Poisoning from organophosphorus (OP) compounds is a serious medical emergency that frequently occurs in developing nations, particularly in agricultural settings where these compounds are widely employed as pesticides. Due to its high morbidity and mortality, which are frequently made worse by delayed presentation, limited access to treatment, and ignorance of the potential severity of the toxicity, OP poisoning remains a significant public health concern.

Acetylcholinesterase (AChE) is irreversibly inhibited in the mechanism of toxicity, which causes acetylcholine to build up at cholinergic synapses and overstimulate muscarinic and nicotinic receptors in the autonomic, central, and peripheral nervous systems. Clinically, this presents as a collection of cholinergic symptoms, such as bronchorrhea, bradycardia, fasciculations, miosis, hypotension, seizures, and, in extreme situations, respiratory failure brought on by cerebral depression and respiratory muscle paralysis[1,2].

Early detection of the severity of OP poisoning is essential for managing the condition since it helps determine the best course of treatment, forecast clinical results, and lessen consequences. Clinical severity has historically been evaluated using a variety of grading systems, including the Glasgow Coma Scale (GCS), the Acute Physiology and Chronic Health Evaluation (APACHE II) score, and the Peradeniya Organophosphorus Poisoning (POP) scale. These clinical scoring methods, however, may be subjective and rely on the experience of the examiner. Biochemical markers, on the other hand, provide a more impartial and possibly early way to gauge the extent of poisoning. Among these, the predictive importance of serum amylase, total leukocyte count (TLC), and C-reactive protein (CRP) in acute OP poisoning has been investigated.[3,2]

Total Leukocyte Count serves as a broad indicator of systemic inflammation and immune response. In OP poisoning, the stimulation of the sympathetic and parasympathetic systems may result in stress leukocytosis, reflecting the systemic inflammatory burden. Elevations in TLC can occur in response to the inflammatory and hypoxic stress associated with OP poisoning, especially in the presence of respiratory distress, aspiration pneumonia, or multi-organ dysfunction. Increased leukocyte counts can therefore serve as a surrogate marker of disease severity, systemic inflammation, or secondary infections, which commonly complicate OP toxicity. Although leukocytosis is not specific to OP poisoning, its trends can provide important information about disease progression, especially when used in conjunction with other markers.[3,4]

C-Reactive Protein is an acute-phase protein produced by the liver in response to interleukin-6 (IL-6) and other pro-inflammatory cytokines. Its levels rise rapidly in response to inflammation, infection, or tissue injury. In the context of OP poisoning, the systemic inflammatory response triggered by oxidative stress, hypoxia, and neuronal injury contributes to elevated CRP levels. Moreover, severe OP poisoning is often associated with complications like aspiration pneumonia, acute respiratory distress syndrome (ARDS), and sepsis, all of which can significantly raise CRP levels. As such, CRP can act as an early biomarker to indicate the extent of inflammation and tissue damage, as well as a predictor of complications and prognosis. Additionally, CRP levels have the advantage of rising early during the acute phase of illness, offering timely insights into the patient's condition before overt clinical deterioration becomes evident.[4,5]

Serum Amylase, predominantly a pancreatic enzyme, is another potential biomarker that has been increasingly investigated in the assessment of OP poisoning. Pancreatic involvement in OP poisoning has been described in literature, with acute pancreatitis being a recognized though underdiagnosed complication. The pathophysiology of pancreatitis in OP poisoning is not fully elucidated but is believed to involve cholinergic overstimulation of the pancreatic acini, increased ductal pressure, and direct cytotoxic effects leading to enzymatic leakage. As a result, elevated serum amylase levels are frequently observed in moderate to severe OP poisoning cases. Moreover, OP-induced hypoxia and oxidative stress may contribute to pancreatic injury and enzyme elevation. It is important to note that hyperamylasemia in these patients may not always correlate with clinical pancreatitis but may still serve as an early warning of subclinical organ involvement and systemic toxicity.[5,6]

The usefulness of these biomarkers lies not just in their individual values but also in their dynamic changes and correlation with the overall clinical picture. When used together, TLC, CRP, and serum amylase provide a composite understanding of the severity and systemic involvement in OP poisoning. For example, elevated TLC in combination with high CRP can signify systemic inflammatory response or infectious complications, while elevated amylase suggests pancreatic or gastrointestinal involvement. These markers are cost-effective, widely available, and do not require specialized laboratory infrastructure, making them particularly valuable in resource-limited settings.[6,7]

Furthermore, these parameters can also be useful in risk stratification and triaging of patients. Patients presenting with significantly elevated TLC, CRP, and serum amylase at admission may require intensive monitoring, early ventilatory support, and prolonged hospital stay. Conversely, patients with normal or mildly elevated levels may be suitable for close observation and conservative management in a high-dependency unit. Serial monitoring of these markers can also provide insights into treatment response and early detection of complications, such as infections, pancreatitis, or respiratory failure. As such, they can serve both diagnostic and prognostic roles in the clinical setting.[4,5]

In an effort to forecast the severity and consequences of OP poisoning, recent research has tried to determine cut-off values for these indicators. Serum amylase levels above 200 IU/L, CRP levels over 6 mg/dL, and TLC levels over 11,000 cells/mm³ have all been found to be substantially linked to the need for mechanical ventilation, ICU hospitalization, and higher mortality. These findings underline the usefulness of adding simple laboratory testing into the conventional strategy for OP poisoning evaluation.[6,7]

This study examined the use of serum amylase, C-reactive protein, and total leukocyte count as indicators to gauge the severity of organophosphorus chemical poisoning.

The study used a cross-sectional design to assess the predictive significance of serum amylase, C-reactive protein (CRP), and total leukocyte count (TLC) in organophosphorus chemical (OPC) poisoning. The purpose of the design was to measure these characteristics at admission and link them with clinical outcomes (such as mortality or the requirement for ventilation) while the patient remained in the hospital. Patients who were admitted to the hospital within 24 hours of being poisoned had their data gathered, and they were monitored until they were discharged or passed away. The cross-sectional method made it possible to analyze correlations between biomarkers and severity as determined by the Peradeniya Organophosphorus Poisoning Scale (POP Scale) in an effective manner. Study Setting The study was conducted in the Department of General Medicine at Shimoga Institute of Medical Sciences (SIMS), Shivamogga, a tertiary care hospital serving rural and urban populations in Karnataka, India. The hospital’s high patient inflow of OPC poisoning cases provided an adequate sample. The McGann Teaching District Hospital, affiliated with SIMS, was the primary site for patient recruitment and data collection. The setting ensured access to standardized laboratory facilities for biomarker estimation (e.g., TLC, CRP, serum amylase) and critical care support for severe cases. Study Duration The study spanned 12 months, from October 2023 to October 2024. This duration accounted for seasonal variations in poisoning cases (e.g., higher incidence during agricultural seasons) and ensured sufficient time to enroll the target sample size of 126 patients. Data collection was completed prospectively during this period. Inclusion Criteria (in points): • Patients aged >14 years of either sex. • History of acute OPC ingestion confirmed by clinical history or circumstantial evidence. • Presentation to the hospital within 24 hours of exposure. • Willingness to provide informed consent (or consent from guardians for minors). Exclusion Criteria (in points): • Mixed poisoning (e.g., OPC + other toxins). • Recent trauma, burns, surgery, or sepsis at admission. • History of pancreatic disorders (to avoid confounding serum amylase levels). • Recent myocardial infarction (to exclude secondary inflammation affecting CRP). Study Sampling A convenience sampling method was used, enrolling all eligible patients admitted during the study period. This approach was pragmatic given the emergency nature of OPC poisoning and the need for timely intervention. Patients were screened against inclusion/exclusion criteria at admission. Ethical Considerations Approval: Obtained from the Institutional Ethics Committee of SIMS. Informed Consent: Written consent from participants/guardians; vernacular language used. Confidentiality: Patient identifiers were anonymized in datasets. Risk Mitigation: No additional risks imposed; standard care was prioritized. Withdrawal: Participants could leave the study without treatment penalties.

Age Distribution of Study Participants (n = 126)

Among the 126 study participants, the highest proportion belonged to the 21–30 years age group (32 cases, 25.4%), followed by 31–40 years (29 cases, 23.0%). The 51–60 years group accounted for 23 cases (18.3%), while 41–50 years included 17 cases (13.5%). Participants aged ≤20 years constituted 14 cases (11.1%), and 61–70 years represented 11 cases (8.7%) of the study population.

Table 1: Age Distribution of Study Participants (n = 126)

Gender Distribution (n = 126)

Among the 126 study participants, males constituted 84 cases (66.7%), while females accounted for 42 cases (33.3%). The distribution indicates that males represented approximately two-thirds of the study population, whereas females comprised about one-third of the total cases included in the study.

Table 2: Gender Distribution

Mode of Poisoning (n = 126)

The majority of poisoning cases occurred through ingestion, accounting for 124 cases (98.4%), while inhalation was reported in 2 cases (1.6%). These findings show that ingestion was the predominant route of exposure among the study participants, with inhalational exposure contributing to only a very small proportion of cases.

Table 3: Mode of Poisoning

Compound Consumed (n = 126)

Among the compounds consumed, chlorpyrifos was the most common with 91 cases (72.2%), followed by quinalphos with 14 cases (11.1%). Other compounds included ethion in 6 cases (4.8%), monocrotophos and profenofos in 4 cases each (3.2%), dimethoate and thimet in 2 cases each (1.6%), and dichlorvas, malathion, and parathion in 1 case each (0.8%).

Table 4: Compound Consumed

Severity of Poisoning (n = 126)

Among the 126 cases, mild poisoning was observed in 84 patients (66.7%), moderate poisoning in 24 patients (19.0%), and severe poisoning in 18 patients (14.3%). The findings indicate that mild cases constituted the majority of the study population, while moderate and severe cases represented smaller proportions.

Table 5: Severity of Poisoning

Distribution of Clinical Parameters According to Severity of Organophosphorus Poisoning (n = 126)

Clinical parameters varied according to severity. Pinpoint pupils were observed in 13 mild, 16 moderate, and 18 severe cases, while pupil size <2 mm was seen in 42 mild and 8 moderate cases. Respiratory rate <20/min occurred in 77 mild cases, whereas >20/min with cyanosis was present in 16 severe cases. Generalised continuous fasciculations were seen in 17 severe cases, and no response level of consciousness was recorded in 13 severe cases.

The aim of the present study was to evaluate the role of total leukocyte count, C-reactive protein, and serum amylase as biochemical markers for assessing the severity of organophosphorus compound poisoning, and to compare their relationship with serum cholinesterase, clinical severity, ventilator requirement, and patient outcome. The study is significant because organophosphorus poisoning remains a major medical emergency, particularly in agricultural regions, with high risk of respiratory failure, multi-organ involvement, and death. Early identification of severe poisoning is essential for prompt triage, intensive monitoring, and timely intervention. While serum cholinesterase is a recognized marker, it may not always be rapidly available in all settings. In contrast, total leukocyte count, C-reactive protein, and serum amylase are simple, cost-effective, and widely accessible investigations. Demonstrating their association with severity and prognosis provides practical value in improving bedside assessment and guiding management decisions, especially in resource-limited healthcare environments. Age The present study showed that the highest proportion of organophosphorus poisoning cases occurred in the 21–30 years age group (25.4%), followed by 31–40 years (23.0%), indicating predominance among young adults. This trend suggests that individuals in the economically productive age group are more frequently exposed, possibly due to occupational and environmental factors. Gender In the present study, males constituted 84 cases (66.7%), while females accounted for 42 cases (33.3%), demonstrating clear male predominance in organophosphorus poisoning. This predominance may be attributed to greater occupational exposure among males, particularly in agricultural activities where organophosphorus compounds are commonly used. A major strength of the present study lies in its comprehensive evaluation of simple, routinely available biochemical markers—total leukocyte count, C-reactive protein, serum amylase, and serum cholinesterase—in relation to severity, ventilator requirement, and clinical outcome in organophosphorus poisoning. The study included a reasonably sized cohort of 126 patients, allowing meaningful subgroup comparison across mild, moderate, and severe poisoning categories. Another important strength is the integration of both clinical and laboratory parameters, including pupil size, respiratory rate, heart rate, fasciculations, level of consciousness, Peradeniya score, biochemical markers, and outcomes such as mortality and ventilator requirement. The demonstration of statistically significant trends across severity categories strengthens the internal consistency of the findings. The study also highlights cost-effective markers that are practical in emergency and resource-limited settings. By correlating inflammatory and enzymatic markers with cholinesterase and outcome, the study offers clinically relevant data for early risk stratification and bedside prognostication. Implication The findings of the present study have important clinical implications for the assessment and management of organophosphorus poisoning. The significant rise in total leukocyte count, C-reactive protein, and serum amylase with increasing poisoning severity, along with the decline in serum cholinesterase, suggests that these parameters can support early identification of high-risk patients. This is particularly useful in emergency settings where rapid decision-making is required and where advanced toxicological assays may not be readily available. The strong association of these markers with mortality and ventilator requirement indicates that they may help clinicians prioritize monitoring, intensive care admission, and aggressive supportive treatment. The study also implies that systemic inflammation and pancreatic enzyme elevation are meaningful components of organophosphorus toxicity rather than incidental findings. Incorporating these markers into initial evaluation protocols may improve prognostic accuracy, optimize triage, and potentially reduce delays in escalation of care for patients likely to deteriorate. Recommendation Based on the present findings, routine estimation of total leukocyte count, C-reactive protein, serum amylase, and serum cholinesterase should be considered in all patients presenting with organophosphorus poisoning. These tests are widely available, economical, and capable of providing valuable early information regarding severity and probable clinical course. Patients with markedly elevated TLC, CRP, and serum amylase, or substantially reduced serum cholinesterase, should be monitored more intensively for respiratory failure, neurological deterioration, and poor outcome. Clinical scoring systems such as the Peradeniya score should be used in conjunction with biochemical markers for more accurate bedside assessment. Hospitals managing poisoning cases should develop structured protocols that integrate these laboratory parameters into emergency triage and management pathways. Training of emergency and critical care teams regarding the prognostic significance of these markers may further enhance clinical use. Standardized early evaluation using combined clinical and biochemical assessment may improve risk stratification and guide timely therapeutic intervention. Limitations Despite its important findings, the present study has certain limitations. It was conducted in a single-center setting, which may limit the generalizability of the results to other populations, healthcare systems, or regions with different pesticide exposure patterns. The sample size, although adequate for primary analysis, may still be limited for more detailed subgroup comparisons, especially in severe poisoning and mortality categories. Serial measurements of inflammatory and enzymatic biomarkers were not presented, which restricts assessment of dynamic trends over time and their relationship with treatment response. The study mainly evaluated a selected group of biochemical markers and did not include broader inflammatory mediators, pancreatic imaging correlation, or additional organ dysfunction markers that could have provided deeper pathophysiological insight. Information regarding confounding factors such as coexisting infection, prior medical illness, or exact pre-hospital treatment may also influence some laboratory values. The observational design allows identification of associations but does not establish causality between biomarker changes and adverse outcomes.

The current study found that young individuals, especially those between the ages of 21 and 30, were most commonly impacted by organophosphorus chemical poisoning, with a notable male predominance. The main method of exposure was ingestion, with chlorpyrifos being the most frequently ingested substance. The majority of patients experienced mild poisoning, but a significant percentage experienced moderate and severe toxicity, which was linked to clinical symptoms that got worse over time, such as pinpoint pupils, respiratory distress with cyanosis, generalized fasciculations, altered sensorium, ventilator need, and death. The study unequivocally shown that whereas serum cholinesterase dramatically dropped with increasing poisoning severity, biochemical markers such total leukocyte count, C-reactive protein, and serum amylase significantly increased. Serum amylase increased from 36.70 U/L to 114.67 U/L, CRP climbed from 28.80 to 181.33, mean TLC increased from 10637.74 in moderate instances to 17130.56 in severe cases, and serum cholinesterase reduced from 3216.89 U/L in light poisoning to 1261.00 U/L in severe poisoning. Compared to patients who recovered, those who passed away had significantly lower cholinesterase levels and significantly higher CRP, serum amylase, and TLC values.

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