Acute organophosphate (OP) poisoning remains an important cause of preventable morbidity and mortality, particularly in low- and middle-income countries where agricultural pesticides are widely available and access to highly hazardous compounds is often insufficiently regulated. Organophosphates are extensively used for crop protection because of their effectiveness and relatively low cost; however, the same accessibility that supports agricultural productivity also creates an important public health concern when these compounds are involved in accidental exposure or intentional self-poisoning. Pesticide poisoning contributes substantially to poisoning-related hospital admissions in many agricultural communities, and intentional ingestion of pesticides continues to account for a considerable proportion of self-harm deaths worldwide. Consequently, the World Health Organization and the Food and Agriculture Organization have emphasized restriction of highly hazardous pesticides as an important component of suicide prevention and pesticide-risk reduction strategies (1).

The problem is particularly relevant to Pakistan, where agriculture remains a major economic activity and organophosphate insecticides are readily accessible in both rural and peri-urban settings. Available national and regional evidence suggests that pesticide ingestion, including exposure to OP compounds, constitutes an important proportion of intentional poisoning presentations to emergency departments. Studies evaluating self-harm and poisoning patterns have also highlighted limitations in compound-specific surveillance, inconsistent reporting systems, and continued community access to potentially lethal pesticides (2,3). These factors complicate efforts to estimate the true burden of OP poisoning and to develop targeted preventive interventions. Recent observations from Jinnah Postgraduate Medical Centre (JPMC), Karachi, further indicate that organophosphates remain among the prominent agents used for self-poisoning, particularly among adolescents and young adults, demonstrating that acute OP toxicity continues to be a clinically and socially relevant problem in the local population (4,5).

The clinical effects of OP poisoning primarily result from inhibition of acetylcholinesterase, followed by excessive accumulation of acetylcholine at muscarinic, nicotinic, and central nervous system synapses. Patients may therefore present with a characteristic acute cholinergic syndrome that includes excessive secretions, gastrointestinal symptoms, pupillary constriction, bradycardia, altered consciousness, muscle fasciculations, weakness, seizures, and respiratory compromise. Although prompt administration of atropine, appropriate use of oximes, airway protection, and supportive critical care can substantially improve survival, the clinical course remains difficult to predict at initial presentation. Some patients recover after successful treatment of the acute cholinergic crisis, whereas others experience persistent or delayed neuromuscular dysfunction, respiratory failure, prolonged mechanical ventilation, infectious complications, or death. This variability makes early recognition of patients at increased risk of deterioration an important component of emergency and critical care management (6-8).

One of the most clinically important delayed complications is intermediate syndrome (IMS), which typically develops after the acute cholinergic manifestations have begun to resolve and before the expected onset of delayed organophosphate-induced neuropathy. It generally occurs within approximately 24 to 96 hours after exposure and is characterized by weakness involving the neck flexors, proximal limb muscles, respiratory muscles, and selected cranial nerve-innervated muscles (9-11). Respiratory muscle weakness is particularly important because affected patients may deteriorate rapidly and require endotracheal intubation and mechanical ventilation. In settings with limited intensive care resources, failure to anticipate this complication may contribute to preventable adverse outcomes. IMS therefore represents more than a neurological manifestation of poisoning; it is a clinically significant complication that may influence intensive care requirements, duration of hospitalization, resource utilization, and survival.

Reported frequencies of IMS vary considerably across studies because of differences in pesticide compounds, ingested dose, severity of poisoning, definitions used for the syndrome, timing of clinical assessment, referral patterns, and availability of intensive care. Contemporary literature suggests that IMS occurs in approximately 15% of patients in some populations, although substantially higher and lower frequencies have been reported (6-9,12-16). Mortality among patients who develop IMS is similarly variable and is strongly influenced by the severity of respiratory muscle involvement, delays in ventilatory support, associated complications, and the overall quality of critical care. Such variation emphasizes the importance of locally generated clinical data rather than assuming that estimates obtained from other countries or healthcare systems can be directly applied to patients treated in Pakistan.

Prediction of mortality in OP poisoning is another major clinical challenge. Decisions regarding intensive monitoring, early airway management, transfer to critical care, and allocation of limited resources often need to be made soon after hospital presentation. Several clinical and biochemical indicators have therefore been investigated as potential markers of severe poisoning and poor outcome. These include level of consciousness, Glasgow Coma Scale (GCS) score, respiratory failure, hemodynamic instability, delayed presentation, serum cholinesterase activity, metabolic abnormalities, requirement for mechanical ventilation, and various bedside severity scores. More recent studies have also explored combinations of clinical parameters, laboratory biomarkers, and multivariable prediction models to improve early risk stratification (17). Despite these developments, complex prognostic tools may not always be practical in busy emergency departments or resource-constrained hospitals. Easily identifiable clinical variables that are routinely available during initial assessment may therefore have greater value for day-to-day decision-making.

Important knowledge gaps nevertheless remain in the Pakistani setting. Published local literature has largely focused on the general epidemiology, management, or outcomes of pesticide poisoning, while fewer studies have simultaneously characterized the clinical profile of acute OP poisoning, quantified the occurrence of IMS, and examined clinical factors associated with in-hospital mortality. Differences in referral delays, pesticide availability, patterns of intentional exposure, pre-hospital treatment, critical care capacity, and patient characteristics may substantially influence both IMS and survival. Establishing locally relevant estimates is therefore necessary not only for epidemiological purposes but also for improving clinical vigilance, identifying high-risk patients early, anticipating ventilatory requirements, and guiding the appropriate use of emergency and intensive care resources (18,19).

Against this background, the present study was designed to determine the clinical profile of patients presenting with acute organophosphate poisoning, estimate the incidence of intermediate syndrome, and identify clinical factors associated with in-hospital mortality. The principal research question was whether routinely identifiable characteristics at presentation and during hospitalization could distinguish patients at increased risk of death. It was hypothesized that a lower GCS score, delayed presentation to hospital, requirement for critical care support, and development of intermediate syndrome would be associated with a greater likelihood of in-hospital mortality. By examining these clinically accessible predictors within a local tertiary-care population, the study aimed to generate evidence that could support earlier risk stratification, closer monitoring, timely escalation of care, and improved management of patients with acute organophosphate poisoning.

A prospective observational cohort study was conducted in the Department of Accident and Emergency, Jinnah Postgraduate Medical Centre (JPMC), Karachi, from March to May 2026. Patients were enrolled at presentation and subsequently followed through the medical wards or medical intensive care unit, as clinically indicated, until completion of the index hospital admission, defined as either discharge alive or in-hospital death. The study was designed to describe the clinical profile of acute organophosphate poisoning, determine the incidence of intermediate syndrome (IMS), and evaluate clinical factors associated with in-hospital mortality. The required sample size was calculated using an anticipated IMS frequency of 12.8%, a 95% confidence level, and a 5% margin of error. On this basis, a minimum sample of 172 patients was included. Non-probability consecutive sampling was employed, whereby all eligible patients presenting during the study period were screened for participation. Recruitment and consent procedures were undertaken after initial clinical stabilization so that emergency treatment was not delayed. All 172 enrolled patients had complete information regarding the primary outcomes and were therefore included in the final analysis. Patients of either sex aged 14 years or older were eligible if they presented within 24 hours of a documented organophosphate exposure, demonstrated at least two clinical manifestations consistent with cholinergic toxicity, required hospital admission, and provided written informed consent either personally or through a legal guardian where appropriate. Patients were excluded if poisoning involved more than one toxic substance, exposure was attributable exclusively to a carbamate compound, pregnancy was present, or there was a pre-existing neuromuscular disorder likely to interfere with assessment of muscle weakness. Patients with chronic respiratory failure requiring home ventilatory support were also excluded because baseline respiratory impairment could confound evaluation of poisoning-related respiratory failure. In addition, patients whose subsequent transfer to another hospital prevented ascertainment of the final in-hospital outcome, those who declined consent, and moribund patients who died within one hour of presentation despite resuscitative measures were excluded. Data were collected prospectively using a structured study proforma. Baseline variables included age, sex, sociodemographic characteristics, intent of exposure, location and route of exposure, estimated quantity of the organophosphate involved, pre-hospital interventions, and time elapsed between exposure and hospital presentation. Clinical assessment at admission included vital signs, pupillary size, manifestations of muscarinic and nicotinic cholinergic toxicity, level of consciousness assessed using the Glasgow Coma Scale (GCS), and serum acetylcholinesterase levels when clinically available. Severity of poisoning was additionally assessed using the Peradeniya Organophosphorus Poisoning (POP) scale. The six-item POP score ranged from 0 to 11 and was categorized as mild for scores of 0–3, moderate for scores of 4–7, and severe for scores of 8–11. Treatment-related variables were recorded throughout hospitalization and included atropine administration, time required to achieve atropinisation, use of pralidoxime, gastric decontamination, admission to the intensive care unit, and requirement for invasive mechanical ventilation. Following resolution of the initial cholinergic crisis, patients were clinically assessed on a daily basis during the period from 24 to 96 hours after admission for features suggestive of IMS. The assessment included weakness of the neck flexors, proximal limb or shoulder-girdle weakness corresponding to a Medical Research Council muscle power grade of 3/5 or less, cranial nerve weakness, and evidence of respiratory muscle weakness. For the purposes of the study, IMS was diagnosed when at least two of these four clinical features developed after improvement of the acute cholinergic phase. Patients continued to be followed until discharge or death, allowing both the development of IMS and in-hospital mortality to be recorded prospectively. Data were entered and analyzed using IBM SPSS Statistics version 26. Continuous variables were summarized as mean ± standard deviation when approximately normally distributed and as median with interquartile range when distributions were skewed. Categorical variables were expressed as frequencies and percentages. The incidence of IMS and the proportion of in-hospital mortality were reported with 95% Wilson confidence intervals. Comparisons between survivors and non-survivors were performed using the independent-samples t-test for normally distributed continuous variables and the Mann–Whitney U test for non-normally distributed variables. Categorical variables were compared using the Pearson chi-square test, with Fisher's exact test used where expected cell frequencies were insufficient for reliable chi-square testing. Binary logistic regression was used to identify independent predictors of in-hospital mortality. The prespecified model included age, admission GCS score, POP score, time from exposure to hospital presentation, requirement for mechanical ventilation, and development of IMS. Associations were reported as adjusted odds ratios with corresponding 95% confidence intervals. Overall model significance was assessed using the omnibus likelihood-ratio test, explanatory performance using Nagelkerke R², and calibration using the Hosmer–Lemeshow goodness-of-fit test. Overall classification accuracy was also reported. All statistical tests were two-sided, and a p-value of ≤0.05 was considered statistically significant. The study was conducted after approval from the Institutional Review Board of Jinnah Postgraduate Medical Centre, Karachi. Written informed consent was obtained from eligible participants or their legal guardians before enrollment. Participation did not alter or delay standard emergency, medical, or critical care management, and all therapeutic decisions remained under the responsibility of the treating clinical team. Patient confidentiality was maintained throughout data collection and analysis, and identifying information was excluded from the analytical dataset.

A total of 172 patients with acute organophosphate poisoning were included in the analysis, and complete outcome data for both intermediate syndrome (IMS) and in-hospital survival were available for all participants. The mean age was 29.6 ± 10.5 years, and 99 (57.6%) patients were male. Urban residents accounted for 115 (66.9%) patients, while 99 (57.6%) were unmarried. Deliberate self-harm was the predominant exposure intent, occurring in 145 (84.3%) patients, whereas 20 (11.6%) had accidental exposure and 7 (4.1%) had occupational exposure. Ingestion was the principal route of exposure in 160 (93.0%) cases. Chlorpyrifos was the most frequently identified organophosphate compound, accounting for 54 (31.4%) cases, followed by diazinon in 31 (18.0%), malathion in 27 (15.7%), and dichlorvos in 20 (11.6%). The specific organophosphate compound remained unidentified in 40 (23.3%) patients. Median time from exposure to hospital presentation was 3.0 hours (IQR 1.9–4.9).

At initial clinical assessment, the median Glasgow Coma Scale (GCS) score was 13 (IQR 10–15), while the median Peradeniya Organophosphate Poisoning (POP) score was 5 (IQR 3–7). Based on POP grading, 52 (30.2%) patients had mild poisoning, 83 (48.3%) had moderate poisoning, and 37 (21.5%) had severe poisoning. Pinpoint pupils were documented in 130 (75.6%) patients. Among patients with an available biochemical assay, the median serum acetylcholinesterase level was 3278.5 U/L (IQR 2432.5–4274.0). Pralidoxime was administered to 131 (76.2%) patients. Sixty-five (37.8%) patients required admission to the intensive care unit, and 38 (22.1%) underwent mechanical ventilation.

Intermediate syndrome developed in 26 of 172 patients, corresponding to an incidence of 15.1% (95% CI 10.5–21.2). The median reported time to onset of IMS was 4 days after admission. Individual neuromuscular manifestations included neck-flexor weakness in 38 (22.1%) patients, proximal-limb weakness in 36 (20.9%), cranial nerve weakness in 21 (12.2%), and respiratory muscle weakness in 10 (5.8%). During hospitalization, aspiration pneumonia occurred in 56 (32.6%) patients, shock in 27 (15.7%), cardiac arrhythmia in 22 (12.8%), and acute kidney injury in 19 (11.0%). The median duration of hospitalization was 5 days (IQR 3–7).

Eighteen patients died during hospitalization, yielding an in-hospital mortality of 10.5% (95% CI 6.7–15.9), while 154 (89.5%) survived to discharge. Respiratory failure accounted for 11 of the 18 deaths (61.1%), followed by cardiac arrhythmia in 3 (16.7%), shock in 2 (11.1%), and aspiration-related complications in 2 (11.1%). Compared with survivors, non-survivors had a lower median GCS score [9.5 (IQR 8–10) vs 13 (IQR 11–15); p<0.001], higher median POP score [9.5 (IQR 8–11) vs 5 (IQR 2.3–6.8); p<0.001], lower mean oxygen saturation (83.7 ± 4.1% vs 90.0 ± 4.6%; p<0.001), and higher median respiratory rate [28.5/min (IQR 25.3–31.8) vs 23/min (IQR 19–27); p<0.001]. Serum acetylcholinesterase levels were also lower among non-survivors [1563 U/L (IQR 1166–2318) vs 3349 U/L (IQR 2747–4429); p<0.001]. Age (p=0.763) and time to presentation (p=0.560) did not differ significantly between the two groups.

Mortality occurred in 11 of 38 mechanically ventilated patients (28.9%) compared with 7 of 134 non-ventilated patients (5.2%), corresponding to an unadjusted odd ratio (OR) of 7.39 (95% CI 2.63–20.80). Among patients who developed IMS, 8 of 26 (30.8%) died compared with 10 of 146 (6.8%) without IMS (OR 6.04; 95% CI 2.11–17.30). Mortality was also higher among patients with aspiration pneumonia (25.0% vs 3.4%; OR 9.33; 95% CI 2.91–29.96) and shock (37.0% vs 5.5%; OR 10.07; 95% CI 3.50–29.00). ICU admission was more frequent among non-survivors than survivors (61.1% vs 35.1%; p=0.031).

The six-variable binary logistic regression model was statistically significant overall (likelihood-ratio χ²=44.31, p<0.001), with a Nagelkerke R² of 0.465 and a Hosmer–Lemeshow χ² of 2.08 (p=0.978). Overall classification accuracy was 91.9%, with a specificity of 97.4% and sensitivity of 44.4%. After simultaneous adjustment, none of the prespecified individual predictors reached statistical significance: age (aOR 0.968; 95% CI 0.912–1.027; p=0.282), GCS score (aOR 0.724; 95% CI 0.428–1.224; p=0.228), POP score (aOR 1.516; 95% CI 0.936–2.457; p=0.091), time to presentation (aOR 1.011; 95% CI 0.870–1.174; p=0.890), mechanical ventilation (aOR 2.419; 95% CI 0.648–9.026; p=0.189), and IMS (aOR 1.338; 95% CI 0.344–5.209; p=0.675).

Table 1: Demographic and exposure profile of patients with acute organophosphate poisoning (n=172)

Values are n (%), mean ± SD, or median (IQR). OP: organophosphate.

Table 2: Clinical severity, treatment, intermediate syndrome and outcomes (n=172)

Values are n (%) or median (IQR). GCS: Glasgow Coma Scale; ICU: intensive care unit; POP: Peradeniya Organophosphate Poisoning.

Table 3: Univariable comparison of survivors and non-survivors

Values are n (%), mean ± SD, or median (IQR). P-values derive from independent t, Mann-Whitney U, chi-square or Fisher exact tests as appropriate.

Table 4: Multivariable logistic regression for in-hospital mortality

Dependent outcome: in-hospital death. CI: confidence interval; GCS: Glasgow Coma Scale; OR: odds ratio; POP: Peradeniya Organophosphate Poisoning.

This prospective cohort study identified several clinically relevant features of acute organophosphate poisoning. The affected population was predominantly young, male, and exposed through intentional oral ingestion. Intermediate syndrome (IMS) developed in 15.1% of patients, while in-hospital mortality occurred in 10.5%. Non-survivors had lower Glasgow Coma Scale (GCS) scores, lower oxygen saturation and acetylcholinesterase levels, together with higher Peradeniya Organophosphate Poisoning (POP) scores and respiratory rates. Mechanical ventilation, IMS, aspiration pneumonia, shock, and intensive care admission were also more frequent among patients who died. Although these variables demonstrated important unadjusted associations with mortality, none retained independent statistical significance after simultaneous adjustment in the multivariable model. The demographic profile was broadly consistent with contemporary evidence from South Asia, where acute organophosphate poisoning continued to affect younger age groups disproportionately and was frequently associated with deliberate self-harm. A recent study from Sindh reported that 57.2% of affected patients were male, 82% were aged 30 years or younger, and 92.2% had intentional exposure (6). The proportion of deliberate self-harm in the present cohort, 84.3%, was similarly consistent with Pakistani literature describing pesticides as a major means of intentional self-poisoning (2,3). Previous hospital-based data from Jinnah Postgraduate Medical Centre had also identified pesticides among the most important toxic agents, while more recent local evidence demonstrated a substantial contribution of organophosphate compounds to poisoning among younger patients (4,5). Collectively, these findings indicated that organophosphate poisoning remained not only a toxicological problem but also an important manifestation of self-harm behavior, particularly among younger individuals with ready access to agricultural chemicals. The incidence of IMS in the present study was 15.1%, which closely approximated the 15.5% reported in an earlier Taiwanese cohort and remained within the range described in other clinical studies (10,12). This finding reinforced the importance of continued neuromuscular surveillance after apparent improvement of the initial cholinergic crisis. Weakness of the neck flexors, proximal limb muscles, cranial nerves, and respiratory musculature could emerge after muscarinic manifestations had begun to resolve, creating a period in which clinical improvement might otherwise have been overestimated. Earlier reports had demonstrated that IMS, particularly when respiratory muscles were involved, was associated with prolonged mechanical ventilation, aspiration, secondary infection, and greater use of intensive care resources (10,11,13). In the present study, mortality among patients with IMS reached 30.8%, compared with 6.8% among those without IMS, producing a strong unadjusted association with death. Although this association was attenuated after adjustment, the finding remained clinically important because IMS appeared to occur within the same pathway of severe neuromuscular toxicity that also contributed to ventilatory failure and critical illness. The observed in-hospital mortality of 10.5% was higher than the pooled estimate of approximately 3.7% reported in a recent systematic review, but remained comparable with mortality reported in several single-center cohorts from resource-limited settings (9,15). A prospective study from Sindh reported mortality of 5.5%, whereas other studies from lower-income regions demonstrated considerable variation according to poisoning severity, delays in presentation, availability of ventilatory support, and characteristics of the ingested compound (6,15). Such differences likely reflected heterogeneity in referral pathways, dose and type of pesticide, pre-hospital management, availability of oximes, intensive care capacity, and thresholds for mechanical ventilation. Respiratory failure accounted for 61.1% of deaths in the present cohort, which was consistent with the recognized pathophysiology of severe organophosphate toxicity. Excessive bronchial secretions, aspiration, pulmonary edema, central respiratory depression, neuromuscular weakness, and cardiovascular dysfunction could act together to produce progressive respiratory compromise and death (10,20). Several bedside indicators clearly differentiated survivors from non-survivors. Lower GCS, higher POP score, hypoxemia, increased respiratory rate, and markedly reduced acetylcholinesterase levels were all associated with mortality in univariable analysis. These findings were consistent with previous studies that had examined level of consciousness, clinical severity scores, SOFA or MODS scores, serum lactate, and cholinesterase activity as prognostic indicators in acute organophosphate poisoning (14,16-21). More recent prediction studies had increasingly favored models combining multiple clinical and biochemical variables rather than relying on a single marker. Nomograms incorporating bedside and laboratory parameters had demonstrated encouraging discriminatory performance in recent studies, although such models still required external validation before routine clinical use (21-23). The present findings supported the continued value of simple bedside assessment, particularly GCS, POP score, oxygenation, and respiratory status, because these variables were rapidly available and directly relevant to early escalation of care. The loss of statistical significance in the adjusted model required cautious interpretation. Mechanical ventilation and IMS had substantial unadjusted odds ratios, yet their adjusted estimates became smaller and imprecise. This did not establish absence of clinical importance. Only 18 deaths occurred, while six predictors were entered simultaneously into the regression model, resulting in a relatively low number of outcome events per variable and an increased risk of unstable coefficients, wide confidence intervals, and model overfitting. In addition, GCS, POP score, mechanical ventilation, and IMS reflected overlapping dimensions of poisoning severity and might have introduced collinearity or shared causal pathways. Mechanical ventilation and IMS also developed during hospitalization and were therefore more appropriately interpreted as markers or mediators of disease progression rather than purely baseline predictors. Future multicenter studies with larger numbers of deaths, fewer prespecified predictors, assessment of collinearity, and penalized regression methods would provide more reliable estimates. The findings nevertheless had practical implications. Patients presenting with severe POP grades, depressed consciousness, oxygen desaturation, increasing respiratory effort, or evolving neuromuscular weakness required closer observation and timely critical care assessment. Continued monitoring for IMS for at least 96 hours after the acute cholinergic phase was clinically justified, particularly in patients with severe poisoning. At a public health level, the predominance of intentional exposure supported previously advocated measures aimed at restricting access to highly hazardous pesticides, strengthening safe-storage practices, improving compound-specific surveillance, and integrating mental health assessment and suicide-prevention services into poisoning care pathways (1-3, 24). The study had several strengths, including its prospective design, consecutive recruitment, standardized assessment of poisoning severity, systematic surveillance for IMS, and complete ascertainment of both IMS and survival outcomes in all 172 participants. However, important limitations remained. The study was conducted at a single tertiary referral center and used non-probability sampling, which might have increased representation of more severe cases and limited generalizability. Exposure was not analytically confirmed in every patient, and the responsible compound remained unknown in 23.3%. Acetylcholinesterase testing was not uniformly documented in all participants and could have been influenced by timing and laboratory variability. The relatively small number of deaths limited the stability of multivariable estimates, while some variables included in the model represented post-admission events rather than true baseline predictors. Larger multicenter prospective cohorts with standardized toxicological confirmation, uniform biomarker measurement, detailed dose information, and externally validated prediction models were therefore warranted.

Acute organophosphate poisoning predominantly affected young individuals and was frequently related to intentional exposure, with intermediate syndrome representing an important delayed complication and in-hospital mortality remaining clinically relevant. Severe poisoning, impaired consciousness, hypoxemia, respiratory compromise, mechanical ventilation, and intermediate syndrome identified patients with a higher risk of adverse outcomes, although no single factor independently predicted mortality after multivariable adjustment. These findings support early severity assessment, close respiratory monitoring, continued surveillance for intermediate syndrome after resolution of the initial cholinergic crisis, and timely escalation to critical care in patients showing signs of clinical deterioration.

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