|Year : 2022 | Volume
| Issue : 1 | Page : 6-10
Management of aluminium phosphide poisoning with a holistic approach at NHL municipal medical college and hospital, Ahmedabad
Dheeraj B More1, Mahendra N Wankhede2, Harshad Malve3
1 Department of Cardiology, Seth GS Medical College and KEM Hospital, Mumbai, Maharashtra, India
2 Department of Forensic Medicine, HBT Medical College and Cooper Hospital, Mumbai, Maharashtra, India
3 Department of Pharmacology, Vedanta Institute of Medical Sciences, Dahanu, Maharashtra, India
|Date of Submission||30-Jul-2021|
|Date of Decision||25-Sep-2021|
|Date of Acceptance||27-Sep-2021|
|Date of Web Publication||17-Mar-2022|
Department of Pharmacology, Vedanta Institute of Medical Sciences, Dahanu, Maharashtra
Source of Support: None, Conflict of Interest: None
Background: Aluminium phosphide is a usual ingredient of rodenticide and its poisoning is a common cause of suicide in India. Signs and symptoms of its toxicity are well-known. Its toxic effects are mainly due to liberation of phosphine gas which causes cell hypoxia due to inhibition of oxidative phosphorylation and results in circulatory failure. Aims and Objectives: Mortality with aluminium phosphide is high as there is no specific antidote available yet. And hence we need to explore holistic treatment approach to improve patient outcomes in aluminium phosphide poisoning. Materials and Methods: Present study discusses a holistic treatment approach to aluminium phosphide poisoning in this retrospective analysis of 100 cases from a tertiary care hospital in this study. Results: Around 65% patients survived due to the holistic treatment approach and correct treatment protocol with supportive therapy. Conclusions: The aggressive and appropriate management with continuous hemodynamic monitoring and holistic treatment approach can reduce the mortality significantly in aluminium phosphide poisoning.
Keywords: Aluminum phosphide toxicity, holistic treatment, rodenticide poisoning
|How to cite this article:|
More DB, Wankhede MN, Malve H. Management of aluminium phosphide poisoning with a holistic approach at NHL municipal medical college and hospital, Ahmedabad. J Forensic Sci Med 2022;8:6-10
|How to cite this URL:|
More DB, Wankhede MN, Malve H. Management of aluminium phosphide poisoning with a holistic approach at NHL municipal medical college and hospital, Ahmedabad. J Forensic Sci Med [serial online] 2022 [cited 2022 May 16];8:6-10. Available from: https://www.jfsmonline.com/text.asp?2022/8/1/6/339794
| Introduction|| |
Aluminum phosphide is commonly used as rodenticide and pesticide in grain storage facility. Aluminum phosphide poisoning occurs as a result of excessive exposure to aluminum phosphide, which is readily available as a fumigant for stored cereal grains or as rodenticide and sold under various brand names such as QuickPhos, RatKil, Salphos, and Celphos. It is highly toxic, especially when consumed from a freshly opened container., After ingestion, toxic features usually develop within a few minutes. It has a fatal dose of between 0.15 and 0.5 g. The mortality rates from aluminum phosphide poisoning vary from 35% to 85% in various studies. The major lethal consequence of aluminum phosphide ingestion is profound circulatory collapse and is due to liberation of phosphine gas, a cytotoxic compound that causes free radical-mediated injury, it inhibits vital cellular enzymes and is directly corrosive to tissues, which leads to direct effects on cardiomyocytes, fluid loss, and adrenal gland damage., It produces phosphine gas which is a mitochondrial poison. It has a very destructive effect on myocardial cells and leads to myocarditis. The degree of myocarditis can vary from mild to severe and it can cause heart failure and various cardiac arrhythmias such as atrial fibrillation, ventricular tachycardia, and bradyarrhythmias. It can also cause ventricular fibrillation and sudden death.
The signs and symptoms of aluminum phosphide poisoning are nonspecific, dose dependent, and evolve with time. Severe poisoning also has the potential to induce multi-organ failure. The dominant clinical feature is severe hypotension refractory to dopamine therapy and metabolic acidosis. Other features may include dizziness, fatigue, tightness in the chest, headache, nausea, vomiting, diarrhea, ataxia, numbness, paresthesia, tremor, muscle weakness, diplopia and jaundice.,,, In severe cases, the patient may develop acute respiratory distress syndrome (ARDS), heart failure, arrhythmias, convulsion, and coma and death. Late manifestations include liver and kidney toxicities.,,, Death can result from profound shock, myocarditis, and multi-organ failure. Several electrocardiography (ECG) changes ranging from ST-segment elevation/depression, PR, and QRS interval prolongation complete heart block to ectopic and fibrillations have been observed. Reversible myocardial injury has also been reported.,, The breath of patients who have ingested aluminum phosphide has a characteristic garlic-like odor. Confirmation of diagnosis is based on the patient's history.
Previously, the laws and legislations for sale of such chemicals were not that strict and it was easily available over the counter. In the last few years, stricter norms have reduced its easy availability. However, it is not enough to reduce the suicidal rate due to its consumption, which traumatizes many families. Since 1992, when aluminum phosphide became freely available in the market, it had, reportedly, overtaken all other forms of deliberate poisoning, such as organophosphorus and barbiturate poisoning, particularly in North India. In a 25-year-long study on 5933 unnatural deaths in Northwest India, aluminum phosphide poisoning was found to be the major cause of death among all cases of poisonings. It has been reported to be the most common method of suicidal death in North India.
The management of aluminum phosphide poisoning remains purely supportive because there is no specific antidote or cure for aluminum phosphide poisoning. Treatment consists of gastric lavage with potassium permanganate solution, oral administration of charcoal and sorbitol suspension, intravenous administration of fluids, inotropes, sodium bicarbonate, magnesium sulfate, calcium gluconate, corticosteroids, and other supportive care. Correction of metabolic acidosis is a cornerstone of treatment., The present study is a retrospective analysis of the registered cases of aluminum phosphide poisoning at the intensive care unit (ICU) of the hospital. The adoption of a holistic approach with the help of physician, intensivist, cardiologist, nephrologist, neurologist, psychiatrist, and clinical pharmacologist as well as a toxicologist for the treatment of aluminum phosphide poisoning helped in better patient outcomes. Hence, this analysis was aimed at observing the clinical profile and outcome of aluminum phosphide poisoning with a holistic approach in the institute.
| Materials and Methods|| |
This study was planned to understand the factors impacting the management of aluminum phosphide poisoning and patient outcomes at NHL Municipal Medical College and Hospital, Ahmedabad. The data were curated for the period of 10 years from January 2011 to December 2020 from the database of registered cases at ICU of the hospital. Data for patients with an alleged history of aluminum phosphide poisoning was curated and compiled for detailed analysis. Till 2014, data was compiled for 40 patients; however, it was decided to further curate the data to get a minimum sample size of 100 patients.
Profiles of patients of aluminum phosphide poisoning along with the investigations and treatment protocols were studied retrospectively. Patient outcomes were also studied in detail. As a routine practice, all the patients were informed on admission regarding possible use of the data for publication. Data were compiled using Microsoft Excel sheets. Statistical analysis was carried out and data were presented as mean and percentages.
| Results|| |
Data of a total of 100 patients who had a diagnosis of aluminum phosphide poisoning were curated. The age of patients ranged from 14 to 85 years with a mean age of 39.5 years. The majority of patients were young with 50% of patients in 20–40 years age group. Out of 100 patients, 85 were male and 15 female. According to educational level, 33 patients were illiterate, 47 were studied up to secondary school, 14 patients were graduates, and six patients were postgraduates, indicating that aluminum phosphide was seen less likely in educated than illiterate people, as summarized in [Figure 1]. According to professional status, 48 people were not working or unemployed, 15 were employed, and 37 were self-employed.
Most of the patients had features of hypotension, cardiogenic shock, and arrhythmias, whereas few got admitted with respiratory distress and the rest of them had a multitude of symptoms related to different organ systems. On admission, sinus tachycardia was present in 72 patients. Wide complex tachycardia was present in 16 patients; sinus bradycardia was seen in six patients. Complete heart block was seen in four patients, and junctional rhythm was seen in two patients, both of which required temporary pacemaker, and patients later resumed spontaneous sinus rhythm. On admission, left ventricular (LV) dysfunction was present in 70 patients (mild 50, moderate 14, and severe 6). Forty-eight patients out of 50 survived with mild LV systolic dysfunction, 12 patients out of 14 survived with moderate LV systolic dysfunction, and 3 patients out of 6 survived with severe LV systolic dysfunction. It indicates that LV ejection fraction/systolic dysfunction has an important impact on survival of patients with aluminum phosphide. The maximum number of patients (85%) presented clinically with cardiovascular system involvement, either in the form of tachycardia, hypotension, or arrhythmias, ST-T changes, which was clinically significant. Clinical presentation of these patients is summarized in [Table 1].
Out of the 100 patients, 30 patients required mechanical ventilation and 70 patients needed inotropic support for maintaining stable hemodynamic parameters. Twenty-seven patients needed defibrillation or other antiarrhythmic treatment, three patients required temporary pacemaker insertion, and all the patients later regained spontaneous sinus rhythm. Only two patients required hemodialysis for renal impairment. The stay in ICU varied from 3 to 16 days, with a mean stay of 8 days. Out of 100, 76 patients survived without any end-organ damage, which is quite significant, but the rest 24 succumbed to poisoning.
The mortality increased with progressive involvement of the number of organ systems. Organ system involvement and mortality is summarized in [Table 2], it indicated that the mortality reached 100% if four or more organs are involved.
Thirteen patients consumed three or more than three tablets of the aluminum phosphide containing poison, whereas 28 patients were brought to the hospital almost more than 4 h of ingestion of these pellets which are believed to be the reasons for increased mortality rate.
Biochemical changes included rise in aspartate transaminase, creatine phosphokinase-MB, and lactate dehydrogenase. Histopathological reports showed myocytolysis, multiple areas of necrosis, and congestion.
Treatment protocol used was as follows, extensive gastric lavage was done with potassium permanganate and charcoal on admission to casualty. Initial 30-ml lavage was sent to forensic laboratory for toxicological analysis. On admission to ICU, the patients were made comfortable on the bed, monitoring gadgets were attached for heart rate and rhythm, noninvasive blood pressure (BP) monitoring, ECG, and pulse oximetry (SpO2). Bedside two-dimensional (2D) echo with Doppler was done in all patients, with inferior vena cava (IVC) measurement which helped in inotropic management. Endotracheal intubation for indicated patients was done with appropriate size cuffed endotracheal tube and patients were put on mechanical ventilation. Symptomatic treatment was initiated on a patient-to-patient basis. Intravenous normal saline, magnesium sulfate, dopamine, dobutamine, amiodarone infusions, antibiotics, and other appropriate intravenous drugs were given depending on the patient's clinical presentation and symptomatology, as well as arrhythmias and BP variations. Urine output was monitored through Foley's catheter attached to urobag with uroflowmeter. Patients who required mechanical ventilation were kept sedated with injection midazolam and paralyzed with injection vecuronium. During this period, strict and vigil monitoring of all vital parameters was done and treatment regimens were titrated according to the clinical condition of the patients.
All patients were managed in ICU with an objective to provide symptomatic and supportive aid as follows:
- Central venous line for central venous pressure monitoring, IV fluids, and inotropic support
- Arterial line for invasive BP monitoring in most of the patients
- Intravenous sodium bicarbonate for metabolic acidosis
- Patients who required mechanical ventilation were kept sedated with injection midazolam and paralyzed with injection vecuronium
- Magnesium sulfate 2 g in dextrose IV every 6 hourly
- Continuous cardiac monitoring and if needed injection amiodarone, defibrillation, or temporary pacemaker insertion
- Prophylactic antibiotics
- Bedside 2D echo for all patients.
| Discussion|| |
Rodenticide and insecticides such as Celphos are formulated as greenish or gray tablet of aluminum phosphide, which releases phosphine gas in the presence of moisture or hydrogen chloride. Phosphine gas gets rapidly absorbed from the gastric mucosa and, once it gains access to bloodstream, it reaches various tissues and at cellular level inhibits the mitochondrial respiratory chain and hence leads to cell necrosis and death. It inhibits myocardial cellular metabolism and necrosis of the cardiac tissue, resulting in the release of reactive oxygen intermediates. Refractory myocardial depression from aluminum phosphide toxicity is not uncommon and carries a very high mortality.,, These cardiotoxic effects were quite marked in patients, as 70% of the patients required inotropic support. Vascular changes may lead to marked low BP/hypotension that does not respond well to vasopressor agents. Cardiotoxicity or toxic chemical myocarditis is manifested as depressed LV ejection fraction, ECG changes varying from ST-segment elevation or depression, PR prolongation, broad QRS complexes, and right or left bundle branch block, supraventricular ectopic or ventricular tachycardia, and bradyarrhythmias. Bedside 2D echo should be used often in such cases.
Pathological changes in heart such as myocytolysis, necrosis, and congestion of liver are common with aluminum phosphide poisoning. Hypomagnesemia has been known to cause arrhythmias in aluminum phosphide poisoning and magnesium supplementation has been suggested as a therapeutic option., The findings of the present study do correlate with all the above studies, as most of the patients presented with arrhythmias of varying nature and it proved fatal in some of the patients who died in the ICU.
The incidence of aluminum phosphide poisoning was seen in working and the nonworking population, highlighting the fact that employment stress is not the only factor, but rather, it is the social and family factors which drive these people to commit suicide.
Aluminum phosphide toxicity that occurs after inhalation is characterized by chest tightness, cough, and shortness of breath. Severe exposure can cause accumulation of fluid in the lungs, pulmonary edema, and ARDS, which may have a delayed onset of 72 h or more after exposure. Children may be more vulnerable because of relatively increased minute ventilation per kilogram and failure to evacuate an area promptly when exposed. Phosphine gas is eliminated through the lungs; hence, due to high concentration in the respiratory alveoli, it is responsible for direct alveolar damage. In the present study, 25% of patients also presented with respiratory distress, either alone or in combination with other organ dysfunction. Four patients developed severe pulmonary edema during the initial course of the treatment and were ventilated with 100% oxygen and high PEEP as the patients developed severe hypoxemia which was evident in ABG report. Studies in the past have shown increased levels of inflammatory markers (cytokines and interleukins) in ARDS, which increase the capillary permeability. This combined effect of an increase in capillary permeability due to global hypoxia and ARDS could be responsible for the exudative effusion seen predominantly in the pleural cavity and not in other serous cavities.
Gastrointestinal symptoms are usually one of the first to occur after exposure. Symptoms may include nausea, vomiting, abdominal pain and diarrhea, and hematemesis. Death due to acute hepatocellular toxicity and fulminant hepatic failure has also been reported in acute poisoning. Hematuria and proteinuria with acute kidney failure due to shock can occur.Analysis of blood gases may reveal combined respiratory and metabolic acidosis. Furthermore, there have been reports of significant hypomagnesemia and hypomagnesemia associated with massive focal myocardial damage., In this study, mortality increased with the increasing number of organ system involvement. In patients with involvement of four or more than four organ system involvement, mortality was 100%.
Gastric lavage is important in the initial stage. The management principles aim to save life with appropriate resuscitation and supportive measures until phosphine is excreted from the body. If phosphides have been ingested, do not induce emesis. Gastric lavage with saline or sodium bicarbonate or potassium permanganate (1:1000) has also been recommended by earlier studies. As the poison itself causes a lot of gastric mucosal damage, it exposes a lot of raw area for phosphine absorption.
Putting patient on mechanical ventilation after sedation, helps enhancing phosphine excretion through lungs by increasing the respiratory rate. Phosphine is excreted through urine also. Therefore, adequate hydration and renal perfusion by low-dose dopamine 4–6 μg/kg/min can be considered. Arterial line is a must for invasive BP monitoring in most of the patients. Intravenous sodium bicarbonate helps to reverse metabolic acidosis. Magnesium sulfate in dextrose IV every 6 hourly helps with its antioxidant and antiarrhythmic action. Continuous cardiac monitoring is essential. Injection of amiodarone and defibrillation for timely control of ventricular arrhythmia and temporary pacemaker insertion for heart block should be considered whenever needed. Prophylactic antibiotic for prevention of nosocomial infection is also essential. It is important to keep serum magnesium, serum potassium and serum sodium within normal level along-with taking care of other hemodynamic parameters and metabolic acidosis. It helps in better survival of such patients.There is significantly better survival rate of patients with aluminum phosphide poisoning. Bedside 2D echo helps in the management of intravenous fluids, diuretics, and inotropes.
Besides considering the expertise of a physician, intensivist, cardiologist, nephrologist, neurologist, and psychiatrist in treating aluminum phosphide poisoning, involvement of clinical pharmacologist and toxicologist helped management of such cases optimally. Clinical pharmacologist can be of great help in such cases with their expertise in drug actions and adverse effects.,,
| Conclusion|| |
Aluminum phosphide poisoning patients can survive without any end-organ damage if aggressive and appropriate management with continuous hemodynamic monitoring is done along with a holistic treatment approach. The patient outcomes correlate best with the severity of hypotension, severity of acidosis, LV dysfunction or LV ejection fraction, arrhythmias, and number of organ systems involved. The management of aluminum phosphide poisoning remains purely supportive because no specific antidote exists. Correction of metabolic acidosis is the cornerstone of treatment. The role of magnesium sulfate, defibrillation, and antiarrhythmic medicines as therapy in aluminum phosphide poisoning should decrease the likelihood of a fatal outcome. With the holistic treatment approach, lives of 65% of patients of aluminum phosphide poisoning were saved and it is recommended to use such an approach by all the intensivists and physicians. This holistic treatment approach can possibly save the lives of so many patients from this emergency.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Parekh U, Gupta S. Epidemio-toxicological profile of poisoning cases – A five years retrospective study. J Forensic Leg Med 2019;65:124-32.
Yadav D, Bhattacharyya R, Banerjee D. Acute aluminum phosphide poisoning: The menace of phosphine exposure. Clin Chim Acta 2021;520:34-42.
Hashemi-Domeneh B, Zamani N, Hassanian-Moghaddam H, Rahimi M, Shadnia S, Erfantalab P, et al
. A review of aluminium phosphide poisoning and a flowchart to treat it. Arh Hig Rada Toksikol 2016;67:183-93.
Çakın Ö, Tazegul G, Gümüş A, Cengiz M, Ramazanoğlu A. Incidental aluminum phosphide poisoning: Case report and current management. Folia Med (Plovdiv) 2018;60:464-7.
Sikary AK. Homicidal poisoning in India: A short review. J Forensic Leg Med 2019;61:13-6.
Chugh SN, Kumar P, Aggarwal HK, Sharma A, Mahajan SK, Malhotra KC. Efficacy of magnesium sulphate in aluminium phosphide poisoning--comparison of two different dose schedules. J Assoc Physicians India 1994;42:373-5.
Goel A, Aggarwal P. Pesticide poisoning. Natl Med J India 2007;20:182-91.
Sudakin DL. Occupational exposure to aluminium phosphide and phosphine gas? A suspected case report and review of the literature. Hum Exp Toxicol 2005;24:27-33.
Farahani MV, Soroosh D, Marashi SM. Thoughts on the current management of acute aluminum phosphide toxicity and proposals for therapy: An Evidence-based review. Indian J Crit Care Med 2016;20:724-30.
] [Full text]
Agrawal VK, Bansal A, Singh RK, Kumawat BL, Mahajan P. Aluminum phosphide poisoning: Possible role of supportive measures in the absence of specific antidote. Indian J Crit Care Med 2015;19:109-12.
] [Full text]
Mathai A, Bhanu MS. Acute aluminium phosphide poisoning: Can we predict mortality? Indian J Anaesth 2010;54:302-7.
] [Full text]
Singh D, Jit I, Tyagi S. Changing trends in acute poisoning in Chandigarh zone: A 25-year autopsy experience from a tertiary care hospital in northern India. Am J Forensic Med Pathol 1999;20:203-10.
Singh D, Dewan I, Pandey AN, Tyagi S. Spectrum of unnatural fatalities in the Chandigarh zone of north-west India--a 25 year autopsy study from a tertiary care hospital. J Clin Forensic Med 2003;10:145-52.
Siwach SB, Gupta A. The profile of acute poisonings in Harayana-Rohtak study. J Assoc Physicians India 1995;43:756-9.
Wiwanitkit V. Aluminum phosphide poisoning. Indian J Crit Care Med 2009;13:171.
] [Full text]
Sahoo D, Kujur ST, Das DS, Dey A, Devi S. Aluminium phosphide poisoning: Early suspicion of cardiotoxicity is necessary for improved outcomes. Cureus 2020;12:e10237.
Meena MC, Mittal S, Rani Y. Fatal aluminium phosphide poisoning. Interdiscip Toxicol 2015;8:65-7.
Eshraghi A, Rajaei N, Mood MB, Vakili V, Ramezani J. Changes of QT dispersion in patients suffering from aluminium phosphide poisoning (Rice Pill). Open Access Maced J Med Sci 2019;7:2251-5.
Karanth S, Nayyar V. Rodenticide-induced hepatotoxicity. J Assoc Physicians India 2003;51:816-7.
Suman RL, Savani M. Pleural effusion-a rare complication of aluminium phosphide poisoning. Indian Pediatr 1999;36:1161-3.
Anand R, Binukumar BK, Gill KD. Aluminum phosphide poisoning: An unsolved riddle. J Appl Toxicol 2011;31:499-505.
Malve HO. Forensic pharmacology: An important and evolving subspecialty needs recognition in India. J Pharm Bioallied Sci 2016;8:92-7.
Malve H. Understanding forensic pharmacology: What Indian physicians need to know? J Assoc Physicians India 2017;65:74-5.
Malve H. Understanding forensic pharmacology: What Indian pharmacologists need to know? Toxicol Int 2016;23:205-6.
[Table 1], [Table 2]