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Cardiovascular toxicity is the most common cause of fatality in the first 24 hours of poisoning with aluminium phosphide (AlP). Most often manifesting itself in cardiac dysrhythmias. The aim of this study was to evaluate the benefits of amiodarone prophylaxis against cardiac dysrhythmia in 46 patients with acute AlP poisoning. They were divided in two groups of 23: one receiving amiodarone and the other not (control). The treatment group received amiodarone prophylaxis in the initial intravenous bolus dose of 150 mg, followed by a drip of 1 mg/min for six hours and then of 0.5 mg/min for eighteen hours. Both groups were Holter-monitored for 24 hours since admission. Save for amiodarone, both groups received the same standard treatment. Amiodarone had a significant beneficial effect in reducing the frequency of ST-segment elevation and ventricular fibrillation plus atrial fibrillation (P=0.02 and P=0.01, respectively), but the groups did not differ significantly in mortality (9 vs 11 patients, respectively). The mean time between ICU admission and death (survival time) was significantly longer in the treatment group (22 vs 10 h, respectively; P=0.03). Regardless its obvious limitations, our study suggests that even though amiodarone alone did not reduce mortality, it may provide enough time for antioxidant therapy to tip the balance in favour of survival and we therefore advocate its prophylactic use within the first 24 h of AlP poisoning.

Aluminum phosphide (AlP) poisoning is a severe toxicity with 30-70% mortality rate. However, several case reports presented AlP-poisoned patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency and extensive hemolysis who survived the toxicity. This brought to our mind that maybe G6PD deficiency could protect the patients from severe fatal poisoning by this pesticide. In this research, we investigated the protective effect of 6-aminonicotinamide (6-AN)- as a well-established inhibitor of the NADP + - dependent enzyme 6-phosphogluconate dehydrogenase- on isolated rat hepatocytes in AlP poisoning. Hepatocytes were isolated by collagenase perfusion method and incubated into three different flasks: control, AlP, and 6-AN+ALP. Cellar parameters such as cell viability, reactive oxygen species (ROS) formation, mitochondria membrane potential collapse (MMP), lysosomal integrity, content of reduced (GSH) and oxidized glutathione (GSSG) and lipid peroxidation were assayed at intervals. All analyzed cellular parameters significantly decreased in the third group (6-AN+AlP) compared to the second group (AlP), showing the fact that G6PD deficiency induced by 6-AN had a significant protective effect on the hepatocytes. It was concluded that G6PD deficiency significantly reduced the hepatotoxicity of AlP. Future drugs with the power to induce such deficiency may be promising in treatment of AlP poisoning., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Background/aim: Aluminum phosphide (AlP) is commonly used as a fumigant in developing countries. Induction of oxidative stress is one of the most important mechanisms of its toxicity. In this regard, and considering that there is no specific antidote for its treatment, the aim of this study was to evaluate the effect of vitamin E in the treatment of acute AlP poisoning., Materials and Methods: This was a clinical trial on acute AlP poisoned patients. All patients received supportive treatment. In addition, the treatment group received vitamin E (400 mg/BD/IM). Level of malondialdehyde (MDA) and total antioxidant capacity of plasma were measured., Results: There was no significant difference between the treatment and control groups with regard to demographic, clinical, or paraclinical data or Simplified Acute Physiology Score II (SAPS II ) on admission. Systolic blood pressure significantly increased during the first 24 h in the treatment group (P < 0.05). The plasma MDA level significantly decreased in the treatment group (P < 0.05). Vitamin E administration decreased the necessity (30% vs. 62%, P < 0.05) and duration of intubation and mechanical ventilation (P < 0.05). It significantly reduced the mortality rate in the treatment group compared to the control group (15% vs. 50%, respectively, P < 0.05)., Conclusion: Vitamin E along with supportive treatment could have a therapeutic effect in acute AlP poisoning.

The use of pesticides such as aluminium phosphide (AlP) has increased in the recent years and improved the quantity and quality of agricultural products in a number of developing countries. The downside is that AlP causes severe chronic and acute health effects that have reached major proportions in countries such as India, Iran, Bangladesh, and Jordan. Nearly 300,000 people die due to pesticide poisoning in the world every year. Poisoning with AlP accounts for many of these deaths. Unfortunately, at the same time, there is no standard treatment for it. The aim of this article is to give a brief review of AlP poisoning and propose a treatment flowchart based on the knowledge gained so far. For this purpose we reviewed all articles on the management of AlP poisoning published from 2000 till now. Using a modified Delphi design, we have designed a handy flowchart that could be used as a guide for AlP poisoning management of patients in emergency centres.

In pulse CO-oximetry of aluminium phosphide (ALP)-poisoned patients, we discovered that carboxyhaemoglobin (CO-Hb) level was elevated. We aimed to determine whether a higher CO level was detected in patients with severe ALP poisoning and if this could be used as a prognostic factor in these patients. In a prospective case-control study, 96 suspected cases of ALP poisoning were evaluated. In the ALP-poisoned group, demographic characteristics, gastric and exhalation silver nitrate test results, average CO-Hb saturation, methaemoglobin saturation, and blood pressure and blood gas analysis until death/discharge were recorded. Severely poisoned patients were defined as those with systolic blood pressure ≤80 mmHg, pH ≤7.2, or HCO3 ≤15 meq/L or those who died, while patients with minor poisoning were those without any of these signs/symptoms. A control group (37 patients) was taken from other medically ill patients to detect probable effects of hypotension and metabolic acidosis on CO-Hb and methaemoglobin saturations. Of 96 patients, 27 died and 37 fulfilled the criteria for severe poisoning. All patients with carbon monoxide saturation >18% met the criteria to be included in the severe poisoning group and all with a SpCO >25% died. Concerning all significant variables in univariate analysis of severe ALP toxicity, the only significant variable which could independently predict death was carbon monoxide saturation. Due to high mortality rate and need for intensive care support, early prediction of outcome is vital for choosing an appropriate setting (ICU or ordinary ward). CO-oximetry is a good diagnostic and prognostic factor in patients with ALP poisoning even before any clinical evidence of toxicity will develop., (© 2016 Nordic Association for the Publication of BCPT (former Nordic Pharmacological Society).)

Objective: Aluminum phosphide is used as a fumigant. It produces phosphine gas (PH₃). PH₃ is a mitochondrial poison which inhibits cytochrome c oxidase, it leads to generation of reactive oxygen species; so one of the most important suggested mechanisms for its toxicity is induction of oxidative stress. In this regard, it could be proposed that a drug like N-acetylcysteine (NAC) as an antioxidant would improve the tolerance of aluminum phosphide-intoxicated cases. The objective of this study was to evaluate the protective effects of NAC on acute aluminum phosphide poisoning., Methods: This was a prospective, randomized, controlled open-label trial. All patients received the same supportive treatments. NAC treatment group also received NAC. The blood thiobarbituric acid reactive substances as a marker of lipid peroxidation and total antioxidant capacity of plasma were analyzed., Results: Mean ingested dose of aluminum phosphide in NAC treatment and control groups was 4.8 ± 0.9 g vs. 5.4 ± 3.3 g, respectively (p = 0.41). Significant increase in plasma malonyldialdehyde level in control group was observed (139 ± 28.2 vs. 149.6 ± 35.2 μmol/L, p = 0.02). NAC infusion in NAC treatment group significantly decreased malondialdehyde level (195.7 ± 67.4 vs. 174.6 ± 48.9 μmol/L, p = 0.03), duration of hospitalization (2.7 ± 1.8 days vs. 8.5 ± 8.2 days, p = 0.02), rate of intubation and ventilation (45.4% vs. 73.3%, p = 0.04). Mortality rate in NAC treatment and control groups were 36% and 60%, respectively with odds ratio 2.6 (0.7-10.1, 95% CI)., Conclusion: NAC may have a therapeutic effect in acute aluminum phosphide poisoning.

Aluminium phosphide (AlP) poisoning has a high mortality due to cardiovascular involvement. In this study, we evaluated the frequency of cardiac manifestations and electrocardiographic (ECG) findings in 20 patients with acute AlP poisoning, who were admitted to the intensive care unit (ICU) in Tehran, Iran, over a period of 6 months (between October 2008 and April 2009). The sex, age, cause and manner of ingestion, number of ingested AlP tablets, cardiac and ECG manifestations, creatine phosphokinase (CPK), CPK-myocardial band (CPK-mb) and troponin-T (TnT) were extracted from the patients' files. All data were analysed with Statistical Package for the Social Sciences (SPSS) software. The majority (60%) of patients were male. The mean age was 27 ± 8.7 years. The mortality rate was 40%. In all of the patients, the cause of poisoning was intentional suicide and ingestion was the route of exposure. The mean number of ingested AlP tablets per patient was 2.2 ± 1.1. The average time interval between admission and cardiovascular manifestations or ECG findings was 168.8 ± 116.2 min. The range of systolic (SBP) and diastolic blood pressure was 60-130 mmHg and 40-70 mmHg, respectively. Dysrhythmia was observed in nine (45%) cases. Elevation of the ST segment was seen in nine cases (45%). Seven patients (35%) had prolonged QTc intervals. Bundle branch block (BBB) was observed in four (20%) patients. In nine (45%) patients, the serum cardiac TnT qualitative assay was positive. There were no significant differences between normal and abnormal ECG groups according to sex, age, number and manner of ingested AlP tablets and SBP. There was a significant correlation between cardiac manifestations and ECG findings and TnT-positive results with mortality in acute AlP poisoning., (Copyright © 2012 Elsevier Ltd and Faculty of Forensic and Legal Medicine. All rights reserved.)

Background: Aluminum phosphide (AlP) is also known as "rice tablet" in Iran. Due to the high incidence of acute AlP poisoning and its associated mortality in Iran, the authorities banned AlP-containing tablets in 2007. The aim of this study is to evaluate the trend of acute fatal AlP poisoning subsequent to this restriction., Materials and Methods: 0 This is a retrospective chart review of patients with acute "rice tablet" poisoning who were admitted to Loghman Hakim Hospital Poison Center, Tehran, Iran, from 2007 to 2010. Collected information included gender, age, type of poisoning, marital status, duration of hospitalization, and outcome., Results: There were 956 cases with a mortality rate of 24.06%. The incidence of fatal AlP poisoning was 2.1 and 5.81 per one million populations of Tehran in 2007 and 2010, respectively. In 223 of the fatal cases (97%) and 697 of the non-fatal cases (96%), the poisoning was intentional. The male to female ratio in the fatal and non-fatal cases was 1.04:1 and 1:1.3, respectively. Most of the fatal cases (n = 122, 53%) were unmarried. The mean age was 27.32 ± 11.31 and 24.5 ± 8.19 years in fatal and non-fatal cases, respectively. In 196 (85.2%) of the fatal cases and in 577 (79%) of non-fatal cases, the duration of hospitalization was less than 24 hours and between 48-72 hours, respectively., Conclusion: The results of this study showed the incidence of "rice tablet" poisoning, and its mortality increased since 2007 in spite of the ban. It seems that legislative means alone without other interventions, such as suicide prevention and public education, will not always be able to control or prevent acute intentional poisonings.

Introduction: Acute aluminum phosphide (AlP) poisoning is one of the most common causes of acute pesticide poisoning in Iran. Hydrogen phosphide or phosphine gas is produced following reaction of AlP with water even at ambient humidity. Methemoglobinemia is a rare finding following phosphine poisoning. In this paper, two cases of fatal AlP poisoning complicated by methemoglobinemia are reported., Case Report: Two patients presented following suicidal ingestion of AlP tablets. In the Emergency Department (ED), they received gastric lavage with sodium bicarbonate and potassium permanganate. Both of them received supportive care. In each case, hematuria and hemolysis were significant events. The patients also showed a decrease in O(2) saturation in spite of high FIO(2). Methemoglobin levels of 40% and 30% were detected by co-oximetry. Neither patient responded to treatment (ascorbic acid in one case, methylene blue in the other). Both patients died due to systemic effects of phosphine poisoning., Discussion and Conclusion: Hemolysis and methemoglobinemia may complicate the course of phosphine poisoning that seems resistant to methylene blue and ascorbic acid. Therefore, other treatments including hyperbaric oxygen therapy and exchange blood transfusion should be considered.

Background: Acute aluminum phosphide (AlP) poisoning is one of the most common cause of acute pesticide poisoning in Iran. Spontaneous ignition is a rare finding in AlP poisoning., Objective: To present two cases of fatal AlP poisoning that involved spontaneous ignition., Case Report: Two patients presented with suicidal ingestion of AlP tablets. In the Emergency Department (ED), they received gastric lavage. During insertion of a nasogastric tube, both patients experienced spontaneous ignition, and flames were witnessed by the medical personnel. Unfortunately, both patients died due to systemic effects of AlP poisoning., Conclusion: Patients who present with acute aluminum phosphide poisoning may experience spontaneous ignition in the ED., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Background: Aluminum phosphide (AlP) is used as a fumigant. It produces phosphine gas, which is a mitochondrial poison. Unfortunately, there is no known antidote for AlP intoxication, and also, there are few data about its prognostic factors., Aims: The aim of this study was to determine the impact of the Simplified Acute Physiology Score II (SAPS II ) in the prediction of outcome in patients with acute AlP poisoning requiring admission to the Intensive Care Unit (ICU)., Materials and Methods: This was a prospective study in patients with acute AlP poisoning, admitted to the ICU over a period of 12 months. The demographic data were collected and SAPSII was recorded. The patients were divided into survival and non-survival groups due to outcome., Statistical Analysis: The data were expressed as mean ± SD for continuous or discrete variables and as frequency and percentage for categorical variables. The results were compared between the two groups using SPSS software. Results : During the study period, 39 subjects were admitted to the ICU with acute AlP poisoning. All 39 patients required endotracheal intubation and mechanical ventilation in addition to gastric decontamination with sodium bicarbonate, permanganate potassium, and activated charcoal, therapy with MgSO 4 and calcium gluconate and adequate hydration. Among these patients, 26 (66.7%) died. SAPSII was significantly higher in the non-survival group than in the survival group (11.88 ± 4.22 vs. 4.31 ± 2.06, respectively) (P < 0.001)., Conclusion: SAPSII calculated within the first 24 hours was recognized as a good prognostic indicator among patients with acute AlP poisoning requiring ICU admission.

Aluminium phosphide is used to control rodents and pests in grain storage facilities. It produces phosphine gas, which is a mitochondrial poison. Unfortunately, there is no known antidote for aluminium phosphide intoxication, but our recent experience with a case showed that rapid prevention of absorption by coconut oil might be helpful. In the present case, we used the same protocol in a 28-year-old man who had ingested a lethal amount (12 g) of aluminium phosphide with suicidal intent and was admitted to hospital approximately 6 hours postingestion. The patient had signs and symptoms of severe toxicity, and his clinical course included metabolic acidosis and liver dysfunction. Treatment consisted of gastric lavage with potassium permanganate solution, oral administration of charcoal and sorbitol suspension, intravenous administration of sodium bicarbonate, magnesium sulphate and calcium gluconate, and oral administration of sodium bicarbonate and coconut oil. Conservative and supportive therapy in the Intensive Care Unit was also provided. The patient survived following rapid treatment and supportive care. It is concluded that coconut oil has a positive clinical significance and can be added to the treatment protocol of acute aluminium phosphide poisoning in humans.

A response from the authors of the article "Carbamzepine-induced toxic epidermal necrolysis" in the 2011 issue is presented.