European Journal of Cardiovascular Medicine

Aluminium phosphide (ALP) poisoning is a major public health concern, particularly in developing countries such as India where it is widely used as an agricultural fumigant for the preservation of stored grains. Due to its easy availability, low cost, and high toxicity, aluminium phosphide has become one of the most common agents involved in suicidal poisoning. Following ingestion, aluminium phosphide reacts with water and gastric acid to release phosphine gas, a highly toxic compound that interferes with cellular respiration by inhibiting mitochondrial oxidative phosphorylation. This leads to severe metabolic disturbances, multiorgan dysfunction, and high mortality rates.¹

One of the most critical complications of aluminium phosphide poisoning is its profound effect on the cardiovascular system. Phosphine toxicity leads to myocardial depression, circulatory collapse, refractory hypotension, and life-threatening arrhythmias.² Cardiovascular manifestations such as ventricular tachycardia, ventricular fibrillation, and severe left ventricular dysfunction are frequently reported and are considered major contributors to mortality. In addition to direct myocardial toxicity, metabolic acidosis, electrolyte imbalance, and systemic hypoperfusion further aggravate cardiovascular compromise.³

Despite advances in supportive care, aluminium phosphide poisoning continues to have a very high case fatality rate because there is no specific antidote available. Management primarily focuses on early recognition, aggressive supportive therapy, hemodynamic stabilization, and treatment of complications.⁴ In recent years, advanced supportive modalities such as extracorporeal membrane oxygenation (ECMO) have been used in selected cases with severe cardiogenic shock and refractory circulatory failure. Early identification of cardiovascular involvement and timely intervention may play an important role in improving patient outcomes.⁵

Several studies have evaluated the clinical and biochemical parameters associated with aluminium phosphide poisoning; however, detailed evaluation of cardiovascular manifestations and their prognostic significance remains limited. Understanding the cardiovascular profile of patients with aluminium phosphide poisoning may help clinicians identify high-risk patients early and guide appropriate management strategies.⁶

Therefore, the present study was undertaken to evaluate the cardiovascular profile of patients with aluminium phosphide poisoning. The study also aimed to assess the clinical outcomes and determine the association of cardiovascular, metabolic, and laboratory parameters with patient survival. Such insights may contribute to improved management and better prognostication in this potentially fatal poisoning.

Study Design and Setting This was a prospective observational study conducted in the Department of Medicine and Intensive Care Unit at Geetanjali Medical College and Hospital (GMCH), Udaipur (Raj). The study was carried out over a period of six months. Study Population All patients presenting with confirmed or suspected aluminium phosphide poisoning during the study period were included. Patients were admitted through the emergency department and managed in the intensive care unit according to institutional protocols. Inclusion Criteria • Patients aged ≥14 years. • Patients with history of aluminium phosphide ingestion or exposure confirmed clinically or by history from relatives. • Patients admitted to GMCH during the study period. Exclusion Criteria • Patients with mixed or unknown poisoning. • Patients with pre-existing severe cardiac disease or chronic liver disease. • Patients with incomplete clinical or laboratory data. Data Collection After obtaining detailed history and performing clinical examination, relevant demographic, clinical, and laboratory data were recorded in a structured proforma. Cardiovascular Evaluation All patients underwent electrocardiographic (ECG) monitoring to detect rhythm abnormalities and myocardial involvement. Echocardiography was performed to assess left ventricular ejection fraction (LVEF) at admission and during recovery. Outcome Measures The primary outcome of the study was in-hospital mortality. Secondary outcomes included cardiovascular complications, arrhythmias, changes in metabolic and laboratory parameters, and duration of hospital stay. Statistical Analysis Data were entered into Microsoft Excel and analyzed using statistical software. Continuous variables were expressed as mean ± standard deviation, while categorical variables were presented as frequency and percentage. Comparisons between survivors and non-survivors were performed using the Student’s t-test for continuous variables and Chi-square test for categorical variables. A p-value <0.05 was considered statistically significant. Ethical Considerations The study was conducted after obtaining approval from the Institutional Ethics Committee of Government Medical College and Hospital (GMCH). Patient confidentiality was maintained throughout the study.

A total of 50 patients with aluminium phosphide poisoning were included in the study. The mean age of the patients was 33.39 ± 11.72 years. Among them, 28 (57.1%) were males and 21 (42.9%) were females, indicating a slight predominance of male patients in the study population. The clinical outcomes of the study population are presented in Table 1. The majority of patients survived the poisoning episode, while a substantial proportion succumbed during hospitalization.

Hemodynamic parameters at admission are summarized in Table 2. Patients commonly presented with features of circulatory compromise, characterized by hypotension and tachycardia.

Assessment of cardiac function is shown in Table 3. A markedly reduced left ventricular ejection fraction (LVEF) was observed at admission, indicating significant myocardial depression. However, a statistically significant improvement in LVEF was noted at discharge, suggesting recovery of cardiac function following treatment.

The types of arrhythmias observed in the study population are presented in Table 4. Ventricular arrhythmias were the most frequently encountered rhythm abnormalities, with ventricular tachycardia or ventricular fibrillation being the predominant findings.

Comparison of cardiovascular and metabolic parameters between survivors and non-survivors is presented in Table 5. No statistically significant difference was observed in baseline LVEF, pH, or lactate levels between the two groups.

Arterial blood gas (ABG) parameters comparing survivors and non-survivors are shown in Table 6. Significant differences were observed in pH, PaCO₂, PaO₂, and lactate levels, indicating that disturbances in acid–base balance and tissue perfusion were associated with poorer outcomes.

Changes in laboratory and metabolic parameters between admission and discharge or death are summarized in Table 7. Significant alterations were noted in lactate levels and hemoglobin during the course of hospitalization. Additionally, liver function parameters, including bilirubin and transaminases, showed significant elevation, reflecting hepatic injury associated with aluminium phosphide toxicity. Electrolyte abnormalities, particularly sodium and potassium levels, also demonstrated significant differences.

Further comparison of laboratory parameters between survivors and non-survivors is shown in Table 8. Non-survivors had significantly lower bicarbonate levels and higher lactate levels at admission, indicating more severe metabolic acidosis. Elevated leukocyte counts and liver enzyme levels were also observed among non-survivors, suggesting greater systemic toxicity and organ damage.

Time-related clinical characteristics of the patients are summarized in Table 9. Most patients presented to the hospital within a short duration after ingestion. The duration of hospitalization varied considerably among patients, reflecting differences in disease severity. Similarly, the duration of ECMO support and mechanical ventilation also varied, highlighting the heterogeneous clinical course of aluminium phosphide poisoning.

Table 1. Clinical Outcome of Patients

Table 2. Hemodynamic Parameters at Admission

Table 3. Cardiac Function Assessment

Table 4. Arrhythmias Observed

Table 5. Comparison of Cardiovascular and Metabolic Parameters Between Survivors and Non-Survivors

Table 6: Comparison ABG Parameters Between Survivors and Non-Survivors

Table 7: Comparison of Laboratory and ABG Parameters at Admission and Discharge/Death in Patients with Aluminium Phosphide Poisoning (n = 50)

Table 8: Comparison of Laboratory and ABG Parameters Between Survivors and Non-Survivors in Aluminium Phosphide Poisoning

Table 9: Time-Related Clinical Characteristics of Patients with Aluminium Phosphide Poisoning

Aluminium phosphide (ALP) poisoning remains a major cause of morbidity and mortality in developing countries, particularly in agricultural regions where the compound is easily accessible. The present study evaluated the cardiovascular profile and clinical outcomes of patients with aluminium phosphide poisoning and demonstrated significant cardiovascular involvement associated with the toxic effects of phosphine gas. The findings highlight the importance of early recognition of cardiovascular compromise and aggressive supportive management in improving patient outcomes.

In the present study, the majority of patients were young adults with a slight predominance of males. Similar demographic patterns have been reported in previous studies, where aluminium phosphide poisoning is frequently seen among young individuals due to its easy availability and frequent use in suicidal attempts. The overall mortality observed in the present study was considerable, reflecting the well-known high fatality rate associated with aluminium phosphide poisoning. Bajwa et al., also reported CELPHOS poisoning in a younger cohort.⁷

Hemodynamic parameters at admission indicated features of circulatory compromise. Hypotension and tachycardia were common findings among the study population, which is consistent with previous studies reporting profound circulatory collapse as a hallmark of aluminium phosphide toxicity. The toxic effects of phosphine on myocardial cells lead to impaired oxidative phosphorylation and severe myocardial depression, ultimately resulting in cardiogenic shock. Bogale et al., also reported similar observations due to Aluminum Phosphide Poisoning.⁸

Assessment of cardiac function revealed markedly reduced left ventricular ejection fraction at admission, suggesting significant myocardial dysfunction. However, a substantial improvement in ejection fraction was observed among survivors at discharge. This finding indicates that myocardial depression associated with aluminium phosphide poisoning may be reversible with adequate supportive management, including inotropic support and advanced circulatory assistance when required.

Arrhythmias were frequently observed in the present study, with ventricular tachycardia and ventricular fibrillation being the most common rhythm abnormalities. These malignant ventricular arrhythmias are known complications of aluminium phosphide poisoning and are considered important contributors to sudden cardiac death. The mechanism of arrhythmogenesis is thought to involve direct myocardial toxicity, metabolic acidosis, and electrolyte imbalance. Moghadamnia⁹ also reported arrythmias in similar settings and Bogale et al. also published similar findings.⁸

Metabolic and laboratory parameters also showed significant alterations during the course of illness. Elevated lactate levels, metabolic acidosis, and electrolyte disturbances were common findings, reflecting severe tissue hypoxia and impaired cellular metabolism caused by phosphine toxicity. Significant elevations in liver enzymes and bilirubin levels observed during hospitalization suggest hepatic involvement and systemic toxicity.

Kakavandi et al., also reported electrocardiographic, hemodynamic, echocardiographic, and biochemical changes due to CELPHOS poisoning.¹⁰

Comparison between survivors and non-survivors demonstrated that patients with poor outcomes had more severe metabolic derangements, higher inflammatory markers, and greater hepatic dysfunction. These findings are consistent with earlier reports indicating that metabolic acidosis, elevated lactate levels, and organ dysfunction are important predictors of mortality in aluminium phosphide poisoning.

The duration of hospitalization, ECMO support, and mechanical ventilation varied among patients, reflecting differences in clinical severity. The use of advanced supportive modalities such as ECMO may provide temporary circulatory support in cases of refractory cardiogenic shock and has shown promising outcomes in selected patients.

A study by Mohan et al. demonstrated that low baseline LVEF is an important predictor of mortality in AlP poisoning patients and ECMO therapy can be useful for survival.¹¹ Another study by Eltokhy et al  reported a survival rate of severely poisoned ALP patients receiving ECMO as 80% which is fairly good making ECMO a viable option.¹²

Overall, the findings of the present study emphasize that cardiovascular dysfunction plays a central role in the pathophysiology and prognosis of aluminium phosphide poisoning. Early recognition of myocardial involvement, prompt correction of metabolic abnormalities, and aggressive supportive care are essential to improve survival in affected patients.

Aluminium phosphide poisoning is associated with significant cardiovascular toxicity and remains a life-threatening medical emergency with high mortality. The present study demonstrated that myocardial depression, malignant ventricular arrhythmias, metabolic acidosis, and multiorgan dysfunction are common manifestations of aluminium phosphide poisoning and play a crucial role in determining patient outcomes. Markedly reduced left ventricular ejection fraction at admission indicates severe myocardial involvement; however, improvement in cardiac function among survivors suggests that myocardial dysfunction may be reversible with timely and aggressive supportive management. Significant metabolic disturbances, including elevated lactate levels, electrolyte imbalance, and hepatic enzyme elevation, were observed during the course of illness, reflecting systemic toxicity caused by phosphine. Patients with poorer outcomes exhibited more severe metabolic derangements and laboratory abnormalities, highlighting the importance of early identification of high-risk patients. Advanced supportive modalities such as extracorporeal membrane oxygenation (ECMO) can play a valuable role in the management of patients with refractory cardiogenic shock due to aluminium phosphide poisoning by providing temporary circulatory support and allowing recovery of myocardial function. Early initiation of ECMO in selected patients may improve survival in otherwise fatal cases. Overall, early diagnosis, prompt hemodynamic stabilization, correction of metabolic abnormalities, continuous cardiac monitoring, and timely use of advanced supportive therapies are essential to improve clinical outcomes in aluminium phosphide poisoning. Further multicenter studies with larger sample sizes are required to better understand prognostic factors and to establish standardized treatment protocols for the management of this highly fatal poisoning.

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