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Research Article
Acute Chlorine Gas Poisoning and Ecg Changes
Latif A*
, Zehra SRE, Makki K and Rauf S
Department of Medicine, Liaquat National Hospital, National Stadium Road, Karachi - 74800, Pakistan
*
Corresponding author:
Anum Latif,
Department of Medicine, Liaquat National Hospital,
National Stadium Road, Karachi - 74800, Pakistan,
Tel: 03212770334, E-mail: dranumlatif@yahoo.com
Received: 13 Aug 2021
Accepted: 02 Sep 2021
Published: 08 Sep 2021
Copyright:
©2021 Latif A. This is an open access article distributed
under the terms of the Creative Commons Attribution Li-
cense, which permits unrestricted use, distribution, and
build upon your work non-commercially.
Citation:
Latif A, Acute Chlorine Gas Poisoning and Ecg Changes.
Ann Clin Med Case Rep. 2021; V7(7): 1-5
http://www.acmcasereport.com/ 1
Annals of Clinical and Medical
Case Reports
ISSN 2639-8109 Volume 7
Keywords:
Acute Gas Poisoning; Chlorine Gas; ECG; Poisoning
1. Abstract
1.1. Introduction: Chlorine is a yellow-green gas at room tem-
perature. It is an extremely reactive element and a strong oxidizing
agent. It has intermediate water solubility and it can cause acute
damage to upper and lower respiratory tract. It can be detected
easily because of its strong odor (1,2). Common cause of chlorine
gas poisoning these days are accidental industrial exposure. Tox-
icity of chlorine depends upon the dose and duration of exposure.
1.2. Objectives of the Study: 1) To assess the frequency of hy-
peracute T waves on electro cephalogram (ECG) among patients
diagnosed with chlorine gas poisoning. 2) To evaluate the relation-
ship between incidence of hyperacute T waves and the troponin I
levels among patients.
1.3. Methodology: A prospective observational study was con-
ducted between October and November 2020 for a duration of
1 month at Liaquat National Hospital, Karachi. All patients be-
tween ages of 18-65 years diagnosed with chlorine gas poisoning
presented to the hospital were included in the study. All patients
with inconclusive diagnosis or those with diabetes mellitus, hy-
pertension, chronic kidney, or liver disease, were excluded from
the study. The demographic data, clinical characteristics and ECG
findings were retrieved by reviewing patients file retrospectively.
Data was compiled and analyzed using statistical package for so-
cial sciences (SPSS) version 25. A p-value of < 0.05 was consid-
ered as statistically significant.
1.4. Results: A total of 37 patients were diagnosed with chlorine
poisoning. 27 (73%) patients had mild, 8 (21.6%) had moderate,
and 2/37 had severe symptoms i.e. ARDS, edema, or pneumonitis.
Out of 37 patients, 36 (97.3%) had hyperacute T waves on ECG
and troponin I was positive in only one patient. The one patient
in which troponin I was positive presented with severe symptoms
of chlorine poisoning albeit the association was not significant
(p=0.054). No significant association was found between ECG
changes and the severity of chlorine poisoning (p>0.05).
2. Introduction
Chlorine is a yellow-green gas at room temperature. It is an ex-
tremely reactive element and a strong oxidizing agent. It has in-
termediate water solubility and it can cause acute damage to upper
and lower respiratory tract. It can be detected easily because of its
strong odor [1-2]. Common cause of chlorine gas poisoning these
days are accidental industrial exposure. Toxicity of chlorine de-
pends upon the dose and duration of exposure [2]. Inhalation poi-
soning substances are usually divided into three categories, simple
asphyxiants, pulmonary irritants and chemical axphyxiants. Chlo-
rine gas belongs to pulmonary irritants and it is considered as the
most common toxic inhalant.
Low level poisoning at concentrations of 1 to 3 ppm chlorine gas
act as an eye and oral mucosa membrane irritant. At high concen-
tration of up to 15 ppm it produces pulmonary symptoms and it can
be fatal at concentration of 450ppm [3]. The source of exposure
includes industrial or chemical accidents, school chemistry lab or
release of gas from swimming pool [2-5]. Findings due to chlorine
gas poisoning include conjunctival irritation, sore throat, rhinor-
rhea, lacrimation, dyspnea, laryngeal edema and stridor [6]. Acute
manifestation can be tracheitis and dyspnea but in the long run it
can permanently damage the lungs [7-8]. Complication includes
ARDS or respiratory failure [2, 4, 9].
Chlorine gas cause myocardial depression. In world war chlorine
gas was used as chemical weapon and it causes severe myocardi-
al depression and Right heart dilatation [10]. Cardiac dysfunction
http://www.acmcasereport.com/ 2
Volume 7 Issue 7 -2021 Reserach Article
could result from pulmonary hypertension and release of vasoac-
tive mediators [11]. Multiple human and animal studies showed the
involvement of cardiovascular system in chlorine poisoning [12-
14]. In previous study they have reported different ECG changes
including ST depletion, sinusoidal tachycardia and extrasystoles
[15]. Due to the discrepancies in the previous literature, the present
study was undertaken to observe and assess the changes such as
hyper acute T waves among the patients who suffered from chlo-
rine gas poisoning and its role as the early indicator of cardiac
involvement. We wanted to assess the relationship between inci-
dence of hyperacute T waves and the cardiac damage as indicated
by troponin I levels.
3. Methodology
A prospective observational study was conducted between Octo-
ber and November 2020 for a duration of 1 month at Liaquat Na-
tional Hospital, Karachi. After procuring ethical clearance from
the institutional review board of Liaquat National Hospital, data
collection was initiated. A total of 37 number of patients were in-
cluded in the study using a non-probability convenience sampling
technique. All patients between ages of 18 and 65 years, with di-
agnosed case of inhalational chlorine gas poisoning presenting to
the emergency department within 12 hours of the onset of adverse
symptoms were included in the study. All patients with incon-
clusive diagnosis or those with diabetes mellitus, hypertension,
chronic kidney, or liver disease, were excluded from the study.
The demographic data, clinical characteristics and ECG findings
were retrieved by reviewing patients file retrospectively. The se-
verity of symptoms of chlorine poisoning were stratified into three
groups: i) Mild Symptoms indicated by conjunctival irritation and
oral mucosal membrane burning, ii) Moderate Symptoms indicat-
ed by sore throat and dyspnea (shortness of breath), and iii) Severe
Symptoms denoted by dyspnea, edema, pneumonitis, and Acute
Respiratory Distress Syndrome (ARDS).
Data was compiled and analyzed using statistical package for so-
cial sciences (SPSS) version 25. Mean and standard deviations
were calculated for the quantitative variables. Frequencies and
percentages were calculated for the qualitative variables. The se-
verity of symptoms and its correlations with the ECG findings (hy-
per acute T waves) were observed. Chi square test was applied
for finding association between these categorical variables taking
p-value of ≤ 0.05 as statistically significant.
4. Results
A total of 37 patients who were eligible as per inclusion and exclu-
sion criteria were included in the study. All patients had a present-
ing history of accidental exposure to chlorine gas. All participants
were males and the majority of them were in their middle age as
depicted by figure 1.
A total of 33/37 patients presented to the emergency room within
12 hours out of which four patients arrived with delayed presen-
tation (more than six hours of onset of symptoms of chlorine gas
poisoning). 27/37 (73%) patients had mild symptoms including ir-
ritation and mucosal membrane burning, 8 (21.6%) had moderate
symptoms of shortness of breath and sore throat, while 2/37 had
severe symptoms i.e. ARDS, edema, or pneumonitis as depicted
by table 1.
A total of 9/37 (24.3%) patients were admitted to the hospital for
further assessment and observation. Five of these were admitted to
the ward setup while other four patients were in critical condition
so were shifted to the intensive care unit (ICU) at LNH.
Out of 37 patients 36 (97.3%) had hyperacute T waves on ECG
and troponin I was positive in only one patient as shown in table 1.
Figure 1: Bar chart of number of patients in respective age group.
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Volume 7 Issue 7 -2021 Reserach Article
Figure 2: Bar chart showing association of symptoms with T waves.
Figure 3: Bar chart showing association of Troponin I with T waves.
Table 1: Demographic of patients
Characteristics n (%)
Patient arrived
Within 6 hours 33(89.2)
After 6 hours 4(10.8)
Symptoms
Mild 27(73)
Moderate 8(21.6)
Severe 2(5.4)
Hyper Acute -T waves
Yes 36(97.3)
No 1(2.7)
Troponin I positive
Yes 1(2.7)
No 36(97.3)
Admission
Yes 9(24.3)
No 28(75.7)
Admitted to ward
Yes 5(13.5)
Monitoring setup
Yes 4(10.8)
Outcome
Discharge 27(73)
Admission 9(24.3)
LAMA 1(2.7)
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Volume 7 Issue 7 -2021 Reserach Article
Table 2: Association of clinical characteristics of patients with incidence of hyperacute T waves on electro cephalogram (ECG)
Characteristics Total n (%)
Hyper Acute T waves P-value
Yes No
Admission
Yes 9(24.3) 9(25) 0(0) 1
No 28(75.7) 27(75) 1(100)
Symptoms
Mild 27(73) 26(72.2) 1(100) 1
Moderate 8(21.6) 8(22.2) 0(0)
Severe 2(5.4) 2(5.6) 0(0)
Patient arrived
Within 6 hrs 33(89.2) 33(91.7) 0(0) 0.1
After 6 hrs 4(10.8) 3(8.3) 1(100)
Troponin I positive
Yes 1(2.7) 1(2.8) 0(0) 1
No 36(97.3) 35(97.2) 1(100)
Outcome
Discharge 27(73) 26(72.2) 1(100) 1
Admission 9(24.3) 9(25) 0(0)
LAMA 1(2.7) 1(2.8) 0(0)
*Significant at p-value <0.05
In this study there was no significant association between incidence of hyperacute T waves on ECG of patients and the severity
of chlorine poisoning, nevertheless, ECG changes were observed in majority of the patients as stated earlier.
Table 3. Association of clinical characteristics of patients with the severity of symptoms
Characteristics Total n (%) Symptoms Mild Moderate Severe P-value
Admission
Yes 9(24.3) 0(0) 7(87.5) 2(100) <0.001*
No 28(75.7) 27(100) 1(12.5) 0(0)
Patient arrived
Within 6 hrs 33(89.2) 24(88.9) 7(87.5) 2(100) 1.000**
After 6 hrs 4(10.8) 3(11.1) 1(12.5) 0(0)
Troponin I positive
Yes 1(2.7) 0(0) 0(0) 1(50) 0.054
No 36(97.3) 27(100) 8(100) 1(50)
Monitoring setup
Yes 4(10.8) 0(0) 2(25) 2(100) <0.001*
No (non monitoring setup) 5(13.5) 0(0) 5(62.5) 0(0)
Outcome
Discharge 27(73) 26(96.3) 1(12.5) 0(0) <0.001*
Admission 9(24.3) 0(0) 7(87.5) 2(100)
LAMA 1(2.7) 1(3.7) 0(0) 0(0)
*Significant at p-value <0.05
The one patient in which troponin I was positive presented with severe symptoms of chlorine poisoning albeit the association was not
significant (p=0.054).
5. Discussion
Chlorine gas is a most common pulmonary irritant. It is very vola-
tile and has moderate solubility in water. It primarily effects the re-
spiratory system [1, 2]. The set of symptoms starts from irritation
of mucosal membranes to fatal pneumonitis and Acute respiratory
distress syndrome. Chlorine gas is been commonly used in various
aspects of industries and its exposure to human environment is
relatively frequent [5, 13]. This gas also effects the cardiovascu-
lar system. As mentioned in previous studies chlorine poisoning is
attributed to the myocardia depression and ECG changes that in-
cludes ST depression, sinus tachycardia and extrasystoles [11, 14].
Chlorine gas released free oxygen species that was thought to be
the cause of cellular damage. But recent studies have shown that
oxidization of different components of cell results in damage to
tissue. When chlorine reacts with water it formed an acid which
irritates the mucosal and conjunctival membranes and cause burn-
ing sensations. Experimental studies showed that majority of gas is
absorbed from the upper respiratory mucosa and only 5 percent is
absorbed from the lower respiratory mucosa [16]. It was observed
in World War 1 that chlorine poisoning causes Right sided heart
dilation as described above.
In an experimental animal study chlorine poisoning cause release
of calcium in myocytes that cause impairment in cytoskeleton and
causes myocardial dysfunction that results in depression of systol-
ic and diastolic blood pressure [17].
http://www.acmcasereport.com/ 5
Volume 7 Issue 7 -2021 Reserach Article
In our study we observed that after an industrial accident and ex-
posure to chlorine gas poisoning the majority only developed mild
symptoms and required no additional treatment while a small per-
centage of patients experienced more severe symptoms of the poi-
soning and required admission and supportive treatment. Almost
all patients had ECG changes indicating the hyperacute T waves.
Troponin I was not a prominent finding. As mentioned above pre-
vious studies showed some ECG changes in patients with chlorine
poisoning but by far our knowledge none of the studies mentioned
about hyperacute T waves in ECG. T waves represent ventricu-
lar repolarization and hyperacute T waves are usually present in
coronary artery occlusion either by a mechanical obstruction or
vasospasms. This change in ECG can be a predictor of outcome in
patients of chlorine poisoning with myocardial dysfunction.
Due to a small sample size, the findings of the current study can-
not be generalized to a larger population. Hence, future research
should come up with better and more elaborated study designs
keeping the current findings as a foundation and recruit a larger
sample size from different tertiary care centers of Pakistan.
6. Conclusion
The present study indicated that there may be an unexplored as-
sociation of severity of chlorine gas poisoning and cardiovascular
damage as indicated by the changes detected on the electro cepha-
lograms. It is further advised to perform an ECG in patients diag-
nosed with chlorine gas inhalation poisoning to observe any early
manifestations of cardiac damage.
References
1. Beach FX, Jones ES, Scarrow GD. Respiratoryeffects of chlorine
gas. Br J Ind Med. 1969; 26,231}236.
2. Bresnitz E. Simple asphyxiants and pulmonary irritants.In‘‘Gold-
frank’s Toxicological Principles’’ (L. R. Goldfrank, Ed.), 1994; pp.
1183, Appleton & Lange, East Norwalk, CT
3. Chauhan S, Chauhan S, D’Cruz R, Faruqi S, Singh KK, Varma S,
et al. Chemical warfare agents. Environ. Toxicol. Pharmacol. 2008
Sep; 26(2): 113-22.
4. Deschamps D, Soler P, Rosenberg N, Baud F, Gervais, P. Persistent
asthma after inhalation of a mixtureof sodium hypochlorite and hy-
drochloric acid. Chest. 1994; 105,1895}1896.
5. Ellenhorn MJ, Barceloux DG. Medical Toxicol-ogy: Diagnosis and
Treatment of Human Poisoning. Elsevier. 1988. New York.
6. Donnelly SC, FitzGerald MX. Reactive airways dysfunction syn-
drome (RADS) due to chlorine gas exposure. Ir. J. Med. Sci. 1990:
159,275}276; discussion 276}277.
7. Fleta J, Calvo C, Zuniga J, Castellano, M, Bueno M. Intoxication of
76 children by chlorine gas. Hum. Toxicol. 1986: 5,99}100.
8. Gapany-Gapanavicius M, Yellin A, Almog S, Tirosh M. Pneumome-
diastinum: A complication of chlorineexposure from mixing house-
hold cleaning agents. J Am Med. Assoc. 1982; 248, 349}350.
9. Heidemann SM, Goetting M G. Treatment of acutehypoxemic re-
spiratory failure caused by chlorine exposure. Pediatr Emerg Care.
1991; 7, 87}88.
10. Arthur Hurst MA. WWI Gas-poisoning: Effects of chlorine gas poi-
soning. 1971
11. Pham H, Bonham AC, Pinkerton KE. Chen CY. Central neuroplasti-
city and decreased heart rate variability after particulate matter expo-
sure in mice. Environ Health Perspect. 2009; 117: 1448-1453.
12. Winternitz MC, Lambert RA, Jackson L. Smith GH. The pathophys-
iology of chlorine poisoning. New Haven: Yale University Press;
1920.
13. Gunnarsson M, Walther SM, Seidal T, Bloom GD, Lennquist S. Ex-
posure to chlorine gas: effects on pulmonary function and morpholo-
gy in anaesthetised and mechanically ventilated pigs. J Appl Toxicol.
1998; 18: 249-255.
14. Wang J, Abu-Zidan FM. Walther SM. Effects of prone and supine
posture on cardiopulmonary function after experimental chlorine gas
lung injury. Acta Anaesthesiol. Scand. 2002; 46: 1094-1102.
15. C Güloğlu, İ Kara, P Erten. Acute Accidental Exposure to Chlorine
Gas in the Southeast of Turkey: A study of 106 Cases. 2002.
16. Chlorine Gas Toxicity SPEX. StatPearls PubMed Reference for iOS
Access to thousands of questions and PubMed indexed medical ar-
ticles.
17. Ahmad S, Ahmad A, Hendry-Hofer TB, Loader JE, Claycomb WC,
Mozziconacci O, et al. Sarcoendoplasmic reticulum Ca2+ ATPase.
A critical target in chlorine inhalation-induced cardiotoxicity. Am J
Respir Cell Mol Biol. 2015; 52: 492-502.

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ACUTE CHLORINE GAS POISONING AND ECG CHANGES

  • 1. Research Article Acute Chlorine Gas Poisoning and Ecg Changes Latif A* , Zehra SRE, Makki K and Rauf S Department of Medicine, Liaquat National Hospital, National Stadium Road, Karachi - 74800, Pakistan * Corresponding author: Anum Latif, Department of Medicine, Liaquat National Hospital, National Stadium Road, Karachi - 74800, Pakistan, Tel: 03212770334, E-mail: dranumlatif@yahoo.com Received: 13 Aug 2021 Accepted: 02 Sep 2021 Published: 08 Sep 2021 Copyright: ©2021 Latif A. This is an open access article distributed under the terms of the Creative Commons Attribution Li- cense, which permits unrestricted use, distribution, and build upon your work non-commercially. Citation: Latif A, Acute Chlorine Gas Poisoning and Ecg Changes. Ann Clin Med Case Rep. 2021; V7(7): 1-5 http://www.acmcasereport.com/ 1 Annals of Clinical and Medical Case Reports ISSN 2639-8109 Volume 7 Keywords: Acute Gas Poisoning; Chlorine Gas; ECG; Poisoning 1. Abstract 1.1. Introduction: Chlorine is a yellow-green gas at room tem- perature. It is an extremely reactive element and a strong oxidizing agent. It has intermediate water solubility and it can cause acute damage to upper and lower respiratory tract. It can be detected easily because of its strong odor (1,2). Common cause of chlorine gas poisoning these days are accidental industrial exposure. Tox- icity of chlorine depends upon the dose and duration of exposure. 1.2. Objectives of the Study: 1) To assess the frequency of hy- peracute T waves on electro cephalogram (ECG) among patients diagnosed with chlorine gas poisoning. 2) To evaluate the relation- ship between incidence of hyperacute T waves and the troponin I levels among patients. 1.3. Methodology: A prospective observational study was con- ducted between October and November 2020 for a duration of 1 month at Liaquat National Hospital, Karachi. All patients be- tween ages of 18-65 years diagnosed with chlorine gas poisoning presented to the hospital were included in the study. All patients with inconclusive diagnosis or those with diabetes mellitus, hy- pertension, chronic kidney, or liver disease, were excluded from the study. The demographic data, clinical characteristics and ECG findings were retrieved by reviewing patients file retrospectively. Data was compiled and analyzed using statistical package for so- cial sciences (SPSS) version 25. A p-value of < 0.05 was consid- ered as statistically significant. 1.4. Results: A total of 37 patients were diagnosed with chlorine poisoning. 27 (73%) patients had mild, 8 (21.6%) had moderate, and 2/37 had severe symptoms i.e. ARDS, edema, or pneumonitis. Out of 37 patients, 36 (97.3%) had hyperacute T waves on ECG and troponin I was positive in only one patient. The one patient in which troponin I was positive presented with severe symptoms of chlorine poisoning albeit the association was not significant (p=0.054). No significant association was found between ECG changes and the severity of chlorine poisoning (p>0.05). 2. Introduction Chlorine is a yellow-green gas at room temperature. It is an ex- tremely reactive element and a strong oxidizing agent. It has in- termediate water solubility and it can cause acute damage to upper and lower respiratory tract. It can be detected easily because of its strong odor [1-2]. Common cause of chlorine gas poisoning these days are accidental industrial exposure. Toxicity of chlorine de- pends upon the dose and duration of exposure [2]. Inhalation poi- soning substances are usually divided into three categories, simple asphyxiants, pulmonary irritants and chemical axphyxiants. Chlo- rine gas belongs to pulmonary irritants and it is considered as the most common toxic inhalant. Low level poisoning at concentrations of 1 to 3 ppm chlorine gas act as an eye and oral mucosa membrane irritant. At high concen- tration of up to 15 ppm it produces pulmonary symptoms and it can be fatal at concentration of 450ppm [3]. The source of exposure includes industrial or chemical accidents, school chemistry lab or release of gas from swimming pool [2-5]. Findings due to chlorine gas poisoning include conjunctival irritation, sore throat, rhinor- rhea, lacrimation, dyspnea, laryngeal edema and stridor [6]. Acute manifestation can be tracheitis and dyspnea but in the long run it can permanently damage the lungs [7-8]. Complication includes ARDS or respiratory failure [2, 4, 9]. Chlorine gas cause myocardial depression. In world war chlorine gas was used as chemical weapon and it causes severe myocardi- al depression and Right heart dilatation [10]. Cardiac dysfunction
  • 2. http://www.acmcasereport.com/ 2 Volume 7 Issue 7 -2021 Reserach Article could result from pulmonary hypertension and release of vasoac- tive mediators [11]. Multiple human and animal studies showed the involvement of cardiovascular system in chlorine poisoning [12- 14]. In previous study they have reported different ECG changes including ST depletion, sinusoidal tachycardia and extrasystoles [15]. Due to the discrepancies in the previous literature, the present study was undertaken to observe and assess the changes such as hyper acute T waves among the patients who suffered from chlo- rine gas poisoning and its role as the early indicator of cardiac involvement. We wanted to assess the relationship between inci- dence of hyperacute T waves and the cardiac damage as indicated by troponin I levels. 3. Methodology A prospective observational study was conducted between Octo- ber and November 2020 for a duration of 1 month at Liaquat Na- tional Hospital, Karachi. After procuring ethical clearance from the institutional review board of Liaquat National Hospital, data collection was initiated. A total of 37 number of patients were in- cluded in the study using a non-probability convenience sampling technique. All patients between ages of 18 and 65 years, with di- agnosed case of inhalational chlorine gas poisoning presenting to the emergency department within 12 hours of the onset of adverse symptoms were included in the study. All patients with incon- clusive diagnosis or those with diabetes mellitus, hypertension, chronic kidney, or liver disease, were excluded from the study. The demographic data, clinical characteristics and ECG findings were retrieved by reviewing patients file retrospectively. The se- verity of symptoms of chlorine poisoning were stratified into three groups: i) Mild Symptoms indicated by conjunctival irritation and oral mucosal membrane burning, ii) Moderate Symptoms indicat- ed by sore throat and dyspnea (shortness of breath), and iii) Severe Symptoms denoted by dyspnea, edema, pneumonitis, and Acute Respiratory Distress Syndrome (ARDS). Data was compiled and analyzed using statistical package for so- cial sciences (SPSS) version 25. Mean and standard deviations were calculated for the quantitative variables. Frequencies and percentages were calculated for the qualitative variables. The se- verity of symptoms and its correlations with the ECG findings (hy- per acute T waves) were observed. Chi square test was applied for finding association between these categorical variables taking p-value of ≤ 0.05 as statistically significant. 4. Results A total of 37 patients who were eligible as per inclusion and exclu- sion criteria were included in the study. All patients had a present- ing history of accidental exposure to chlorine gas. All participants were males and the majority of them were in their middle age as depicted by figure 1. A total of 33/37 patients presented to the emergency room within 12 hours out of which four patients arrived with delayed presen- tation (more than six hours of onset of symptoms of chlorine gas poisoning). 27/37 (73%) patients had mild symptoms including ir- ritation and mucosal membrane burning, 8 (21.6%) had moderate symptoms of shortness of breath and sore throat, while 2/37 had severe symptoms i.e. ARDS, edema, or pneumonitis as depicted by table 1. A total of 9/37 (24.3%) patients were admitted to the hospital for further assessment and observation. Five of these were admitted to the ward setup while other four patients were in critical condition so were shifted to the intensive care unit (ICU) at LNH. Out of 37 patients 36 (97.3%) had hyperacute T waves on ECG and troponin I was positive in only one patient as shown in table 1. Figure 1: Bar chart of number of patients in respective age group.
  • 3. http://www.acmcasereport.com/ 3 Volume 7 Issue 7 -2021 Reserach Article Figure 2: Bar chart showing association of symptoms with T waves. Figure 3: Bar chart showing association of Troponin I with T waves. Table 1: Demographic of patients Characteristics n (%) Patient arrived Within 6 hours 33(89.2) After 6 hours 4(10.8) Symptoms Mild 27(73) Moderate 8(21.6) Severe 2(5.4) Hyper Acute -T waves Yes 36(97.3) No 1(2.7) Troponin I positive Yes 1(2.7) No 36(97.3) Admission Yes 9(24.3) No 28(75.7) Admitted to ward Yes 5(13.5) Monitoring setup Yes 4(10.8) Outcome Discharge 27(73) Admission 9(24.3) LAMA 1(2.7)
  • 4. http://www.acmcasereport.com/ 4 Volume 7 Issue 7 -2021 Reserach Article Table 2: Association of clinical characteristics of patients with incidence of hyperacute T waves on electro cephalogram (ECG) Characteristics Total n (%) Hyper Acute T waves P-value Yes No Admission Yes 9(24.3) 9(25) 0(0) 1 No 28(75.7) 27(75) 1(100) Symptoms Mild 27(73) 26(72.2) 1(100) 1 Moderate 8(21.6) 8(22.2) 0(0) Severe 2(5.4) 2(5.6) 0(0) Patient arrived Within 6 hrs 33(89.2) 33(91.7) 0(0) 0.1 After 6 hrs 4(10.8) 3(8.3) 1(100) Troponin I positive Yes 1(2.7) 1(2.8) 0(0) 1 No 36(97.3) 35(97.2) 1(100) Outcome Discharge 27(73) 26(72.2) 1(100) 1 Admission 9(24.3) 9(25) 0(0) LAMA 1(2.7) 1(2.8) 0(0) *Significant at p-value <0.05 In this study there was no significant association between incidence of hyperacute T waves on ECG of patients and the severity of chlorine poisoning, nevertheless, ECG changes were observed in majority of the patients as stated earlier. Table 3. Association of clinical characteristics of patients with the severity of symptoms Characteristics Total n (%) Symptoms Mild Moderate Severe P-value Admission Yes 9(24.3) 0(0) 7(87.5) 2(100) <0.001* No 28(75.7) 27(100) 1(12.5) 0(0) Patient arrived Within 6 hrs 33(89.2) 24(88.9) 7(87.5) 2(100) 1.000** After 6 hrs 4(10.8) 3(11.1) 1(12.5) 0(0) Troponin I positive Yes 1(2.7) 0(0) 0(0) 1(50) 0.054 No 36(97.3) 27(100) 8(100) 1(50) Monitoring setup Yes 4(10.8) 0(0) 2(25) 2(100) <0.001* No (non monitoring setup) 5(13.5) 0(0) 5(62.5) 0(0) Outcome Discharge 27(73) 26(96.3) 1(12.5) 0(0) <0.001* Admission 9(24.3) 0(0) 7(87.5) 2(100) LAMA 1(2.7) 1(3.7) 0(0) 0(0) *Significant at p-value <0.05 The one patient in which troponin I was positive presented with severe symptoms of chlorine poisoning albeit the association was not significant (p=0.054). 5. Discussion Chlorine gas is a most common pulmonary irritant. It is very vola- tile and has moderate solubility in water. It primarily effects the re- spiratory system [1, 2]. The set of symptoms starts from irritation of mucosal membranes to fatal pneumonitis and Acute respiratory distress syndrome. Chlorine gas is been commonly used in various aspects of industries and its exposure to human environment is relatively frequent [5, 13]. This gas also effects the cardiovascu- lar system. As mentioned in previous studies chlorine poisoning is attributed to the myocardia depression and ECG changes that in- cludes ST depression, sinus tachycardia and extrasystoles [11, 14]. Chlorine gas released free oxygen species that was thought to be the cause of cellular damage. But recent studies have shown that oxidization of different components of cell results in damage to tissue. When chlorine reacts with water it formed an acid which irritates the mucosal and conjunctival membranes and cause burn- ing sensations. Experimental studies showed that majority of gas is absorbed from the upper respiratory mucosa and only 5 percent is absorbed from the lower respiratory mucosa [16]. It was observed in World War 1 that chlorine poisoning causes Right sided heart dilation as described above. In an experimental animal study chlorine poisoning cause release of calcium in myocytes that cause impairment in cytoskeleton and causes myocardial dysfunction that results in depression of systol- ic and diastolic blood pressure [17].
  • 5. http://www.acmcasereport.com/ 5 Volume 7 Issue 7 -2021 Reserach Article In our study we observed that after an industrial accident and ex- posure to chlorine gas poisoning the majority only developed mild symptoms and required no additional treatment while a small per- centage of patients experienced more severe symptoms of the poi- soning and required admission and supportive treatment. Almost all patients had ECG changes indicating the hyperacute T waves. Troponin I was not a prominent finding. As mentioned above pre- vious studies showed some ECG changes in patients with chlorine poisoning but by far our knowledge none of the studies mentioned about hyperacute T waves in ECG. T waves represent ventricu- lar repolarization and hyperacute T waves are usually present in coronary artery occlusion either by a mechanical obstruction or vasospasms. This change in ECG can be a predictor of outcome in patients of chlorine poisoning with myocardial dysfunction. Due to a small sample size, the findings of the current study can- not be generalized to a larger population. Hence, future research should come up with better and more elaborated study designs keeping the current findings as a foundation and recruit a larger sample size from different tertiary care centers of Pakistan. 6. Conclusion The present study indicated that there may be an unexplored as- sociation of severity of chlorine gas poisoning and cardiovascular damage as indicated by the changes detected on the electro cepha- lograms. It is further advised to perform an ECG in patients diag- nosed with chlorine gas inhalation poisoning to observe any early manifestations of cardiac damage. References 1. Beach FX, Jones ES, Scarrow GD. Respiratoryeffects of chlorine gas. Br J Ind Med. 1969; 26,231}236. 2. Bresnitz E. Simple asphyxiants and pulmonary irritants.In‘‘Gold- frank’s Toxicological Principles’’ (L. R. Goldfrank, Ed.), 1994; pp. 1183, Appleton & Lange, East Norwalk, CT 3. Chauhan S, Chauhan S, D’Cruz R, Faruqi S, Singh KK, Varma S, et al. Chemical warfare agents. Environ. Toxicol. Pharmacol. 2008 Sep; 26(2): 113-22. 4. Deschamps D, Soler P, Rosenberg N, Baud F, Gervais, P. Persistent asthma after inhalation of a mixtureof sodium hypochlorite and hy- drochloric acid. Chest. 1994; 105,1895}1896. 5. Ellenhorn MJ, Barceloux DG. Medical Toxicol-ogy: Diagnosis and Treatment of Human Poisoning. Elsevier. 1988. New York. 6. Donnelly SC, FitzGerald MX. Reactive airways dysfunction syn- drome (RADS) due to chlorine gas exposure. Ir. J. Med. Sci. 1990: 159,275}276; discussion 276}277. 7. Fleta J, Calvo C, Zuniga J, Castellano, M, Bueno M. Intoxication of 76 children by chlorine gas. Hum. Toxicol. 1986: 5,99}100. 8. Gapany-Gapanavicius M, Yellin A, Almog S, Tirosh M. Pneumome- diastinum: A complication of chlorineexposure from mixing house- hold cleaning agents. J Am Med. Assoc. 1982; 248, 349}350. 9. Heidemann SM, Goetting M G. Treatment of acutehypoxemic re- spiratory failure caused by chlorine exposure. Pediatr Emerg Care. 1991; 7, 87}88. 10. Arthur Hurst MA. WWI Gas-poisoning: Effects of chlorine gas poi- soning. 1971 11. Pham H, Bonham AC, Pinkerton KE. Chen CY. Central neuroplasti- city and decreased heart rate variability after particulate matter expo- sure in mice. Environ Health Perspect. 2009; 117: 1448-1453. 12. Winternitz MC, Lambert RA, Jackson L. Smith GH. The pathophys- iology of chlorine poisoning. New Haven: Yale University Press; 1920. 13. Gunnarsson M, Walther SM, Seidal T, Bloom GD, Lennquist S. Ex- posure to chlorine gas: effects on pulmonary function and morpholo- gy in anaesthetised and mechanically ventilated pigs. J Appl Toxicol. 1998; 18: 249-255. 14. Wang J, Abu-Zidan FM. Walther SM. Effects of prone and supine posture on cardiopulmonary function after experimental chlorine gas lung injury. Acta Anaesthesiol. Scand. 2002; 46: 1094-1102. 15. C Güloğlu, İ Kara, P Erten. Acute Accidental Exposure to Chlorine Gas in the Southeast of Turkey: A study of 106 Cases. 2002. 16. Chlorine Gas Toxicity SPEX. StatPearls PubMed Reference for iOS Access to thousands of questions and PubMed indexed medical ar- ticles. 17. Ahmad S, Ahmad A, Hendry-Hofer TB, Loader JE, Claycomb WC, Mozziconacci O, et al. Sarcoendoplasmic reticulum Ca2+ ATPase. A critical target in chlorine inhalation-induced cardiotoxicity. Am J Respir Cell Mol Biol. 2015; 52: 492-502.