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| ORIGINAL ARTICLE |
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| Year : 2017 | Volume
: 5
| Issue : 2 | Page : 18-24 |
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Electrocardiographic changes in organophosphate poisoning - A prospective study of 50 cases at a tertiary care center in Gujarat
Sanket Makwana1, MN Saiyad2, Vaishali Makwana3
1 Assistant Professor, Department of Medicine, C U Shah Medical College, Surendranagar, Gujarat, India
2 Professor, Department of Medicine, Smt. S C L Municipal General, Ahmedabad, Gujarat, India
3 Assistant Professor, Department of Skin &V.D, C U Shah Medical College, Surendranagar, Gujarat, India
| Date of Web Publication | 31-Aug-2018 |
Correspondence Address:
Sanket Makwana
Assistant Professor, Department of Medicine, C U Shah Medical College, Surendranagar, Gujarat
India
 Source of Support: None, Conflict of Interest: None  | 2 |
DOI: 10.4103/2347-6486.240240
Introduction: Organophosphates (OP) are irreversible cholinesterase inhibitors, producing nicotinic and muscarinic effects. Cardiac complications with these compounds are often fatal. Early recognition of abnormal rhythm protects the patients against acquiring life-threatening arrhythmias. Hence, this study was done to determine the ECG findings in patients with OP poisoning.
Aims & Objectives: To determine the various electrocardiographic changes & its importance in acute Organophosphate poisoning.
Materials and methods: This prospective observational study of 50 cases was conducted for 2 years in a tertiary care institute. All adults with history of OP poisoning, admitted within 12 hours were enrolled. Patients with cardiac disease or treated from outside were excluded. Diagnosis was made by history, clinical features and confirmed by serum cholinesterase level. ECG analysis of each case was done for rate, rhythm, ST-T changes, PR and QTc intervals, and conduction defects etc.
Results: Mean age in the study group was 30.66 ± 11.70(SD). Male:Female ratio was 1.94:1. 78% were suicidal, 22% were accidental and 6(12%) cases expired. Most common mode of poisoning was ingestion 45 cases (90%). Most common ECG abnormality was Sinus Tachycardia in 12(24%) followed by ST-T changes 8(16%), QTc prolongation in 6(12%), Sinus Bradycardia 4(8%), Extrasystole 2(4%), PR Prolongation 1(2%), AF 1(2%) and VT 1(2%).
Conclusion: Poisoning with OP compounds can produce significant ECG abnormalities especially sinus tachycardia, non specific ST-T changes and QTc interval prolongation. Since these abnormalities can cause lethal arrhythmia and cardiac damage, careful observation of the electrocardiogram of the patients exposed to OP compound is necessary, parallel to the appropriate medical management.
Keywords: Organophosphates, Serum cholinesterase, ECG, Sinus tachycardia, QTc prolongation, Atropine, Oximes
How to cite this article:
Makwana S, Saiyad M N, Makwana V. Electrocardiographic changes in organophosphate poisoning - A prospective study of 50 cases at a tertiary care center in Gujarat. J Integr Health Sci 2017;5:18-24 |
How to cite this URL:
Makwana S, Saiyad M N, Makwana V. Electrocardiographic changes in organophosphate poisoning - A prospective study of 50 cases at a tertiary care center in Gujarat. J Integr Health Sci [serial online] 2017 [cited 2023 Mar 28];5:18-24. Available from: https://www.jihs.in/text.asp?2017/5/2/18/240240 |
| Introduction | |  |
Acute organophosphate poisoning represents a major health problem in developing countries, where organophosphate compounds are widely and easily available. OP compounds act as irreversible cholinesterase inhibitors, causing a syndrome of cholinergic excess involving muscarinic, nicotinic and central nervous system receptors.[1] Muscarinic effects include sweating, salivation, lacrimation, urination, diarrhoea, gastrointestinal discomfort, emesis (“SLUDGE” syndrome)[2], rhinorrhea, bronchorrhea, broncho- constriction, dyspnea and miosis. Nicotinic signs include muscle twitching, fasciculations, weakness and, in severe cases, paralysis. Central nervous system effects may include restlessness, tremor, confusion, convulsions, respiratory depression and coma.[3] Cardiac complications that often accompany poisoning with these compounds may be serious and are often fatal .Since early recognization of abnormal rhythm in OP poisoning protects the patients against acquiring life-threatening arrhythmias[4], this study was done to determine the ECG findings in patients with OP poisoning at our tertiary care institute.
Aims & Objectives:
To determine the various electrocardiographic changes and its importance in acute Organophosphate poisoning.
| Methodology | | |
This prospective observational study was conducted from January 2014 to October 2015 in Department of Medicine at Smt SCL Hospital, Ahmedabad. By using random selection method, 50 patients with alleged history of ingestion or exposure to organophosphate compounds were enrolled in study. All adults with history of consumption and/or exposure to OP compound of either sex, admitted in hospital within 12 hours of poisoning and not having been treated outside included in study. All patients with poisoning due to compounds other than organophosphate, prior H/O consumption of organophosphate compounds, patients who received partial treatment outside and referred to this hospital, patients with H/O cardiac disease and patients with pre-existing motor or sensory neuropathy were excluded .A proforma was designed for study which includes detailed history and examination to diagnose organophosphate poisoning. The diagnosis was based on history of ingestion of organophosphate compound, specific clinical features, clinical improvement after Atropine and/or pralidoxime and serum cholinesterase level. The age, sex, mode of exposure, type of poisoning, OP compound involved, time elapsed between exposure and admission to the hospital, duration of hospital stay, need for assisted ventilation, and cardiac and ECG manifestations at the time of presentation and during the hospital stay were recorded. 12 lead ECG with lead II rhythm strip was taken once daily during their hospital stay in ICU and subsequently whenever needed. ECG analysis included the rate, rhythm, ST-T abnormalities, conduction defects, and measurement of PR and QT intervals. The QT intervals were measured from the first deflection of the QRS complex to the point of T-wave offset, defined as the return of the T wave to baseline of the 12-lead ECG. If a U wave was present, the T- wave offset was defined as the nadir of the curve between the T and U waves. The QT interval was corrected according to the formula of Bazett[5]. QTc was considered prolonged when it was longer than 0.41 s in men and longer than 0.42 s in women[6]. All this information was collected for each patient and then descriptive statistical analysis was conducted by SPSS version 18. Values were presented as frequency and mean ± standard deviation.
| Results | | |
In this prospective study, majority of patients (56%) were in age group of 16-30 years. Mean age in the present study was 30.66 ± 11.70.Out of 50 patient with organophosphate poisoning 33(66%) patients were male while 17(34%) patients were female. Male to female ratio in this study group was 1.94:1. In this study, 39(78%) patients had suicidal poisoning while 11(22%) patients consumed organophosphate accidently. Out of 50 patients, 45(90%) patients gave the history of organophosphate ingestion, 3(6%) patients were affected by ingestion as well as topical exposure to OP compounds. 1(2%) patient had history of inhalation and 1(2%) patient had topical exposure to OP compound. Most of the cases 26(52%) were arrived hospital within 2-6 hours of organophosphate consumption and 18(36%) patients arrived in less than 2 hours. More than 6 hours delay between exposure and hospital arrival was found in 6(12%) patients. The mean of time elapsed in hours between exposure to OP compound and hospital arrival was 3.33 ± 2.56.
[Table 1] shows that methyl parathion was the most common organophosphate compound consumed comprising 20% of the cases; in our study, we were not able to find out OP compound in 23(46%) patients either due to patient not given proper history related OP compound or not brought the OP sample. | Table 1: Distribution of study subjects based on type of Organophosphate compound consumed
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[Table 2] shows ECG manifestations that were recorded before the administration of atropine. 35 patients (70%) patients showed ECG abnormality. In male group, it was observed in 20(60.6%) patients while in female group, it was in 15(88.2%) females. In our study, nearly one fourth of the patients had sinus tachycardia (>100 bpm) while bradycardia (<60 bpm) was recorded only in 4 patients. Followed by Sinus tachycardia ST-T changes was the most common ECG abnormality. Elevation of ST segment (>2 mm above the isoelectric line) was seen in 4(8%) patients. This was most striking in the anterolateral leads (V2-V5). T wave inversion was seen in 4(8%) patients and involved anterolateral leads in two cases and inferolateral in two cases. 6 patients(3 males & 3 females)(12%) had a prolongation of QTc interval(>0.41 seconds in males and >0.42 seconds in females). First degree heart block (PR interval >0.23 seconds) occurred in one case. One patient also had atrial fibrillation. Ventricular tachycardia was seen in 1(2%) cases while ventricular premature contractions in 2(4%) cases. | Table 2: Distribution of study subject based on ECG manifestation in acute Organophosphate poisoning
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| Discussion | | |
Organophosphorous compounds account for two million suicide attempts and one million accidental poisoning each year worldwide[7]. In several areas, some pesticides have become the trendiest method of suicide, gaining unsavory reputation amongst both health-care personnel and community.[8] The mechanism by which organophosphates and carbamates induce cardiotoxicity is still uncertain. Possible mechanisms include sympathetic and parasympathetic over-activity, hypoxemia, acidosis, electrolyte derangements, and a direct toxic effect of the compounds on the myocardium. Both sympathetic and parasympathetic over- activity has been shown to cause myocardial damage.[9],[10]
In our study 50 patients were presented with the history of organophosphate poisoning, of which 35 developed ECG manifestations. In our study group, mean age was 30.66 ± 11.70(SD) years, while Yurumez et al reported mean age 32.2 ± 14.9(SD) in their study of 85 patients with OP poisoning.[11] In study by Balouch GH, the overall mean age identified was 27.35±8.63 (SD).4
In this study, most of the victims were in the age group of 16-60 years with maximum numbers of cases (56%) between the ages of 16-30 years. Similarly, in a prospective study by Rafigh Doost et al. in Birjand, of 51 patients with OP poisoning, most of the cases (37%) were in the 15 to 24 year age group.
Out of 50 patients with organophosphate poisoning 33(66%) patients were male while 17(34%) were female. Male to female ratio in this study group was 1.94. In study by Balouch GH of 87 patients with cardiac manifestations, 60(69%) patients were males and 27 (31%) patients were female. Male to female ratio in their study was 2.22.[4]
In this study, 39(78%) patients had suicidal poisoning while 11(22%) patients consumed organophosphate accidently. Agarwal found that 67.4% of the cases had the intention of committing suicide, 16.8% of the cases were the result of occupational exposure, and 15.8% of the cases were from accidental poisoning.[13] Regarding mode of poisoning accidental, suicidal and homicidal was observed in 41(47.1%), 44(50.6%) and 02(2.3%) in study by Balouch GH.[4] Manzoor Ali reported OPc poisoning was suicidal in 58(82.86%) and accidental/incidental in 12(17.14%).[14]
Out of 50 patients, 45(90%) patients gave the history of organophosphate ingestion, 3(6%) patients were affected by ingestion as well as topical exposure to OP compounds. 1(2%) patient had history of inhalation and 1(2%) patient had topical exposure to OP compound. Manzoor Ali also found that there was a high ratio of insecticides (Malathion, Parathion, and Mite/rat
House fly killer Carbamates) by ingestion/inhalation route.[14] Exposure routes were gastrointestinal in 111 patients (77.62%), respiratory in 8 patients (5.59 %), dermal in 10 patients (6.99%) and both dermal and respiratory in 14 (9.79%) patients in study done in Pakistan by Muhammad Imran.[15]
In our study, the mean of time elapsed between exposure to OP compound and hospital arrival was 3.33 ± 2.56(SD) with maximum patients 26(52%) were arrived hospital within 2-6 hours of organophosphate consumption. S. Laudari et al. also noted that the majority of patients (66.1%) presented to the hospital within 2-6 hours post-ingestion.[16]
Among all patients exposed to OP compounds, 10(20%) patients consumed methyl parathion while 7(14%) patients consumed malathion and 6(12%) patients exposed to chlorpyrifos plus cypermethrin. In this study, 2(4%) patients consumed chlorpyrifos, while 1(2%) patient exposed to dichlorvas and 1(2%) patient to monocrotophos. We were not able to find out OP compound in 23(46%) patients either due to patient not given proper history related OP compound or not brought the OP sample. Methyl parathion ingestion is also most common 23(62%) organophosphate ingestion in study of 37 patients by P. Karki et al.[17]
Ludomirsky et al[18] described three phases of cardiac toxicity after organophosphate poisoning: phase 1, is a brief period of increased sympathetic tone; phase 2, is a prolonged period of parasympathetic activity; and in phase 3, Q-T prolongation is followed by torsades de pointes ventricular tachycardia, and then ventricular fibrillation. The cardiac toxicity associated with organophosphate and carbamate poisoning is caused by more than one mechanism.
The electrocardiographic presentation detected in our study was sinus tachycardia, sinus bradycardia, QTc prolongation, PR prolongation, ST-T abnormality, ventricular tachycardia a conduction abnormalities.
The electrocardiographic picture of our study is consistent with the study by P. Karki and study by S. Laudari that also identified similar arrhythmias with different proportions.[16],[17]
In our study, nearly one fourth of the patients had sinus tachycardia while bradycardia was recorded in only 3 patients. Similar observation was made in the study by Karki et al.[17] Sinus tachycardia could be related to nicotinic effects of OP compounds while sinus bradycardia can be attributed to muscarinic effects.[19] Although bradycardia is thought to dominate in the early cholinergic phase of the OP poisoning, sinus tachycardia was a more frequent finding in our study probably due to the fact that most of the patients were visited in antimuscarinic phase of OP toxicity.[19] Karki et al. reported that sinus tachycardia occurred in 40.5% of patients.[17] Yurumez et al. reported that sinus tachycardia was a more frequent finding (in 31.8% cases) in their study.n In another study, Saadeh et al. reported that sinus tachycardia was seen in 35.0% of cases.[6]
Some investigators have described a polymorphic ventricular tachycardia of the torsades de pointes type attributed to a prolongation of the QTc interval associated with organophosphate poisoning[18],[20]. In spite of the presence of a prolonged QTc interval in 6(12%) of patients, none of them had this type of arrhythmia. Administration of atropine in high doses has been implicated in the development of ventricular arrhythmias.[21],[22] In our, study there was no such correlation. Lyzhnikov et al[10] and Ludomirsky et al[18] also found no correlation between atropine therapy and ventricular arrhythmias in organophosphate poisoning.
In general, large QT dispersion (QT dispersion = longest-shortest QT interval on any of the 12 leads of the ECG) is a result of ischemic change, which may conceal the QT prolongation in the affecting vascular area. Muscarinic action induced by OP poisoning causes vagotony and acetylcholine accumulation on nerve endings, which results in spastic contraction of the coronary artery[6]. Although non-specific ST-T changes have generally been recognized as not being directly related to any cardiac disease, they also have been observed before the ST elevation associated with coronary spasm.[23] Thus, the nonspecific ST-T change for the patient with OP poisoning has a considerable clinical meaning.[17] In our study ST-T changes seen in 8(16%) patients. Yurumez et al” noted ST-T changes in 17.6%. Similarly P. Karkii17 noted it in 29.7% while Sadeh et al[6] noted it in 41%.
Extrasystole in form of premature ventricular contraction is also seen in 2(4%) of our patients. In the present study, type 1 atrioventricular (AV) block developed in one patient. This resembles to a Russian series that intraventricular conduction defects and AV block were described in 5.4% of OP poisoned patients.[24] Correspondingly, Paul et al. reported AV block following OP poisoning in 8.4% of patients.[25] Atrial fibrillation was also observed in one patient which was reverted by diltiazem. In our study, one patient developed ventricular tachycardia and which could not be reverted back despite defibrillation, advanced cardiopulmonary resuscitation and correction of hypokalemia, and consequently led to death. In the study by P. Karki et al[17] hospital mortality rate is 8.1%, which is 12% in our study.
| Conclusion | | |
Poisoning with OP compounds can produce significant ECG abnormalities especially sinus tachycardia, non specific ST-T changes and QTc interval prolongation. Since these abnormalities can cause lethal arrhythmia and cardiac damage, careful observation of the electrocardiogram of the patients exposed to OP compound is necessary, parallel to the appropriate medical management.
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[Table 1], [Table 2]
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