Analyzing electrocardiographic, echocardiographic, and cardiac marker changes in organophosphorus poisoning cases at a tertiary care hospital of Jharkhand, India

ABSTRACT

Introduction:

Organophosphorus insecticides, widely used worldwide, are a significant public health risk in developing countries, causing 3 million poisonings and 300,000 deaths annually. Despite a 20% fatality rate in Asia, improved care is reducing mortality. Improper storage and accessibility contribute to frequent suicides, especially among lower socio-economic groups. Cardiac complications, often fatal, are preventable with early treatment. This study examines 60 acute poisoning cases at RIMS, Ranchi, highlighting the need for improved management.

Material and Methods:

This prospective clinical study, conducted from May 2018 to November 2019, involved 60 patients with acute organophosphorus poisoning admitted within 24 hours of ingestion. Comprehensive management included gastric lavage, activated charcoal, antidotes (atropine and pralidoxime), and supportive measures. Clinical and biochemical assessments, including echocardiography, monitored patient progress and treatment outcomes.

Results:

In a study of 60 acute organophosphorus poisoning cases, common early symptoms included lacrimation, salivation, blurring vision, nausea, and vomiting. Pupil constriction was an early sign. Bradycardia occurred in 46.67% of patients. Despite intensive care, 6.67% succumbed, with causes including ventricular fibrillation, aspiration pneumonia, and non-cardiogenic pulmonary edema.

Conclusion:

Future studies should address the infrastructural gaps of this study, as acute organophosphate poisoning constitutes over 75% of hospital poisoning cases. Early recognition and prompt treatment of cardiac complications can prevent fatalities, highlighting the need for improved management protocols and healthcare infrastructure.

Introduction

Organophosphorus compounds are the most widely used insecticides worldwide. They are being utilised in increasing quantities for the control of insects affecting agriculture and residential places. Organophosphorus compound poisoning is an important preventable public health problem in developing countries.[1]

The World Health Organization estimates 3 million annual cases of organophosphorus insecticide poisoning, resulting in approximately 300,000 deaths.[2] In Asia, the case fatality rate after deliberate ingestion is around 20%, but improved supportive care is reducing mortality rates.[3]

Since agriculture is the main occupation in our country, organophosphorus compounds are easily accessible in shops and often stored carelessly, highlighting a significant awareness gap. Suicidal ingestion of TIK-20 or Parathion has been a common issue in lower socioeconomic groups for 30 years. Early recognition and prompt treatment of cardiac complications can significantly reduce fatalities.[4]

In the present study, we describe our experience with sixty adult patients who were admitted in medicine wards of Rajendra Institute of Medical Sciences, Ranchi, with acute organophosphorus insecticide poisoning.

Materials Methods

Patients

This prospective clinical study was conducted from May 1, 2018, to November 1, 2019, at the Department of Medicine, Rajendra Institute of Medical Sciences, Ranchi, with ethical approval (IHEC/RIMS/213/2018. It involved 60 patients diagnosed with acute organophosphorus insecticide poisoning, admitted within 24 hours of ingestion. Consent was obtained from a responsible adult relative after discussing potential prognoses. Inclusion criteria include 1) diagnosis of acute organophosphorus insecticide poisoning in an adult patient irrespective of sex, based on history given by the patient or relatives, and 2) clinical features suggestive of acute organophosphorus poisoning. Exclusion criteria include 1) patients with double insecticide poisoning/multiple poisonings with other drugs such as opioids, diazepam, barbiturates etc., 2) patients with concomitant cardiovascular diseases—either congenital or acquired, and 3) patients who were already treated outside.

Management of poisoning

Initial management of organophosphorus poisoning involves gastric lavage to remove unabsorbed poison, especially if ingested within 4 hours, prioritizing airway protection in unconscious patients. Activated charcoal (30-100 g) minimizes further absorption, while contaminated clothing is removed, and thorough skin washing is performed. For inhalation exposure, extensive eye irrigation is essential. Atropine is administered intravenously, starting at 2–5 mg, doubling every 15 minutes until atropinization occurs, followed by maintenance doses. Pralidoxime (PAM) is given as a cholinesterase reactivator, starting with 1 g IV, then every 6 hours for 48 hours. Supportive care includes airway clearance, IV fluids, anticonvulsants, inotropes, and antibiotics.

Outcomes and data collection

Each patient underwent clinical assessment with detailed history, physical examination, and treatment initiation. Regular monitoring included blood indexes, liver and kidney function, cholinesterase, creatine kinase-Mb (CK-Mb), cardiac troponin I (cTnI), and serum LDH via a rapid test kit.

Owing to unavailability of bed side ECG, it could not be performed before the patient’s condition was stabilized. All the investigations done at admission were repeated after 24 hours and as or when needed. ECG. was repeated daily until the condition of the patient stabilised. Serum LDH measurement was done at 24 hrs, 48 hrs, on day 5, and on day 7; serum CPK-MB was repeated at 24 hours; and cardiac Troponin I (Rapid Test Method) was repeated at 24 hours. In patients with elevated LDH level serum Amylase, lipase level, and serum creatine phosphokinase (CPK) level were measured at 24 hrs, 48 hrs, on day 5, and on day 7 to determine alternate sources of elevated serum LDH. In these patient’s urine, routine microscopical tests (including dip stick test for blood) and ultrasonography of upper abdomen were also done.

Transthoracic echocardiography was done. 2-D, M-mode, and Doppler were done to study the following parameters: a) left ventricular end diastolic diameter (LVEDD), b) left ventricular end systolic diameter (LVESD), c) interventricular septal thickness (diastolic), d) left ventricular posterior wall thickness (diastolic), e) left ventricular fractional shortening normal range, f) left ventricular ejection fraction, g) right ventricular internal dimension, h) left atrial diameter, i) any regional wall motion abnormality (RWMA), j) diastolic dysfunction, and k) M-mode technique had been used to record the rate of relaxation of the left ventricular cavity. Doppler was also used for this l) Condition of the valves.

Results

Sixty cases of acute organophosphorus insecticide poisoning were studied whose diagnosis was based on the history of ingestion of organophosphorus compounds provided by the patient or accompanying persons. The container or label of the container was produced in some cases, and the brand name of the organophosphorus insecticide was provided by others. Characteristics clinical features of acute organophosphorus insecticide poisoning. The earliest symptoms observed was blurring of vision in 54 cases (90%), nausea in 52 cases (86.66%), vomiting in 54 cases (90%), salivation in 56 cases (93.33%), lacrimation in 58 cases (96.67%), and rhinorrhoea in 45 cases (75%). Commonest symptoms were lacrimation and salivation which were also the earliest to appear. Ocular and gastrointestinal symptoms were common followed by respiratory, nicotinic, CNS symptoms, and urinary incontinence, respectively. The earliest sign was constriction of pupil, and it was found in 44 cases (73.33%). Six cases (10%) were associated with normal pupil, and another 10 cases (16.67%) had dilated pupils. Excessive oropharyngeal secretion was present in 41 cases (68.33%), and sweating was present in 38 cases (63.33%). The pulse rate was normal in 19 cases (31.67%), but bradycardia was found in 28 cases (46.67%), and tachycardia was present in 13 cases (21.66%). Pulse was irregular in 14 cases (23.33%).

Blood pressure was normal in 33 patients (55%). Pressure was high in 10 (16.67%) cases, and hypotension was noted in 17 (28.33%) cases [Tables 1–3].

Table 1.

Demographic details, mode and type of organophosphorus poisoning cases

Parameter	Number (Percentage)
Age Group (Years)
• 15–20	18 (30%)
• 21-30	25 (41.67%)
• 31-40	12 (20%)
• 41-50	4 (6.67%)
• >50	1 (1.66%)
Gender Distribution
• Male	26 (43.3%)
• Female	34 (56.7%)
Mode of Poisoning
• Suicidal	56 (93.3%)
• Accidental	4 (6.7%)
Type of Organophosphorus Compound Consumed (Brand Name in Bracket)
• Methyl Parathion (Folidol)	28 (46.67%)
• Sumithion (Tik 20)	22 (36.67%)
• Temphos (Abate)	5 (8.33%)
• Fenthion (Dalf)	2 (3.33%)
• Monocrotophos (Nuvacron)	3 (5%)
Time Interval between Consumption and Time of Admission
• 0–1	18 (30%)
• >1-2	12 (20%)
• >2-3	10 (16.7%)
• >3-4	8 (13.3%)
• >4	12 (20%)
Occupation of the Patients
• Students	10 (16.7%)
• Farmers or Agricultural Labourers	20 (33.33%)
• Housewife	22 (36.70%)
• Service	2 (3.3%)
• Unemployed	6 (10%)
Marital Status of the Patients
• Married	24 (40%)
• Unmarried	30 (50%)
• Widow/Widower	6 (10%)

Table 3.

Clinical sign of the patients presented with Organophosphate poisoning

Signs	No. of Patients (Percentage in brackets)
1. Nutrition
• Good	12 (20%)
• Average	36 (60%)
• Poor	12 (20%)
2. Pulse
Rate
• Normal	19 (31.67%)
• Bradycardia	28 (46.67%)
• Tachycardia	13 (21.66%)
Rhythm
• Regular	46 (76.67%)
• Irregular	14 (23.33%)
Volume
• Normal	46 (76.67%)
• Low	14 (23.33%)
3. Blood pressure
• Normal	33 (55%)
• High	10 (16.67%)
• Low	17 (28.33%)
4. Respiration
• Normal	48 (80%)
• Tachypnea	4 (6.67%)
• Depression	8 (13.33%)
5. Pupils
• Normal	6 (10%)
• Constricted	44 (73.33%)
• Dilated	10 (16.67%)
6. Garlic odour in breath	38 (63.33%)
7. Bronchospasm	32 (53.33%)
8. Fasciculation	24 (40%)
9. Sweating	38 (63.33%)
10. Peristalsis Hurried	32 (53.33%)
11. Basal crepitations in the lung	16 (26.67%)
12. Profuse oropharyngeal secretions	41 (68.33%)
13. Anemia	25 (41.67%)

Table 2.

Clinical symptoms of the patients presented with organophosphate poisoning

Clinical features	Number (Percentage)
Chief Complaints of the Patients
• Vomiting	20 (33.33%)
• Pain abdomen	15 (25%)
• Unconsciousness	8 (13.30%)
• Vomiting with pain abdomen	12 (20%)
• Vomiting with unconsciousness	4 (6.70%)
• Pain abdomen with unconsciousness	1 (1.7%)
Muscarinic Symptoms
Ocular
• Eye ache	50 (83.33%)
• Lacrimation	58 (98.67%)
• Conjunctival redness	52 (86.67%)
• Diminution and blurring of vision	54 (90%)
Respiratory
• Rhinorrhea	45 (75%)
• Wheezing	32 (53.33%)
• Tightness in chest	38 (63.33%)
• Dyspnea	18 (30%)
Gastrointestinal
• Anorexia	48 (80%)
• Nausea	52 (86.66%)
• Vomiting	54 (90%)
• Diarrhoea	22 (36.66%)
• Abdominal cramps	36 (60%)
• Salivation	56 (93.33%)
Genitourinary
• Urinary incontinence	18 (30%)
Sweating	38 (63.30%)
Nicotinic effects
• Fatiguability	40 (66.66%)
• Weakness	45 (75%)
• Muscular twitching	29 (48.33%)
• Palsy	2 (3.33%)
CNS Symptoms
• Confusion	35 (58.33%)
• Unsteadiness	40 (66.66%)
• Convulsion	8 (13.33%)

Electrocardiography

A standard 12 leads electrocardiogram was taken during admission and subsequently repeated daily during the course of therapy [Table 4].

Table 4.

Electrocardiogram (E.C.G.) findings at admission before initiation of atropine therapy

Rate	No. of Patients (percentage in brackets)
Showing Heart Rate from E.C.G. at Admission Before Starting Treatment with Atropine
• Normal	19 (31.67%)
• Bradycardia	28 (46.67%)
• Tachycardia	13 (21.66%)
Showing Conduction disturbance at Admission Before Starting Therapy with Atropine
Conduction Abnormality
• Right bundle branch block	8 (13.33%)
• Left bundle branch block	2 (3.33%)
• Prolonged QTc interval	5 (8.34%)
• No change	45 (75%)
Rhythm Disturbance at Admission Before Starting Therapy with Atropine
Rhythm Disturbance
• Supraventricular tachycardia	2 (3.33%)
• Ventricular premature beats	1 (1.67%)
• Ventricular tachycardia	2 (3.33%)
• Ventricular fibrillation	1 (1.67%)
• Normal rhythm	54 (90%)
Axis Deviations in the E.C.G. at Presentation before Starting Therapy
• Normal Axis	45 (75%)
• Right axis deviation	10 (16.67%)
• Left axis deviation	5 (8.33%)
ST Segments Changes at Admission
• Non Specific Changes	8 (13.33%)
• Depression	2 (3.33%)
• No change	50 (83.33%)
T-Wave Changes at Admission
• Flat	8 (13.33%)
• Inverted	6 (10%)
• Normal upright T-Wave	46 (76.67%)

Serum LDH

Serum LDH was measured on admission, after 24 hours, 48 hours, on 5^th day, and on 7^th day [Figures 1 and 2].

Figure 1.

Serum LDH Level

Figure 2.

Trends of serum LDH in patients no 12, 41, 50

Cardiac troponin-I (Trop-I)

Qualitative estimation of Cardiac Troponin-I by rapid test method was done at admission and 24 hours admission to detect any myocardial damage. However, the tests were negative in all cases. One patient of acute organophosphorus poisoning died within 24 hours of admission.

Mortality and causes of death

The outcome data revealed that the majority of patients survived, with 56 out of 60 patients (93.33%) making a recovery. Unfortunately, 4 patients (6.67%) succumbed to the poisoning. The causes of death were varied: one patient died due to ventricular fibrillation, another due to aspiration pneumonia, and 2 patients succumbed to noncardiogenic pulmonary edema.

Discussion

Organophosphorus compounds, common in insecticides and herbicides, frequently cause poisoning in developing countries like India through ingestion, skin absorption, or inhalation.[5] This can lead to severe cardiac complications, liver dysfunction, or pancreatitis, often fatal without prompt treatment. Owing to limited studies, many medical practitioners are unaware of these complications. This study investigates the extent of cardiac toxicity in organophosphorus poisoning using electrocardiography, echocardiography, and cardiac markers.

Associated epidemiological features

Age incidence

In the present study, the majority of patients (71.67%) were in the 15–30 years age group, with 25 patients (41.67%) aged 21–30 and 18 patients (30%) aged 15–20. Previous studies also showed similar trends. Agarwal S.B. reported most cases in the 21–30 years range,[6] Cherian M.A. observed that most patients were below 30 years,[7,8] and Karki P[9] found a majority in the 15–30 years group.

Sex incidence

In this study 26 patients (43.3%) were male and 34 patients (56.7%) were female with ratio being 1 : 1.31. Chhabra[10] and Adalakha[11] observed that male : female ratio in their study was 4:1 and 7:1 respectively. Eddleston[12] and Shankar[13] found male : female ratio of 6:5 in Karnataka while Dash S.K.[14] found that male patients outnumber females and most cases are in 21-30 years age group. Agarwal S. B[6] found a male : female ratio of 2.1:1. Karki P.[9] found 41% of the patientswere male and 59% of the patients were female with a male: female ratio of 1:1.5.

Mode of poisoning, route of poisoning, and type of poison

Mode of poisoning was suicidal in most patients (56; 93.3%). It was accidental in 4 (6.7%) patients, and no homicidal poisoning was reported. Shankar,[13] Mutalik,[14] and Limaye[15] also observed majority of their cases were suicidal. However, Adalkha,[11] in Punjab observed majority (62%) of his patients were of accidental poisoning.

In the present study, the route of poisoning was oral in all cases. However, majority of the patients vomited and absorption through skin from vomitus and clothes soiled with vomitus might have been an important route of poisoning in some patients. Majority of the studies also reported the oral route as the commonest route of poisoning.

In our study, the most common organophosphorus insecticide used was Methyl Parathion (Folidol), which was implicated in 28 (46.67%) patient followed by Sumithion (Tik-20). Other organophosphorus insecticides found to be involved were Temphos (Abate) in 8.33% patients, Monocrotophos (Nuvacron) in 5% patients, and Fenthion (Dalf) in 3.33% patients. Balani,[16] observed that majority of the poisoning was by Tik -20. Karki P,[9] also reported that the commonest organophosphorus insecticide consumed in this study was Methyl Parathion.

Interval between exposure and admission

Thirty (50%) patients attended the hospital within 2 hours similar to study by Shankar,[13] and reported that most of the patients arrived in the hospital within 1 hour, though Adalkha,[11] reported that the mean time interval between exposure and arrival in the hospital was 9.37 hours. Kariki P,[9] reported that patients presented to the hospital as early as 5 minutes to as long as 12 hours after ingestion of poison. 90% of the patients presented within 2 hours of ingestion, with mean time interval of 1 hour 10 minutes.

Occupation and marital status

The present study found that 36.7% of the patients were housewives, 33.3% of the patients were farmers and agricultural labourers, 16.7% were students, 3.3% were service holders, and 10% were unemployed. Gupta[17] in their studies also found that majority (75%) of their patients were farmers. Karki P,[9] in their study found that 46% were students, 22% were farmer, and 16% each were housewives and service holders. The present study showed that 40% of the patients were married and 60% were single. However, Mutalik,[14] Basu,[18] and Gupta[17] in their studies found that married persons outnumber the unmarried persons. However, in the study of Karki P,[9] majority (23 patients, 62%) were unmarried.

Associated clinical features

Symptoms

The commonest chief complaint was vomiting (33.3%). 20% of the patient had both vomiting and pain abdomen as the chief complaint. The common symptoms observed were blurring of visioning 90% cases; vomiting in 90% cases; and salivation, lacrimation, rhinorrhoea in 93%, 96%, and 75% cases, respectively.[16,19,20] Tightness in the chest was reported in 63% of cases, dyspnea in 30% and increased sweating was reported in 63% cases. Commonest symptom was lacrimation which was reported in 96.67% patients. Ocular symptoms were very frequently observed in this study. Eye ache was found in 83%, conjunctival redness in 86%, and diminished vision in 90%. Singh,[19] observed blurred vision, increased sweating and vomiting in 100%, 95%, and 90% patients, respectively. In the present study abdominal cramps and diarrhoea were found in 60% and 36.6% of the cases respectively. Basu,[18] observed loose motion and abdominal cramp in 16% and 55% patients, respectively. Shankar,[13] observed nausea, vomiting, diarrhoea, abdominal pain, excessive oropharyngeal secretion, sweating, and dimness of vision in 39.9%, 12.7%, 29%, 25.5%, 12.7% and 7.2%, respectively. In the present study, 13 patients (21.67%) were unconscious at admission. 50% of patients of Basu,[18] was unconscious at admission, whereas unconsciousness at admission was described in 45% of patients by Adalkha,[11] in 30% of patients by Balani.[16]

Signs

In this study, the earliest and commonest sign was constriction of pupils in 73.33% of cases, followed by oropharyngeal secretion was in 68.33% of cases. Garlic odour in breath was found in 63.33% of cases. Fasciculations were seen in 40% of cases. Adalkha,[11] found constriction of pupils in 65% of cases. Shankar,[13] in their study of acute organophosphorus poisoning found pupillary constriction in 67.5% cases. In the present study bradycardia was found in 46.67% cases. Another study reported that bradycardia was the earliest noticeable event of acute organophosphorus insecticide poisoning mean while Singh[19] observed bradycardia in 5% patients and Chhabra[10] noticed bradycardia in only 3% patients. Pulmonary edema was observed in 26.6% of patients in this study. Chhabra,[10] detected pulmonary oedema in 100% cases and Singh[19] in 65% cases. In the present study bronchospasm was noted in 53.33% patients. Balani[16] found bronchospasm in 3% and 15% patients respectively. Bladder incontinence was observed in 30% patients in this study, while Chhabra[10] and Singh[19] reported it in 5.7% and in 11% patients respectively.

Electrocardiographic changes

At admission, bradycardia was present in 46.67% of patients, tachycardia was present in 21.66% of patients and heart rate was normal in 31.67% of patients. After treatment with atropine all the surviving patients showed presence of tachycardia. At admission, right bundle branch block (RBBB) was present in 8 (13.33%) of patients and left bundle branch block was present in 2 (3.33%) of patients. With therapy, both RBBB and LBBB reverted to normal. Prolonged QTc interval was present in 5 (8.34%) patients. However, with treatment none of them progressed to polymorphic ventricular tachycardia – but reverted to normal sinus rhythm. Six (12%) patients presented with dysrhythmias: Two (3.33%) patients showed supraventricular tachycardia, 2 (3.33%) patients showed ventricular tachycardia, and 1 (1.67%) patient each presented with ventricular premature beat and ventricular fibrillation.

The patient with ventricular fibrillation died soon after admission despite resuscitative measures. Other patients with dysrhythmias recovered with treatment. At admission, right axis deviation was present in 10 (16.67%) patients and left axis deviation was present in 5 (8.33%) patients. At admission, nonspecific ST segment changes were present in 8 (13.33%) patients and ST segment depression was present in 2 (3.33%) patients. However, the changes disappeared with treatment. At admission, flat T wave was present in 8 (13.33%) patients and inverted T wave was present in 6 (10%) of patients. However, with treatment, they reverted to normal.

Chuang FR[20] studied 223 patients with acute organophosphate poisoning. 43.5% patients had QTc prolongation where the incidence of QTc prolongation was high in patients with severe poisoning as determined by serum Cholinesterase level, compared to mild and moderate poisoning. Kiss Z [21] described 168 patients with acute organophosphate poisoning In 134 patients QTc prolongation, ST and T anomalies were present. 56 patients had arrhythmia including 5 patients who had ventricular arrhythmia.

Echocardiographic changes

In the present study, echocardiography (2-D, M-mode and colour Doppler study) was normal in all 56 patients in whom it was performed. Echocardiography could not be done in 4 patients who died from acute organophosphate compound poisoning even before their condition stabilized enough to allow their transportation to Department of Cardiology for doing echocardiography as our hospital did not have the facilities for bed-side echocardiography in medicine wards. Singh,[19] in their study described parathion poisoning in a 63-year-old woman in whom impressive ECG changes were present from 6 hours after admission and these ECG changes persisted for 6 days. However, echocardiography was normal.

Serum LDH

In this study, elevated serum LDH was observed in three patients. In two cases (Patient No. 12 and 41), serum LDH was elevated at admission, peaked 48 hours later, and returned to normal by Day 7. Patient No. 50, however, had normal LDH on admission, which started rising after 24 hours, peaked at 48 hours, and normalized by Day 7. As LDH isoenzyme testing was unavailable, the specific source of elevated LDH could not be identified.

For Patient No. 12 and 41, a simultaneous increase in serum amylase and lipase, with normal serum CPK and absence of RBCs in urine analysis, along with a negative urine dipstick test for blood, pointed to acute pancreatitis as the source of elevated LDH. Both patients complained of upper abdominal pain, and ultrasonography on Day 7 confirmed acute pancreatitis. Cardiac Troponin-I levels were within normal limits, suggesting the heart was not the source of LDH.

In contrast, Patient No. 50 had elevated serum CPK alongside LDH, with a positive urine dipstick test for blood but normal serum amylase, lipase, and pancreas on ultrasonography. These findings indicate that the elevated LDH in Patient No. 50 was likely due to organophosphate-induced acute rhabdomyolysis rather than myocardial damage. Normal liver function tests (LFT) in all three patients ruled out the liver as a potential source of elevated LDH.

Thus, the source of elevated LDH varied among patients, with the pancreas implicated in two cases and acute rhabdomyolysis in one.

Mortality

In the present study 4 deaths occurred out of the 60 patients admitted in the study giving a mortality rate of 6.7%. 1 patient died due to ventricular fibrillation, 1 patient died due to aspiration pneumonia and 2 patients died due to non cardiognic pulmonary edema. Balani[16] reported a mortality rate of 6%, Singh[19] in his study reported 15% case fatality rate. Eddleston[22] reported a case fatality rate of 10%. In the study of Karki P.[9] 3 patients out of 37 died giving a mortality rate of 8.1%. Two patients died from non cardiogenic pulmonary edema and 1 patient died from ventricular arrhythmia. So the mortality rate in our study compares favorably with the mortality rate of other studies and suggests that prompt and effective treatment will go a long way to reduce the mortality in acute organophosphate insecticide poisoning.[23,24,25]

Conclusion

Future studies on acute organophosphate poisoning should address the limitations of this research, as it accounts for over 75% of acute poisoning cases. Early recognition and prompt treatment can prevent serious, potentially fatal cardiac complications associated with this condition.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.