Organophosphate (OP) poisoning represents one of the most significant causes of pesticide-related morbidity and mortality worldwide, particularly in developing countries where agricultural practices are prevalent and regulations may be less stringent.¹ The World Health Organization estimates that approximately three million cases of pesticide poisoning occur annually, with organophosphates accounting for a substantial proportion of these incidents, resulting in an estimated 300,000 deaths.² The toxicological mechanism of organophosphate compounds primarily involves the inhibition of acetylcholinesterase (AChE), causing accumulation of acetylcholine at synaptic junctions and neuromuscular junctions. This accumulation results in continuous stimulation of cholinergic receptors, manifesting as a characteristic cholinergic crisis.³

Plasma cholinesterase levels have traditionally been a biochemical marker for diagnosing and monitoring OP poisoning. This enzyme, also known as butyrylcholinesterase or pseudocholinesterase, shows a rapid decline in activity following OP exposure, making it a valuable diagnostic tool.⁴ Potassium homeostasis can be significantly disrupted in OP poisoning through multiple mechanisms, including altered cellular membrane permeability, autonomic dysfunction, and respiratory compromise.⁵ Early studies have suggested that hyper- or hypokalemia correlates with the severity of poisoning and could serve as a prognostic indicator when evaluated alongside other clinical and biochemical parameters. The complex pathophysiology of OP poisoning involves multiple mechanisms that can affect both cholinesterase activity and potassium homeostasis. These manifestations can indirectly influence potassium levels through various mechanisms, including respiratory acidosis, tissue hypoxia, and altered cellular transport.⁶

Furthermore, the autonomic effects of OP poisoning can lead to significant cardiovascular complications, which electrolyte disturbances may exacerbate. Studies have shown that patients with severe OP poisoning often exhibit ECG changes, some of which may be attributed to potassium abnormalities.⁷ The assessment of OP poisoning severity has traditionally relied on clinical scoring systems, such as the Peradeniya Organophosphorus Poisoning (POP) scale and the Modified Glasgow Coma Scale. While these scoring systems provide valuable clinical information, integrating biochemical parameters could enhance their predictive value.⁸

Recent research has suggested that the combined evaluation of multiple parameters, including clinical features, cholinesterase levels, and electrolyte status, may provide better prognostic information than any single parameter alone.⁹ The timing of biochemical measurements of poisoning onset and treatment initiation also presents an important consideration. While plasma cholinesterase levels typically show early depression following OP exposure, the temporal pattern of potassium alterations and their relationship to clinical severity may vary. Additionally, therapeutic interventions, particularly atropine and oxime therapy, may influence cholinesterase reactivation and electrolyte balance.¹⁰ This current study aims to find a link between serum potassium levels and plasma cholinesterase activity in acute OP poisoning, emphasizing their combined value in determining poisoning severity.

This cross-sectional study included patients admitted to the medicine ICU/WARDS of  “BLDE(DU) Shri BM Patil Medical College and Research Centre, Vijayapura, from May 2023 to Dec 2024. Patients above 18yrs with a known history of consumption or exposure to OPC poison and typical clinical symptoms of organophosphorous compound poisoning were included. Patients with a history of serious systemic illness, malnutrition, chronic infections and consuming alcohol while poisoning were excluded. Upon admission to the casualty medicine department or ICU, patients were screened for eligibility based on predetermined inclusion and exclusion criteria. Written informed consent was obtained from the patients or their legal representatives before the study was enrolled. The diagnosis of organophosphate poisoning was established based on history of exposure, characteristic clinical features, and confirmation through poison detection center reports.”

Blood samples were collected from all participants at admission before the initiation of specific treatment. The primary parameters of interest - serum potassium and plasma cholinesterase levels - were measured using standardized laboratory techniques. Serum potassium was analysed using the ion-selective electrode method, while plasma cholinesterase activity was determined using spectrophotometric analysis. Patients were classified into two groups - severe and non-severe cases - based on specific clinical manifestations at the time of presentation. The severe category included patients presenting with any of the following: convulsions, significant muscle weakness/fasciculations, or respiratory distress requiring ventilatory support. Mortality outcomes were also recorded for each patient during hospitalization.

Statistical analysis: The data were collected in pro forma and analysed using SPSS v26.0. The data were represented in tables and graphs, such as mean, standard deviation, frequency, and percentage. The mean difference was assessed using an unpaired t-test and categorical data using a chi-square test. For all statistical testing, a p-value <0.05 was considered significant.

83 patients meeting inclusion criteria are included in the present study.

Presence of “vomiting was the most common clinical feature observed in 74.7% of patients, followed by muscle weakness (62.6%) and bronchospasm (30.1%), while less common symptoms included diarrhea (21.7%), salivation (19.3%), abdominal pain (9.6%), convulsions (6%), and lacrimation (1.2%). The majority of patients (66.3%) maintained a good level of consciousness with Glasgow Coma Scale (GCS) scores of 13-15, while 13.3% had moderate impairment (GCS 9-12), and 20.5% presented with severe impairment (GCS 3-8). Mechanical ventilation was required in approximately one-quarter (26.5%) of the patients, while the majority (73.5%) did not require this intervention.”

Patients according to poisoning severity, 37.3% were categorized as having severe organophosphate poisoning, while 62.6% were classified as not severe.

Above Table shows significant associations between severity of poisoning and biochemical parameters, with severely poisoned patients showing significantly lower initial serum potassium (3.32±0.59 vs 4.08±0.47 mEq/L, p<0.001), lower 24-hour potassium (3.6±0.55 vs 4±0.34 mEq/L, p=0.001), lower initial plasma cholinesterase (1465.4±2336.2 vs 3455.4±2785.4, p=0.001), and lower 24-hour plasma cholinesterase levels (1633.5±2620.9 vs 3550.9±2794.6, p=0.01).

The table shows a strong association between GCS scores and poisoning severity, with 51.6% of severe cases having GCS scores of 3-8 compared to only 1.9% of non-severe cases, while 92.3% of non-severe cases had GCS scores of 13-15 compared to only 22.6% of severe cases (p<0.001). Patients with severe organophosphate poisoning had significantly smaller pupil sizes than non-severe cases (1.48±0.67 mm vs 2.37±0.74 mm, p<0.001), reflecting more pronounced cholinergic effects.

The study demonstrates a significant positive correlation between serum potassium levels and acetylcholinesterase activity in severe and non-severe organophosphate poisoning cases. The correlation coefficient (r=0.582) for non-severe cases indicates a moderate positive correlation, while the stronger correlation (r=0.675) in severe cases suggests that this relationship becomes more pronounced with increasing poisoning severity. The statistically significant p-values (p=0.003 and p=0.001, respectively) confirm that these correlations are unlikely to be due to chance.

Table reveals a striking relationship between serum potassium levels and mortality outcomes. Patients who died had markedly lower initial potassium levels (2.86±0.44 mEq/L) compared to those discharged (3.94±0.51 mEq/L), with patients who left against medical advice (AMA) having intermediate values (3.62±0.58 mEq/L). This gradient across outcome groups became highly statistically significant (p<0.001). It also shows dramatically lower initial acetylcholinesterase levels in patients who died (452.8±198.6) compared to those discharged (3212.9±2824.8), with a highly significant p-value (<0.001). This profound depression of enzyme activity in fatal cases reflects severe organophosphate toxicity. At 24 hours, while there was some increase in enzyme levels among deceased patients (985.4±324.7), they remained substantially lower than in discharged patients (3376±2900.9).

OP compounds are extensively used as insecticides, pesticides, and chemical warfare agents, making them a significant cause of poisoning worldwide, particularly in agricultural regions. The majority of organophosphate poisoning cases (67.5%) occurred in the 20-40 years age group, followed by those below 20 years (21.7%). Our study showed a slight male predominance (51.8%) compared to females (48.2%), which differs somewhat from many other studies that report a more pronounced male predominance. For instance, Chaudhary et al. reported a male-to-female ratio of 2.7:1 in their study from Nepal.¹¹ Banday et al. reported similar findings in their study from Kashmir, where 62.8% of OP poisoning cases were in the 21-40 years age group, attributing this to the high levels of stress, emotional instability, and socioeconomic challenges faced by this productive age group.¹² Similarly, Adinew et al., in their Ethiopian study, found that 76.8% of poisoning cases were among those aged 21-30 years.¹³

In the present study, vomiting was the most prevalent clinical feature (74.7%), followed by muscle weakness (62.6%) and bronchospasm (30.1%). These findings are consistent with the established cholinergic toxidrome of OP poisoning but show some variation in frequency compared to other studies. Vomiting as the predominant symptom aligns with findings by Ahmed et al., who reported vomiting in 81.3% of their patients.¹⁴ The significant proportion of patients presenting with muscle weakness (62.6%) in our study reflects the nicotinic effects of OP poisoning. Yurumez et al. observed similar findings with muscle weakness in 58% of their patients.¹⁵ However, Kang et al. reported a lower incidence (34.7%) of neuromuscular manifestations, suggesting potential variations based on the specific OP compound involved, route of exposure, and time elapsed before medical intervention.¹⁶

The present study demonstrated that plasma cholinesterase levels were significantly lower in patients with severe OP poisoning compared to non-severe cases, both initially (1465.4±2336.2 vs 3455.4±2785.4, p=0.001) and at 24 hours (1633.5±2620.9 vs 3550.9±2794.6, p=0.01). This finding is consistent with the established role of cholinesterase inhibition in OP toxicity and supports its utility as a severity marker. Plasma cholinesterase (butyrylcholinesterase) has been widely used as a biomarker of OP exposure and severity assessment. Nouira et al. reported that plasma cholinesterase levels below 1000 IU/L were associated with increased mortality and the need for mechanical ventilation.¹⁷ In our study, this association was even more dramatic, with non-survivors showing profoundly depressed initial enzyme activity (452.8±198.6) compared to survivors (3212.9±2824.8, p<0.001). This extreme reduction in cholinesterase activity in fatal cases represents a nearly 86% depression from typical values and indicates severe enzyme inhibition incompatible with normal physiological function. The slight increase in mean plasma cholinesterase levels after 24 hours observed in our study (from 2712.2±2785.7 to 2803.4±2864.9) likely reflects the effects of therapeutic interventions, particularly oxime therapy. This pattern aligns with observations by Pawar et al., who reported gradual recovery of enzyme activity following appropriate treatment.¹⁸

One of the most novel and significant findings in our study was the strong positive correlation between serum potassium levels and acetylcholinesterase activity in both severe (r=0.675, p=0.001) and non-severe (r=0.582, p=0.003) OP poisoning cases. This correlation has not been extensively investigated in previous studies, but it provides essential insights into the interrelated pathophysiological mechanisms in OP poisoning. The stronger correlation observed in severe cases (r=0.675) compared to non-severe cases (r=0.582) suggests that the relationship between cholinesterase inhibition and potassium dysregulation becomes more pronounced as poisoning severity increases. Sumathi et al.¹⁹ examined various biochemical parameters in OP poisoning and suggested that combined assessment of multiple markers provides superior predictive value compared to single parameter evaluation. Our finding of a significant correlation between potassium and cholinesterase levels supports this integrated approach to severity assessment and risk stratification. Several researchers have reported a correlation between pupil size and poisoning severity. Abedin et al. described progressive miosis with increasing severity of poisoning and proposed pupillary diameter as a simple bedside parameter for initial assessment.²⁰

Strengths: The study is well-structured with a transparent methodology, including a systematic approach to data collection, comprehensive laboratory investigations, and severity classification. Objective biomarkers (serum potassium and plasma cholinesterase levels) enhance the study’s clinical relevance. Additionally, strict quality control measures and a statistically justified sample size improve the reliability of findings. Moreover, the study setting in an agricultural region with high OP exposure rates enhances the external validity of our findings.

Limitations: The single-center study may limit generalizability to other populations. The cross-sectional design prevents the establishment of causality between potassium levels and clinical outcomes. Additionally, potential underreporting of alcohol consumption and limited long-term follow-up may affect the completeness of data on patient outcomes.

The findings contribute to the growing evidence base on prognostic markers in OP poisoning and highlight the potential value of readily available tests like serum potassium in resource-limited settings. The strong correlations between clinical parameters (GCS, pupil size) and biochemical markers (serum potassium, plasma cholinesterase) support an integrated approach to severity assessment. This multi-dimensional evaluation provides complementary information that enhances risk stratification and could guide treatment decisions. Future research should focus on elucidating the mechanisms underlying these associations and evaluating their impact on clinical outcomes when incorporated into management protocols.

Funding: Nil

Conflict of interest: Nil

1. Eddleston M, Phillips MR. Self-poisoning with pesticides. BMJ. 2019;328(7430):42-4. https://doi.org/10.1136/bmj.328.7430.42
2. World Health Organization. The WHO recommended the classification of pesticides by hazard and guidelines for classification 2019-2020. Geneva: WHO; 2020.
3. Gunnell D, Eddleston M, Phillips MR, Konradsen F. The global distribution of fatal pesticide self-poisoning: a systematic review. BMC Public Health. 2018;7:357. https://doi.org/10.1186/1471-2458-7-357
4. Thiermann H, Szinicz L, Eyer P, Worek F. Modern strategies in the therapy of organophosphate poisoning. Toxicol Lett. 2019;107:233-9. DOI: 10.1016/s0378-4274(99)00052-1
5. Roberts DM, Aaron CK. Managing acute organophosphorus pesticide poisoning. BMJ. 2017;334:629-34. https://doi.org/10.1136/bmj.39134.566979.BE
6. Eddleston M, Buckley NA, Eyer P, Dawson AH. Management of acute organophosphorus pesticide poisoning. Lancet. 2018;371:597-607. doi: 10.1016/S0140-6736(07)61202-1.
7. Peter JV, Jerobin J, Nair A, Bennett A. Clinical profile and outcome of patients hospitalized with organophosphate poisoning. JAPI. 2019;58:11-4. DOI: 10.3109/15563650.2010.528425
8. Senanayake N, de Silva HJ, Karalliedde L. A scale to assess severity in organophosphorus intoxication: POP scale. Hum Exp Toxicol. 2018;12:297-9. DOI: 10.1177/096032719301200407
9. Konickx LA, Bingham K, Eddleston M. Is oxygen required before atropine administration in organophosphorus or carbamate pesticide poisoning? Clin Toxicol. 2019;52:531-7. DOI: 10.3109/15563650.2014.915411
10. Eddleston M, Chowdhury FR. Pharmacological treatment of organophosphorus insecticide poisoning: current status and future direction. Expert Rev Clin Pharmacol. 2020;9:1363-73. doi: 10.1111/bcp.12784
11. Chaudhary SC, Singh K, Sawlani KK, Jain N, Vaish AK, Atam V, et al. Prognostic significance of estimating pseudocholinesterase activity and role of pralidoxime therapy in organophosphorus poisoning. Toxicol Int. 2013;20(3):214-7. DOI:10.4103/0971-6580.121669
12. Banday TH, Tathineni B, Desai MS, Naik V. Predictors of morbidity and mortality in organophosphorus poisoning: A case study in a rural hospital in Karnataka, India. N Am J Med Sci. 2015;7(6):259-65. DOI: 10.4103/1947-2714.159331
13. Adinew GM, Asrie AB, Birru EM. The pattern of acute organophosphorus poisoning at the University of Gondar Teaching Hospital, Northwest Ethiopia. BMC Res Notes. 2017;10(1):149-52. DOI: 10.1186/s13104-017-2464-5
14. Ahmed SM, Das B, Nadeem A, Samal RK. Survival pattern in patients with acute organophosphate poisoning on mechanical ventilation: A retrospective intensive care unit-based study in a tertiary care teaching hospital. Indian J Anaesth. 2014;58(1):11-7. DOI: 10.4103/0019-5049.126780
15. Yurumez Y, Durukan P, Yavuz Y, Ikizceli I, Avsarogullari L, Ozkan S, et al. Acute organophosphate poisoning in university hospital emergency room patients. Intern Med. 2007;46(13):965-9. DOI: 10.2169/internalmedicine.46.6304
16. Kang EJ, Seok SJ, Lee KH, Gil HW, Yang JO, Lee EY, et al. Factors for determining survival in acute organophosphate poisoning. Korean J Intern Med. 2009;24(4):362-7. doi: 10.3904/kjim.2009.24.4.362
17. Nouira S, Abroug F, Elatrous S, Boujdaria R, Bouchoucha S. Prognostic value of serum cholinesterase in organophosphate poisoning. Chest. 1994;106(6):1811-4. DOI: 10.1378/chest.106.6.1811
18. Pawar KS, Bhoite RR, Pillay CP, Chavan SC, Malshikare DS, Garad SG. Continuous pralidoxime infusion versus repeated bolus injection to treat organophosphorus pesticide poisoning: A randomized controlled trial. Lancet. 2006;368(9553):2136-41. DOI: 10.1016/S0140-6736(06)69862-0
19. Sumathi ME, Kumar SH, Shashidhar KN, Takkalaki N. Prognostic significance of various biochemical parameters in acute organophosphorus poisoning. Toxicol Int. 2014;21(2):167-71. DOI: 10.4103/0971-6580.139800
20. Abedin MJ, Sayeed AA, Basher A, Maude RJ, Hoque G, Faiz MA. Open-label randomized clinical trial of atropine bolus injection versus incremental boluses plus infusion for organophosphate poisoning in Bangladesh. J Med Toxicol. 2012;8(2):108-17. DOI: 10.1007/s13181-012-0214-6