, the lack of collaboratory
evidence to support the diagnosis of idiopathic
facial palsy, and the possible fifth cranial
nerve involvement raises the possible causal role
of DCM toxicity. Conclussion This is the first
article, as far as we know, that describes a
possible link between acute dichloromethane
exposure and facial nerve palsy.
Introduction Dichloromethane ( DCM or Methylene
chloride ) is a clear, colorless liquid with a
mild sweet odor that can be detected at
concentrations of 100-300 parts per million (ppm)
(1,2, 3). Dichloromethane is lipophilic and is an
excellent solvent for preparations of paint
removers, degreasing agents, aerosol propellants,
paint and varnish thinners, fire extinguishers,
adhesives and in a variety of other industrial
settings (4). Exposures to high concentrations of
Dichloromethane are generally occupationa (2).
The principal route of human exposure is
inhalation. Skin absorption is usually small
because of rapid evaporation. Following
absorption, DCM is distributed mainly to the
liver, brain and adipose tissue (1). In the
liver, it is metabolized to carbon monoxide,
which subsequently binds to hemoglobin producing
carboxyhemoglobin (CO-Hb). This process may
continue for several hours after the exposure, as
fat and other tissues release accumulated DCM
(9). Toxic effects of DCM have been observed
following its inhalation, due to central nervous
system depression or from the effect of carbon
monoxide (5,6,7,8). The most serious
manifestations of DCM toxicity are
unconsciousness and death, and a number of
fatalities have been reported in the literature
(5,7,8,9,11,13,14,15,16,17). Most of these cases
were associated with furniture paint
stripping. The objective of this article is to
describe a case of facial nerve palsy in a
soldier who was acutely exposed to
Dichloromethane in a paint stripping operation.
Case Report Eleven Israeli Air Force soldiers
used a liquid paint stripping formulation named
TURCO 5873, containing DCM to remove old paint
stains from the floor of a small building. Four
soldiers worked in the entrance to this building,
4 soldiers in the hall ( 2 meter width and 10
meter length), and 3 soldiers worked in a closed
small room, 25 square meters in size, with one
door that opened to the hall, and one window 10
cm10 cm in size. There was no ventilation device
in the room. Shortly after they began working
they experienced headache, dizziness and throat
irritation. They left the room every few minutes
as they felt insufficient ventilation and excess
solvent vapor in the room-air. They wore no
appropriate protective gloves or masks. After a
total of about three hours the work was stopped
due to excess vapors in the room, and
exacerbation of symptoms. Two hours later, one of
the soldiers who worked in the small room,
reported to the base clinic. This patient was 21
years old, who was known to have an atrophic left
kidney. He reported of headache, dizziness and
nausea. His vital signs were normal as well as
the rest of his physical examination including a
thorough neurological exam. The attending
physician ordered a change of clothes, and he
then received IV hydration and a mild analgesic.
Upon waking up the next morning the patient
noticed weakness and asymmetry of the left side
of his face an immediately went to the base
clinic. He was re-interviewed and reported no
preceding viral infection, tinnitus, hearing
diminution, pain behind the ear, hyperacussis or
taste loss. Physical examination revealed
features compatible with left peripheral facial
nerve palsy with drooping face and mouth. The
palpebral fissure appeared widened and the
forehead smooth. Upper and lower parts of the
face were affected. There was also a decrease in
sensation over the left side of the face. A
possible mild weakness of the muscles of
mastication on the left side was also noted,
indicating a possible involvement of the fifth
cranial nerve. The rest of the exam was normal
including tympanic membranes and a thorough
neurological examination. The patient was
referred to the emergency department of a nearby
hospital. The diagnosis of peripheral facial
nerve palsy was confirmed. Laboratory tests
revealed normal kidney and liver function tests
and oxygen saturation of 98. Blood
carboxyhemoglobin levels were 0.3-0.4 on serial
tests. He was admitted for observation and
received a short course of 1mg/kg Prendisolone.
After his D/C he had a rapid improvement and an
almost complete recovery after about three weeks
from the event, although he continued to complain
of left temporal headaches for several weeks.
There is currently no facial asymmetry and only a
slight weakness of the affected side. The other
ten soldiers involved in the incident were
summoned after the patient was diagnosed with
facial palsy. Nine soldiers reported symptoms
such as headaches, dizziness and nausea for
several hours after the event, but were all
symptom free by the next morning. They had no
abnormal findings on physical examination and a
laboratory evaluation that included
carboxyhemoglobin levels, liver and kidney
function function tests were normal.
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