Background: Acute aluminium phosphide poisoning is a severe toxicological emergency associated with substantial mortality due to rapid systemic toxicity, cardiovascular dysfunction, metabolic abnormalities, and multiorgan involvement. Early identification of prognostic factors may facilitate risk stratification and timely intensive management.Aims and Objectives: The study aimed to evaluate prognostic factors of mortality in acute aluminium phosphide poisoning. The objectives were to correlate blood sugar levels, arterial pH, and serum bicarbonate levels with clinical outcome and to assess the correlation between electrocardiographic (ECG) changes and clinical outcome.Results: A total of 51 patients were included, with a mean age of 27.75 ± 5.053 years. Of these, 28 (54.9%) were non-survivors and 23 (45.1%) survived. Abnormal ECG findings were observed in 67.9% of non-survivors and 69.6% of survivors, with no significant association with outcome (p=0.896). Mean blood sugar levels were 157.49 ± 46.753 mg/dL among survivors and 134.61 ± 54.105 mg/dL among non-survivors (p=0.117). Mean arterial pH was 7.2165 ± 0.09374 and 7.2764 ± 0.11573, respectively (p=0.051). Mean serum bicarbonate was 11.74 ± 2.862 mEq/L among survivors and 14.29 ± 3.374 mEq/L among non-survivors, showing a statistically significant difference (p=0.008). Serum bicarbonate also demonstrated a significant correlation with clinical outcome (r=−0.381, p=0.006). Diastolic blood pressure differed significantly between survivors and non-survivors (p=0.007), whereas systolic blood pressure was not significantly different (p=0.518). GCS and ECG changes were not significantly associated with clinical outcome.Conclusion: Acute aluminium phosphide poisoning was associated with high mortality in the present study. Serum bicarbonate and diastolic blood pressure showed significant associations with clinical outcome, while serum bicarbonate also demonstrated a significant correlation with outcome. Blood sugar, arterial pH, systolic blood pressure, GCS, and ECG abnormalities did not show statistically significant associations with outcome. Assessment of acid–base and hemodynamic parameters may therefore contribute to prognostic evaluation in acute aluminium phosphide poisoning

The present study was conducted after obtaining approval from the Institutional Ethics Committee. Patients admitted with a history of acute aluminium phosphide poisoning and fulfilling the predefined inclusion and exclusion criteria were enrolled in the study. After enrollment, demographic details, clinical presentation, findings on clinical examination, relevant laboratory investigations, treatment modalities, and clinical outcomes were recorded using a standardized study proforma. All enrolled patients underwent evaluation of blood sugar, arterial blood gas analysis including arterial pH, serum bicarbonate levels, and electrocardiographic (ECG) changes. These parameters were assessed on Day 1 and Day 2 following poisoning and subsequently every three days until the final clinical outcome was determined. Patients were evaluated according to their demographic characteristics, clinical features, laboratory parameters, ECG findings, treatment details, and outcomes. The relationship of blood sugar levels, arterial pH, serum bicarbonate levels, and ECG changes with clinical outcome was assessed to identify potential prognostic factors associated with mortality. Data were entered into Microsoft Excel and analysed using IBM SPSS version 26.0. Categorical variables were summarized as frequencies and percentages, while continuous variables were expressed as mean and standard deviation or median and interquartile range, wherever appropriate. Normality was assessed using the Kolmogorov–Smirnov test. Associations between categorical variables and clinical outcome were evaluated using the Chi-square test. Continuous variables were compared using the unpaired t-test or Mann–Whitney U test for non-parametric data, as appropriate. A p-value <0.05 was considered statistically significant. Results were presented using tables, figures, and graphs wherever necessary.

Table 1. Baseline Demographic and Clinical Characteristics of the Study Participants Parameter Value Age (years), Mean ± SD 27.75 ± 5.053 Age range (years) 19–40 Male, n (%) 27 (52.9) Female, n (%) 24 (47.1) SBP (mmHg), Mean ± SD 89.09 ± 20.651 DBP (mmHg), Mean ± SD 62.35 ± 11.265 In the present study, the mean age of the study participants was 27.75 ± 5.053 years, with an age range of 19–40 years. Among the participants, 27 (52.9%) were males and 24 (47.1%) were females. The mean systolic blood pressure (SBP) was 89.09 ± 20.651 mmHg, while the mean diastolic blood pressure (DBP) was 62.35 ± 11.265 mmHg. Table 2. Laboratory Parameters Among Patients with Acute Aluminium Phosphide Poisoning Parameter Mean ± SD UOP (mL/day) 2457.88 ± 1300.835 Sodium (mEq/L) 141.43 ± 4.365 Potassium (mEq/L) 4.13 ± 0.702 Creatinine (mg/dL) 1.04 ± 0.346 PO₂ (mmHg) 93.54 ± 39.544 WBC 12.67 ± 5.336 Arterial pH 7.2494 ± 0.10957 HCO₃⁻ (mEq/L) 13.14 ± 3.377 HCT (%) 40.12 ± 6.485 Blood sugar (mg/dL) 144.93 ± 51.719 Hemoglobin (g/dL) 12.95 ± 2.221 BUN (mg/dL) 13.85 ± 4.026 In the present study, the mean UOP was 2457.88 ± 1300.835 mL/day, serum sodium was 141.43 ± 4.365 mEq/L, serum potassium was 4.13 ± 0.702 mEq/L, and serum creatinine was 1.04 ± 0.346 mg/dL. The mean PO₂ was 93.54 ± 39.544 mmHg, WBC was 12.67 ± 5.336, arterial pH was 7.2494 ± 0.10957, serum HCO₃⁻ was 13.14 ± 3.377 mEq/L, and HCT was 40.12 ± 6.485%. The mean blood sugar was 144.93 ± 51.719 mg/dL, hemoglobin was 12.95 ± 2.221 g/dL, and BUN was 13.85 ± 4.026 mg/dL. Table 3. Clinical Outcome of Patients with Acute Aluminium Phosphide Poisoning Clinical outcome Frequency Percentage (%) Non-survivors 28 54.9 Survivors 23 45.1 Total 51 100.0 In the present study, out of 51 patients with acute aluminium phosphide poisoning, 28 (54.9%) were non-survivors, while 23 (45.1%) were survivors. The total study population comprised 51 (100.0%) patients. Table 4. Association of ECG Changes with Clinical Outcome ECG finding Non-survivors, n (%) Survivors, n (%) Total, n (%) p-value Normal 9 (32.1) 7 (30.4) 16 (31.4) 0.896 Abnormal 19 (67.9) 16 (69.6) 35 (68.6) Total 28 (100.0) 23 (100.0) 51 (100.0) In the present study, among the 28 non-survivors, 9 (32.1%) had normal ECG findings and 19 (67.9%) had abnormal ECG findings, while among the 23 survivors, 7 (30.4%) had normal ECG findings and 16 (69.6%) had abnormal ECG findings. Overall, 16 (31.4%) patients had normal ECG findings and 35 (68.6%) had abnormal ECG findings among the total 51 (100.0%) patients. The association between ECG findings and clinical outcome was not statistically significant (p=0.896). Table 5. Association of GCS with Clinical Outcome GCS category Non-survivors, n (%) Survivors, n (%) Total, n (%) p-value Moderate (9–12) 6 (21.4) 3 (13.0) 9 (17.6) 0.434 Mild (12–15) 22 (78.6) 20 (87.0) 42 (82.4) Total 28 (100.0) 23 (100.0) 51 (100.0) In the present study, among the 28 non-survivors, 6 (21.4%) had moderate GCS scores of 9–12 and 22 (78.6%) had mild GCS scores of 12–15. Among the 23 survivors, 3 (13.0%) had moderate GCS scores and 20 (87.0%) had mild GCS scores. Overall, 9 (17.6%) patients had moderate GCS scores and 42 (82.4%) had mild GCS scores among the total 51 (100.0%) patients. The association between GCS category and clinical outcome was not statistically significant (p=0.434). Table 6. Comparison of Blood Sugar, Arterial Ph and Serum Bicarbonate According to Clinical Outcome Parameter Survivors, Mean ± SD Non-survivors, Mean ± SD p-value Blood sugar (mg/dL) 157.49 ± 46.753 134.61 ± 54.105 0.117 Arterial pH 7.2165 ± 0.09374 7.2764 ± 0.11573 0.051 HCO₃⁻ (mEq/L) 11.74 ± 2.862 14.29 ± 3.374 0.008 In the present study, the mean blood sugar level was 157.49 ± 46.753 mg/dL among survivors and 134.61 ± 54.105 mg/dL among non-survivors, with no statistically significant difference (p=0.117). The mean arterial pH was 7.2165 ± 0.09374 among survivors and 7.2764 ± 0.11573 among non-survivors, with no statistically significant difference (p=0.051). The mean serum HCO₃⁻ level was 11.74 ± 2.862 mEq/L among survivors and 14.29 ± 3.374 mEq/L among non-survivors, with a statistically significant difference (p=0.008). Table 7. Comparison of Blood Pressure According to Clinical Outcome Parameter Survivors, Mean ± SD Non-survivors, Mean ± SD p-value SBP (mmHg) 91.18 ± 21.992 87.37 ± 19.720 0.518 DBP (mmHg) 59.20 ± 11.709 64.94 ± 10.387 0.007 In the present study, the mean systolic blood pressure (SBP) was 91.18 ± 21.992 mmHg among survivors and 87.37 ± 19.720 mmHg among non-survivors, with no statistically significant difference (p=0.518). The mean diastolic blood pressure (DBP) was 59.20 ± 11.709 mmHg among survivors and 64.94 ± 10.387 mmHg among non-survivors, with a statistically significant difference (p=0.007). Table 8. Correlation Of Blood Sugar, Arterial Ph and Serum Bicarbonate with Clinical Outcome Parameter N Pearson correlation coefficient (r) p-value Blood sugar 51 0.222 0.117 Arterial pH 51 −0.275 0.051 HCO₃⁻ 51 −0.381 0.006 In the present study, blood sugar among 51 patients showed a Pearson correlation coefficient of r=0.222 with clinical outcome, with no statistically significant correlation (p=0.117). Arterial pH among 51 patients showed a correlation coefficient of r=−0.275, which was not statistically significant (p=0.051). Serum HCO₃⁻ among 51 patients showed a correlation coefficient of r=−0.381 with clinical outcome, which was statistically significant (p=0.006).

The present study evaluated prognostic factors associated with mortality in acute aluminium phosphide poisoning, with particular emphasis on blood glucose, arterial pH, serum bicarbonate, blood pressure, Glasgow Coma Scale (GCS), and electrocardiographic changes. Among 51 patients, 28 (54.9%) were non-survivors and 23 (45.1%) survived, demonstrating the substantial mortality associated with aluminium phosphide poisoning. This is consistent with the clinical severity described by Gurjar et al. (2011), who highlighted rapid cardiovascular collapse, severe metabolic disturbances, and multiorgan dysfunction as major challenges in aluminium phosphide poisoning (3). More recently, Karakaya and Yavuz (2025) also emphasized the high toxicity of phosphine and the importance of early recognition and intensive supportive management (1). The mean arterial pH in the present study was 7.2494 ± 0.10957, while the mean serum bicarbonate level was 13.14 ± 3.377 mEq/L. When compared according to clinical outcome, arterial pH was 7.2165 ± 0.09374 among survivors and 7.2764 ± 0.11573 among non-survivors (p=0.051). Serum bicarbonate was 11.74 ± 2.862 mEq/L among survivors and 14.29 ± 3.374 mEq/L among non-survivors, with a statistically significant difference (p=0.008). Furthermore, serum bicarbonate demonstrated a significant correlation with clinical outcome (r=−0.381, p=0.006). Mathai and Bhanu (2010) similarly investigated predictors of mortality in acute aluminium phosphide poisoning and demonstrated the prognostic importance of physiological and biochemical disturbances (13). The relevance of acid–base abnormalities in critically ill patients has also been emphasized by Achanti and Szerlip (2023). Phosphine-induced mitochondrial dysfunction described by Sciuto et al. (2016) provides a biological basis for the profound metabolic abnormalities encountered in severe poisoning (4,6). Blood glucose was another predefined prognostic parameter. Mean blood glucose was 157.49 ± 46.753 mg/dL among survivors compared with 134.61 ± 54.105 mg/dL among non-survivors; however, the difference was not statistically significant (p=0.117). Similarly, its correlation with clinical outcome was not significant (r=0.222, p=0.117). Sharma et al. (2018) specifically evaluated blood glucose alterations in aluminium phosphide poisoning and reported their potential prognostic significance (9). The present findings, however, did not demonstrate a statistically significant relationship between blood glucose and outcome, suggesting that its prognostic value was limited in this study population. Cardiovascular involvement is a prominent manifestation of aluminium phosphide toxicity. In the present study, abnormal ECG findings were observed in 19 (67.9%) non-survivors and 16 (69.6%) survivors. However, ECG abnormalities were not significantly associated with clinical outcome (p=0.896). In comparison, Hadi et al. (2025) evaluated electrocardiographic patterns as predictors of mortality in aluminium phosphide poisoning, supporting the clinical relevance of ECG monitoring (11). The cardiac toxicity associated with severe poisoning has also been discussed by Purkayastha et al. (2006). Nevertheless, the present findings indicate that the presence of an abnormal ECG alone did not differentiate survivors from non-survivors (5). Regarding hemodynamic parameters, mean SBP did not differ significantly between survivors and non-survivors (91.18 ± 21.992 versus 87.37 ± 19.720 mmHg; p=0.518), whereas DBP showed a statistically significant difference (59.20 ± 11.709 versus 64.94 ± 10.387 mmHg; p=0.007). Anbalagan et al. (2023) similarly emphasized that multiple poisoning-related and clinical factors should be considered when assessing prognosis rather than relying on a single parameter (7). Overall, the present study demonstrates that among the investigated parameters, serum bicarbonate and DBP showed statistically significant associations with clinical outcome, while blood glucose, arterial pH, ECG abnormalities, SBP, and GCS did not reach statistical significance. These findings support the importance of combined clinical, biochemical, and cardiovascular assessment for prognostic evaluation in acute aluminium phosphide poisoning.

The present study highlights the high mortality associated with acute aluminium phosphide poisoning, with 54.9% of patients being non-survivors. Evaluation of clinical, biochemical, and cardiovascular parameters demonstrated that serum bicarbonate and diastolic blood pressure were significantly associated with clinical outcome. Serum bicarbonate also showed a statistically significant correlation with outcome, suggesting its potential value in prognostic assessment. Although arterial pH approached statistical significance, blood glucose levels did not demonstrate a significant association with outcome. Similarly, systolic blood pressure, GCS category, and ECG abnormalities were not significantly associated with mortality in the present study. These findings indicate that readily available clinical and biochemical parameters may contribute to early assessment of patients with acute aluminium phosphide poisoning. Careful monitoring of acid–base status and hemodynamic parameters may assist in identifying patients requiring intensive management. Further studies with larger sample sizes are required to establish reliable and independent predictors of mortality in acute aluminium phosphide poisoning

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