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Reactive airway disease after chlorine gas exposure.
S L Demeter and E W Cordasco Chest 1992;102;984b-984 DOI 10.1378/chest.102.3.984b The online version of this article, along with updated information and services can be found online on the World Wide Web at: http://chestjournal.chestpubs.org/content/102/3/984b.citation
Chest is the official journal of the American College of Chest Physicians. It has been published monthly since 1935. Copyright1992by the American College of Chest Physicians, 3300 Dundee Road, Northbrook, IL 60062. All rights reserved. No part of this article or PDF may be reproduced or distributed without the prior written permission of the copyright holder. (http://chestjournal.chestpubs.org/site/misc/reprints.xhtml) ISSN:0012-3692
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wald E, ed. Heart disease, 3rd ed. Philadelphia:
WB Saunders
Co. 1988; 180-227
3 Schamroth
L. An introduction
to electrocardiography,
Oxford, England: Blackwell Scientific Publications,
6th ed. 1982; 140
4 Dunn PM, Levinson WL. The lack of effect of clinical information
on electrocardiographic
diagnosis of acute myocardial infarction,
Arch Intern Med 1990; 150:1917-19
Reactive Airway Disease after Chlorine Gas Exposure
To the Editor:
We read with great interest in the September
1991 issue of Chest
the case report by Moore and Sherman.' Chlorine gas exposure has
multiple toxic effects ate airflow obstruction,
on the respiratory
system, including immedi-
ARDS, and death. The long-term effects
can include abnormalities
in gas transfer, restriction,
and airflow
obstruction.
These generally resolve with time to a variable degree.
Additionally, the severity and resolution of these effects appear to
be related to the degree of exposure, premorbid pulmonary status,
and the degree of hypoxemia
on initial presentation.
In 1990, we reported
two cases of reactive airway dysfunction
syndrome (RADS) following chlorine exposure to chlorine gas.5 Both
patients had an asthmatic diathesis extending over time. One individual has had persistent asthmatic symptoms for the past six
years; the symptoms
have ameliorated
with time, although she
continues to be symptomatic.
She is receiving minimal medication
at the present time, compared with her immediate postexposure needs. Before exposure, she was neither a smoker nor an asthmatic.
The other individual was also exposed to chlorine fumes. There was
no history of preexposure asthma, and he had discontinued
smoking
several years prior to his exposure. Not only did this individual
have asthmatic symptoms,
which responded
to bronchodilators,
but
he also had persistent
hypoxemia,
which has resolved over the
years. His exercise stress test initially accentuated and his primary symptoms were those of dyspnea
his hypoxemia, on exertion. His
condition
has ameliorated
with time.
Thus, chlorine exposure can present with asthmatic and BADS, as described by Brooks et al.' Our experience
symptoms has been
that the amount of asthma (diagnosed either by symptoms or by the
medication needs) ameliorates with time. Hypoxemia
with poor
cardiopulmonary
reserve was observed in one individual, and this
also resolved with time.
Northeastern
Stephen L. Demeter, M.D., EC.C.P,
Ohio Universities
College of Medicine,
Akrrns, Ohio; and
Edward
W Cordasco, Cleveland
M.D.,
Clinic,
Cleveland
REFERENCES
1 Moore BB, Sherman M. Chronic reactive airway disease following
acute chlorine gas exposure in an asymptomatic
atopic patient.
Chest 1991; 100:855-56
2 Demeter
SL, Cordasco
EM. Reactive airways dysfunction
syn-
drome: a subset of occupational
asthma. J Disability 1990; 1:23-
39
3 Brooks SM, Weiss MA, Bernstein IL. Reactive airways dysfunc-
tion syndrome
(RADS): persistent asthma syndrome after high
level irritant exposures.
Chest 1985; 88:376-84
To the Editor:
We welcome the comments agree that our patient probably
of Drs Demeter and Cordasco. We does have BADS, although he does
984
not fulfill all of the criteria set forth by Brooks et al.' Clearly the
cases reported
by Demeter
and Cordasco represent
persistent
hyperactive
airways disease after chlorine gas exposure.2
Our
patient differs from theirs in that his symptoms and level of disability
have not ameliorated
with time. On the contrary, six years after the
exposure this patient still requires home oxygen therapy, oral
corticosteroids
at high doses, frequent use of beta-agonist
inhalers,
and frequent
injections of subcutaneous
epinephrine.
In a recent
telephone
conversation,
he informed us that his symptoms
have
actually worsened since our report was submitted. He is barely
able to perform normal activities of daily living and reported that
his physicians referred him to a transplant center for possible heart-
lung transplantation.
Division
of Allergy,
Brad B.Moo,-e,M.D.,
and
Michael Sherman, M.D., F.C.C.P,
Pulmonary,
and Critical Care Medicine,
Hahenann University Hospital,
Philadelphia
REFERENCES
1 Brooks SM, Weiss MA, Bernsteiis IL. Reactive airways dysfunc-
tion syndrome
(RADS): persistent
asthma syndrome
after high
level irritant exposures. Chest 1985; 88:376-84
2 Demeter
SL, Cordasco EM. Reactive airways dysfunction
syn-
drome: a subset of occupational asthma. J Disability 1990; 1:23-
39
Pulmonary Lymphangioleiomyomatosis
To the Editor:
I read the very interesting
case report by HumI et al,' which
appeared in the December
1991 issue of Chest. I was curious to
know whether the patient described so well by the authors had
sarcoidosis
or a localized sarcoidal reaction. It would be helpful in
making this distinction
if the authors were to state whether
noncaseating
granulomata
were observed outside the thorax in the
organs examined at autopsy. It would also be of interest to know
something of the patient's ethnic background.
Jerome M. Reich, M.D.,
Division of Pulmonary
Disease,
Bess Kaiser Medical Center,
Portland, Oregon
REFERENCE
1 HumI JP, Borkgren
MW, Henley LB, Fahey PJ. Pulmonary
Iymphangioleioniyomatosis
associated with pulmonary parenchy-
mal, hilar, and mediastinal noncaseating
granulomas.
Chest 1991;
100:1726-28
To the Editor:
In our case report, the absence of multiorgan involvement
with
noncaseating
granulomas
speaks against systemic sarcoidosis.
No
evidence of noncaseating
granulomas
was found outside the thorax.
This raises the very interesting
possibility
that an immunologic
mechanism
may play a role in the etiology or that the presence of
noncaseating
granulomas
may represent
a localized insmunologic
reaction to lymphangioleiomyomatosis.
Further study and clinical
correlation
are necessary to prove this hypothesis.
Jeffrey P Hum!, M.D., F.C.C.P,
Marilyn W Borkgren, RN., MS., and
PatnickJ. Fahey, M.D.,
F.C.C.P,
Elk Grove Village, Illinois
Communications
to the Editor
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Reactive airway disease after chlorine gas exposure. S L Demeter and E W Cordasco Chest 1992;102; 984b-984 DOI 10.1378/chest.102.3.984b
This information is current as of October 22, 2010
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