Abstract
Background
Pyrethroid insecticides are commonly used insecticides. This study was undertaken to characterize the clinical profile and outcome of deliberate self-harm (DSH) with type 1 and type 2 pyrethroids and identify factors associated with need for hospitalization.
Methods
This retrospective study was conducted in a tertiary care hospital in South India to study the clinical features, treatment, and outcome of patients with pyrethroid poisoning due to DSH. Patients were categorized as poisoning with type 1 or type 2 pyrethroid compounds. Factors associated with need for hospital admission was explored using bivariate and multivariate regression analysis and expressed as odds ratio (OR) with 95% confidence intervals (CIs).
Results
A total of 379 patients presented with pyrethroid poisoning; 202 (53.3%) patients were male. The median (interquartile range) age was 26 (22–33) years. Transfluthrin (n = 48, 58%) and cypermethrin (n = 149, 50%) were the most frequently implicated type 1 compounds and type 2 compounds, respectively. Of the 130 (34.3%) patients who were admitted, 13 (3.4%) patients required mechanical ventilation. All patients survived. On multivariate logistic regression analysis, ingestion of type 2 pyrethroids (OR: 2.55, 95%CI: 1.31–4.97), history of seizures (OR: 2.62, 95%CI 1.06-6.48), and treatment prior to presentation to the referral hospital (OR: 2.99, 95%CI: 1.87–4.74) were associated with the need for hospitalization.
Conclusion
A third of patients with pyrethroid poisoning require hospitalization. Type 2 pyrethroid poisoning is more frequent in clinical practice. Ingestion of type 2 pyrethroids, seizures, and need for pre-hospital treatment are associated with hospitalization.
Keywords: Pyrethroid, Type 1/type 2 pyrethroid compounds, Human toxicity, Outcomes
Introduction
Deliberate self-harm (DSH) with pesticide ingestion is a global health problem and constitutes 33% of emergency department (ED) visits in South India.1 Previous studies have shown that there are around 1 million cases of DSH per year.2 But recent reviews have shown that if we include unintentional poisoning among agricultural workers, the estimates of pesticide poisonings may be as high as 385 million cases per year.3 The global burden of disease study estimated that in India approximately 230,314 of the cases die annually due to DSH; studies from South India have shown that the suicide rate is very high at 92.1 per 100,000 population, and the common methods used were hanging and insecticide ingestion.4,5
The first pyrethroid pesticide was discovered in 1949. Since then, pyrethroids have been popular household and commercial pesticides.6 They are used as external applicants for the treatment of scabies and head lice.7 Pyrethroids are classified as type 1 pyrethroids (e.g. allethrin) and type 2 pyrethroids (e.g. cypermethrin). Type 1 pyrethroids have a simple cyclopropane carboxylic ester structure while type 2 compounds have an added alpha cyano group that confers enhanced insecticidal activity. Pyrethroids are about 2250 times more toxic to insects when compared to humans; this is because insects have a smaller body size, lower body temperature, and higher sodium channel sensitivity compared to humans. Humans and other mammals have the capacity to rapidly metabolize pyrethroid into nontoxic substances.8 This relative selective toxicity makes pyrethroids the ideal insecticide for domestic use.
Pyrethroids are the second most used pesticides worldwide.9,10 Despite this, the clinical presentation and outcomes of pyrethroid poisoning in humans have not been well characterized. This study was undertaken to describe the clinical profile and outcomes of pyrethroid poisoning, identify differences in clinical profiles and outcomes between type 1 and type 2 pyrethroid poisoning, and determine the factors associated with the need for hospital admission.
Materials and methods
This was a retrospective study of patients treated in the ED, medical wards, and intensive care unit (ICU) in a teaching tertiary care hospital in South India between January 2011 and December 2019. The study was approved by the institutional review board and ethics committee (IRB number 11009/17). The study was conducted in accordance with the Declaration of Helsinki; the ICMR National Ethical Guidelines for Biomedical and Health Research involving Human Participants 2017 and the GCP Guidelines. A written informed consent was taken from all patients. Patients who were diagnosed as pyrethroid poisoning were included in the study and identified through search of the electronic database of the hospital using the terms DSH, pyrethroid, or poisoning. Patients who presented with combination pesticide poisoning (e.g. organophosphorus plus pyrethroid) or with co-ingestion with alcohol or other drugs were excluded.
Patients were managed as per the standard protocol for insecticide poisoning since there is no separate protocol for pyrethroid poisoning. The compound was identified based on the container brought by the patient or his/her relative. Since organophosphorus poisoning is common in this region and some symptoms suggestive of organophosphorus poisoning (e.g. increased salivation, agitation, drowsiness, and seizures) can also be present in patients presenting with pyrethroid poisoning, all patients underwent pseudocholinesterase estimation to ensure that the patient had not co-ingested an organophosphorus compound or had taken a pyrethroid–organophosphate combination pesticide.
All patients were assessed for airway breathing and circulation; patients with low sensorium were intubated for airway protection. Patients received activated charcoal at admission into ED for gastrointestinal decontamination and in case the patient did not produce the compound at admission, symptomatic patients (e.g. increased salivation and drowsiness) were treated with atropine till the compound could be identified or the pseudocholinesterase results were available. Inpatient admission was decided by the treating unit physician and decided mostly on the need for inpatient monitoring for clinical worsening; some medical units had a lower threshold for admitting patients with insecticide poisoning.
Data were extracted from online electronic medical records, entered into MS Excel, and analyzed using IBM SPSS version 25.0. Categorical variables were summarized as frequencies (percentages) and continuous variables as mean with standard deviation (SD). Continuous variables that were not normally distributed were summarized as median with interquartile range (IQR). For the evaluation of factors associated with hospital admission, chi-square was used. Factors associated with hospital admission were explored using bivariate analysis and incorporated into a multivariate logistic regression analysis, and the results were expressed as odds ratio (OR) with 95% confidence intervals (CIs). The goodness of fit for regression was assessed by the R square statistic.
Results
A total of 379 patients presented with pyrethroid poisoning during the study period. The mean (SD) age of the cohort was 29.8 (12.03) years. Although overall more men (53.3%) presented with DSH with pyrethroids, more women (59.3%) had taken type 1 pyrethroid compounds (Table 1). More patients had taken type 2 pyrethroids (78.6%) as compared to type 1 pyrethroids. Transfluthrin (n = 48, 59.2%), allethrin (n = 15, 18.5%), and prallethrin (n = 10.12.3%) were the most common compounds among type 1 pyrethroid poisoning, whereas cypermethrin (n = 149, 50%), deltamethrin (n = 43, 14.4%), lambda-cyhalothrin (n = 42, 14%), and cyhalothrin (n = 38, 12.7%) were the common compounds among type 2 poisoning (Table 2).
Table 1.
Baseline characteristics.
| Variable | All pyrethroids (n = 379) | Type I compounds (n = 81) | Type 2 compounds (n = 298) | P value |
|---|---|---|---|---|
| Age, median (IQR) years | 26 (22–33) | 25 (22–28) | 27 (22–35) | 0.03 |
| Gender, M: F | 202:177 | 33: 48 | 169: 129 | 0.01 |
| Clinical features, n (%) | ||||
| Drowsiness | 76 (20.1) | 20 (24.7) | 56 (18.1) | 0.24 |
| Seizures | 22 (5.8) | 4 (4.9) | 18 (6.0) | 0.71 |
| Salivation | 22 (5.8) | 0 (0) | 22 (7.4) | 0.15 |
| Vomiting | 22 (5.8) | 2 (2.5) | 20 (6.7) | 0.92 |
| Diarrhea | 10 (2.6) | 2 (2.5) | 8 (2.7) | |
| Prior treatment | 160 (42.2) | 21 (25.9) | 139 (46.6) | 0.001 |
| Required admission | 130 (34.3) | 13 (16.0) | 117 (39.3) | <0.01 |
| HLOS∗ median (IQR), h | 12 (5–48) | 6.0 (4–24) | 18 (6–48) | <0.001 |
| Required ventilation | 13 (3.4) | – | 13 (4.3) | |
| Tracheostomy | 2 (0.5) | – | 2 (0.6) | |
| Pneumonia | 8 (2) | – | 8 (2.6) | |
| Laboratory parameters, median (IQR) | ||||
| Biochemical parameters | ||||
| Pseudocholinesterase (U/L) | 7397 (6286–8834) | 7591 (6613–10,154) | 7387 (6280–8661) | 0.17 |
| Sodium (135–145 mmol/l) | 139 (137–141) | 139 (137–141) | 139 (137–141) | 0.24 |
| Potassium (3.5–5.5 mmol/l) | 3.7 (3.3–4) | 3.7 (3.4–3.9) | 3.7 (3.4–3.9) | 0.62 |
| Bicarbonate (23–30 mmol/l) | 19 (17–21) | 19 (16–22) | 19 (17–21) | 0.72 |
| Hematological parameters | ||||
| Hemoglobin (12–14 g/L) | 13.8 (12.3–15.3) | 12.8 (11.8–15) | 14.05 (12.5–15.5) | 0.02 |
| WBC (4000–11,000/cumm | 10,550 (8500–14,800) | 9450 (8075–13,200) | 10,900 (8600–14,900) | 0.04 |
| Platelets (150,000–400,000/cumm) | 264,000 (217,000–305000) | 258,000 (202,000–313,000) | 265,000 (219,000–303250) | 0.40 |
| Sinus tachycardiâ–ECG | 63 (21.2) | 18 (32.7) | 45 (18.6) | 0.02 |
Values specified are number of patients, and the percentages are in parentheses unless specified otherwise; M: F – male: female, LOS – length of stay; IQR – interquartile range; WBC –total white blood count; SD – ŝinus tachycardia on electrocardiogram; h – hours; pneumonia – ventilator-associated pneumonia.
Table 2.
Spectrum of compounds implicated in pyrethroid poisoning.
| Type 1 (n = 81) | Number (%) | Type 2 (n = 298) | Number (%) |
|---|---|---|---|
| Transfluthrin | 48 (59.2) | Cypermethrin | 149 (50) |
| Allethrin | 15 (18.5) | Deltamethrin | 43 (14.4) |
| Prallethrin | 10 (12.3) | Lambda-cyhalothrin | 42 (14) |
| Permethrin | 4 (4.9) | Cyhalothrin | 38 (12.7) |
| Transallethrin | 3 (3.7) | Fenvalerate | 15 (5) |
| Bifenthrin | 1 (1.2) | Alphamethrin | 5 (1.6) |
| Metofluthrin | 1 (1.2) | Fenpropathrin | 3 (1) |
| Flumethrin | 2 (0.6) |
In our cohort, 335 (88.3%) took the liquid formulation, 19 (5%) had ingested the chalk form of pyrethroid, 2 (0.5%) took powdered form, 2 (0.5%) had taken mosquito coils, 2 (0.5%) had poured into their ear, and 2 (0.5%) had injected themselves; details were not available for 17 patients.
Most of the patients with pyrethroid poisoning were asymptomatic. The most common presenting symptoms were drowsiness (n = 76, 20.0%), seizures (n = 22, 5.8%), salivation (n = 22, 5.8%), vomiting (n = 22, 5.8%), and diarrhea (n = 10, 2.6%). Frequency of neither the minor nor the major symptoms such as seizures were significantly different among patients with type 1 and type 2 pyrethroid poisoning.
Laboratory parameters were similar in type 1 and type 2 pyrethroid poisoning patients except for hemoglobin which was significantly (p = 0.02) lower in type 1 poisoning (Table 1). As expected, pseudocholinesterase activity was normal and similar in type 1 and type 2 pyrethroid poisoning. In a majority of the patients, electrocardiogram (ECG) was normal; 63 (21.2%) patients had sinus tachycardia of whom 45 patients had ingested type II pyrethroid and 18 type I pyrethroid (p = 0.02). Only 1 patient had ECG changes suggestive of lateral wall ischemia (patient was a long-term smoker and had stage 4 prostatic malignancy).
A significantly higher number of patients with type 2 poisoning required admission (39.3% vs. 16%, p < 0.01) when compared with type 1 poisoning (Table 1). Presentation with seizures was associated with risk of admission OR 2.43 (C.I. 1.02–5.78) (Table 3). A total of 22 patients presented with history of seizures, and 10 patients were discharged from ED since they had only isolated episode and had no further seizures during their entire period of observation in the ED.
Table 3.
Factors associated with hospitalization.
| Values | Requiring hospitalization n = 130 | Not requiring hospitalization n = 249 | Univariate analysis (OR, 95% CI) | P value | Multivariate analysis (OR, 95% CI) | P value |
|---|---|---|---|---|---|---|
| Age (mean, SD) years | 31.7 (12.7) | 28.6 (11.4) | 1.02 (1.01–1.04) | 0.02 | 1.02 (0.99–1.04) | 0.09 |
| Gender (female, %) | 81 (62.3) | 121 (48.6) | 1.74 (1.13–2.69) | 0.01 | 1.33 (0.82–2.14) | 0.25 |
| Type of pyrethroid (1:2) | 13: 117 | 68: 181 | 3.38 (1.79–6.40) | <0.001 | 2.55 (1.31–4.97) | 0.006 |
| Drowsiness (%) | 29 (22.3) | 47 (18.9) | 1.23 (0.73–2.07) | 0.43 | – | – |
| Seizures (%) | 12 (9.2) | 10 (4) | 2.43 (1.02–5.78) | 0.05 | 2.62 (1.06–6.48) | 0.03 |
| Any CNS (%) | 41 (31.5) | 57 (22.9) | 1.55 (0.97–2.49) | 0.07 | 1.48 (0.89–2.47) | 0.13 |
| Salivation (%) | 10 (7.7) | 12 (4.8) | 1.65 (0.69–3.93) | 0.26 | 1.56 (0.62–3.93) | 0.34 |
| Treated prior to hospitalization (%) | 80 (61.5) | 80 (32.1) | 3.38 (2.17–5.26) | <0.001 | 2.99 (1.87–4.74) | <0.001 |
Values in parentheses indicate percentages unless specified; CNS – central nervous system; multivariate analysis was done incorporating factors that were associated (P < 0.2) with hospitalization on univariate analysis.
None of the patients with type 1 pyrethroid poisoning required mechanical ventilation, whereas 13 (3.7%) of patients with type 2 poisoning were intubated and ventilated. The hospital length of stay was significantly longer in patients who had consumed type 2 compounds median (IQR) 18 h (6–48) compared with patients who had consumed type 1 compounds (6 h (4–24)) p = 0.001).
The factors associated with hospitalization were presented in Table 3. Ingestion of type 2 pyrethroids (OR: 2.55, 95%CI: 1.31–4.97)), history of seizures (OR: 2.62, 95%CI 1.06–6.48), and patients requiring pre-hospital treatment prior to presentation to our center (OR: 2.99, 95% CI: 1.87–4.74) were associated with increased risk of admission in the multivariate analysis.
Discussion
In our study of patients who presented with pyrethroid poisoning, type 2 compound ingestion was more common than type 1. Only a third of the patients required admission. The frequency of symptoms was similar in type 1 and type 2 poisoning except for salivation which was recorded only with type 2 poisoning. Although seizures were more common with type 2 pyrethroid poisoning, this was not statistically significant.
One in three patients had some involvement of the central nervous system (CNS); the most common symptom was drowsiness (20/81 (24.7%) in type 1 poisoning vs. 56/297 (18.1%) in type 2 poisoning). The incidence of seizures was also similar among both the groups (4.9% vs. 6%). Type 2 pyrethroids reduce the opening state of voltage-sensitive chloride channels and inhibit gamma amino butyric acid (GABA) pathway, and this is probably the reason for the higher incidence of CNS effects and seizures in type 2 pyrethroids poisoning.11,12 There are, however, case reports of seizure with type 1 compounds like biphenthrin,13 suggesting that both the types of pyrethroid have a tendency to cause seizures.
We observed from our study cohort that there is no clear toxidrome that can be attributed to patients with pyrethroid toxicity. The majority of our patients were asymptomatic; in these patients, the diagnosis of pyrethroid poisoning could be made only by identifying the toxin through the container that was brought by the patient or patient relatives.
The typical pyrethroid toxidrome suggested by He et al.14 was not observed in a majority of our patients. He classified patients as mild, moderate, and severe. Patients with hypersalivation and fasciculation were categorized to have moderate poisoning while those with altered sensorium, seizures, or pulmonary edema were categorized as severe poisoning. None of our patients had fasciculations or pulmonary edema, and a majority did not report salivation, nausea, or vomiting. A possible reason for not observing some of the manifestations of the toxidrome could be the retrospective nature of the study, wherein the trivial symptoms of patients may not been stated or recorded. The other feature of tremors may not have been observed or recorded unless they were severe and discomforting. Around 40% had received pre-hospital atropine which could have masked some of the symptoms.
Previous studies have shown that pyrethroid poisoning can present with typical type 1 “T” syndrome and type 2 “CS” syndrome (Table 4)15; in our cohort hypersalivation, depressed sensorium and seizures were exclusively seen in patients with type 2 pyrethroid poisoning while nausea, vomiting, and paraesthesias were seen in both type 1 and type 2 poisoning.
Table 4.
Type 1 and Type 2 pyrethroid poisoning clinical features.
| Clinical features | Type 1 pyrethroids | Type 2 pyrethroids |
|---|---|---|
| Classical type 1 syndrome | ||
| Fine tremor | + | − |
| Paraesthesias | + | − |
| Marked reflex hyperexcitability | + | − |
| Classical type 2 syndrome | ||
| Choreoathetosis | − | + |
| Salivation | − | + |
| Coarse tremor | − | + |
| Increased extensor tone | − | + |
| Moderate reflex hyperexcitability | − | + |
Pyrethroids act on the sodium and the chloride channels of the nerves and the muscle cells. They modify the gating properties of the voltage-sensitive sodium channels, delaying closure; this leads to sodium influx and repetitive firing, leading to paraesthesias and proarrthymogenic potential. Type II pyrethroids act on the voltage-dependent chloride channels, especially in the brain, nerves, muscles, and salivary glands. These decreased chloride currents can lead to salivation and myotonia. At higher levels, pyrethroids can act on the GABA chloride channels leading to seizures.15
There was no difference in pseudocholinesterase (Pch) levels between type 1 and 2 pyrethroid poisoning and between those who required mechanical ventilation and the non-ventilated group (Table 1), implying that these patients had not co-ingested organophosphorus compounds. A low-Pch levels in patients with suspected pyrethroid poisoning would indicate ingestion of OP pyrethroid combination.16,17 Pch in this setting can be used to discriminate pyrethroid poisoning from mixed poisoning with pyrethroids and organophosphorus compounds. In contrast to chronic pyrethroid poisoning, our cohort with acute pyrethroid poisoning did not have any blood cell abnormalities.18,19
There was a significant difference in the hemoglobin between both the groups with a lower hemoglobin in type 1 pyrethroid group; this is probably because there were more women in the type 1 group compared to the type 2 group (59.2% versus 43.2%)
The most common ECG change was tachycardia. Both type 1 and type 2 pyrethroids cause profound adrenal activation with the secretion of noradrenaline and adrenalin.20 Adrenal activation is shown to occur with small doses in deltamethrin21; hence, adrenal activation was probably the reason for the ECG recorded tachycardia in both the groups.
There was a higher incidence of symptomatic presentations with type 2 pyrethroid poisoning when compared with type 1 poisoning, albeit not significantly different. It is likely that patients who had taken type 2 compounds were sicker, reflected by the fact that more patients sought medical help prior to being referred to our hospital, and corroborated by the observation that more patients with type 2 poisoning required hospital admission when compared with type I pyrethroid poisoning (39.3% vs. 16%, p < 0.01) (Table 2). These observations suggest that type 2 pyrethroids are more toxic to humans than type 1 compounds.
Our study cohort had good outcomes with supportive therapy and without use of antidotes. Previous studies have suggested that certain drugs can be used as antidotes for pyrethroid poisoning such as Ivermectin which is effective against deltamethrin-induced salivation and repetitive muscle discharges and mephenesin can be used as an antidote for motor and cardiovascular effects of deltamethrin.22,23 Atropine has also been suggested for reducing the salivation seen in type 2 pyrethroid poisoning.24
None of these medications were used in our patients, barring the pre-hospital use of atropine in about 40% of our patients.
Conclusions
Type 2 pyrethroid poisoning is more frequently seen than type 1 poisoning. The most commonly used pyrethroid in DSH was cypermethrin. Poisoning due to pyrethroid is mild; most patients were asymptomatic, and only a small proportion of patients required admission. All patients survived. Ingestion of type 2 compounds, presence of seizure, and treatment prior to hospitalization were associated with the need for hospitalization.
Strengths and limitations
The greatest strength of the study was the number of patients who presented with different compounds used in pyrethroid poisoning due to DSH and could be included in the study. Our study also has the strength of being an in-hospital study and looking at patients with DSH rather than occupational or accidental exposure. The limitations of our study lay in the fact that it is a retrospective study; hence, minor symptoms could have been missed and since it is a retrospective study, blood levels and compound analysis could not be done.
Patients/ Guardians/ Participants consent
Patients informed consent was obtained.
Ethical clearance
Institute/hospital ethical clearance certificate was obtained.
Source of support
Nil.
Disclosure of competing interest
The authors have none to declare.
Acknowledgment
None.
References
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