Correlation of serum potassium and plasma cholinesterase in assessing the severity of acute organophosphate poisoning

Abstract

Introduction: Organophosphate (OP) compounds are widely used as pesticides, particularly in agricultural regions, and constitute a significant cause of poisoning worldwide. The toxicity primarily results from inhibition of acetylcholinesterase enzyme, leading to accumulation of acetylcholine at synapses and manifesting as a characteristic cholinergic toxidrome. While plasma cholinesterase levels have been traditionally used to confirm exposure and assess severity, their correlation with clinical outcomes is not always consistent. Recent studies have suggested alterations in serum electrolytes, particularly potassium, as potential markers of poisoning severity. This study aimed to correlate serum potassium and plasma cholinesterase levels with the clinical severity of acute organophosphate poisoning. Methods: This prospective study was conducted at Shri B.M. Patil Medical College, Hospital and Research Centre, Vijayapura, from May 2023 to December 2024. A total of 83 patients with acute organophosphate poisoning were included. Detailed clinical assessment, including Glasgow Coma Scale (GCS) scoring and pupillary examination, was performed at admission. Serum potassium and plasma cholinesterase levels were measured at admission and after 24 hours. Patients were classified as having severe or non-severe poisoning based on clinical parameters and requirement for mechanical ventilation. Statistical analysis was performed to assess the correlation between biochemical markers and poisoning severity. Results: The majority of patients (67.5%) were between 20-40 years of age, with a slight male predominance (51.8%). Common clinical features included vomiting (74.7%), muscle weakness (62.6%), and bronchospasm (30.1%). Severe poisoning was observed in 37.3% of patients, with 26.5% requiring mechanical ventilation. Patients with severe poisoning had significantly lower serum potassium levels both initially (3.32±0.59 vs 4.08±0.47 mEq/L, p<0.001) and at 24 hours (3.6±0.55 vs 4±0.34 mEq/L, p=0.001) compared to non-severe cases. Similarly, plasma cholinesterase levels were significantly lower in 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). A significant positive correlation was observed between serum potassium and acetylcholinesterase levels in both severe (r=0.675, p=0.001) and non-severe (r=0.582, p=0.003) poisoning cases. Patients requiring mechanical ventilation had markedly lower initial potassium levels (3.12±0.48 mEq/L vs. 3.97±0.54 mEq/L, p<0.001). There was a strong association between mortality and low serum potassium, with non-survivors having dramatically lower potassium levels (2.86±0.44 mEq/L) compared to survivors (3.94±0.51 mEq/L, p<0.001). Similarly, patients who died had profoundly reduced initial acetylcholinesterase levels (452.8±198.6) compared to those who were discharged (3212.9±2824.8, p<0.001). Severe poisoning was also associated with lower GCS scores (p<0.001) and smaller pupil sizes (1.48±0.67 vs 2.37±0.74 mm, p<0.001). Conclusion: Serum potassium levels show a significant correlation with the severity of acute organophosphate poisoning, comparable to the established marker plasma cholinesterase. The combination of these biochemical parameters with clinical indicators like GCS scores and pupillary changes provides a comprehensive approach to severity assessment. Serum potassium measurement can serve as a simple, cost- effective, and readily available tool for early risk stratification, particularly in resource- limited settings.