Aluminum Phosphide Poisoning Research Articles

Role of Aggressive Management on Outcome in Patients of Acute Aluminium Phosphide Poisoning

Aluminium phosphide poisoning is a common medical emergency in the Northern parts of India and South-East Asian nations. This poison is known to have high mortality ranging from 50% to 90% at various medical centres. In the absence of an antidote, an aggressive management is the need of the hour for reducing the mortality. A retrospective analysis of a set of variables was conducted on a group of 25 patients, followed by a prospective study of the same variables on a group of 25 consecutive patients who were enrolled into the study. Both the groups differed from each other principally in terms of management. The outcome of the management in both the groups were studied and analysed statistically. Factors strongly associated with mortality were consumption of fresh tablets, duration between consumption and treatment, low Glasgow coma scale (GCS), low mean arterial pressure (MAP) and metabolic acidosis. The group managed aggressively had lesser mortality rates than the group managed conservatively. Aggressive treatment benefitted even those individuals in whom prognostic variables were adverse. Aggressive management consisting of thorough gastric lavage, good fluid management, correction of metabolic acidosis, administration of magnesium sulphate, hydrocortisone and vitamin C has reduced the mortality rates in acute aluminium phosphide poisoning.

A Case Who Died Due to the Suicidal Intake of Aluminum Phosphide

Introduction: Aluminum phosphide poisoning is an important heath problem due to high mortality rate although it is rarely seen in Turkey and developed countries. Aluminum phosphate tablets in 3 g weight which are placed on the market under the trade name “57% Fumiphos” include 57% aluminum phosphide and 43% ammonium carbonate. In the present report, it was aimed to define clinical, crime scene investigation and autopsy findings of a case of aluminum phosphide poisoning that rarely seen in Turkey and to comparatively discuss data of our case and literature knowledge. Case: 20 years old male patient, hospitalized with ambulance following intake of aluminum phosphide while he was in military service and he was accepted as exitus after intense cardio-pulmonary resuscitation efforts. From witness statements, it was learned that patient taken orally a poison; a pill box written “Fumiphos 57% aluminum phosphide” on it, was found in patient’s jacket pocket; and it was learned that patient shared some words about death in social media. In the performed medico-legal autopsy, macroscopic findings were defined and the tissue samples which obtained in autopsy were examined microscopically. In the results of toxicological analysis of samples which obtained in autopsy, it was reported the presence of 14184 ng/g aluminum in stomach contents and p-toluene sulfonic acid in visceral organ and muscle samples. Discussion: Macroscopic and microscopic findings which obtained at autopsy was found compatible with non-specific findings which defined in the literature. In the result of evaluation of crime scene, autopsy and toxicological analysis findings, it was decided that the person's death occurred due to aluminum phosphide poisoning. Conclusion: In this case report, a case who died due to aluminum phosphide poisoning that was a condition commonly seen in developing countries, but rarely seen in Turkey and developed countries was presented and precautions against aluminum phosphide poisoning were defined. Additionally, we suggest that macroscopic and microscopic autopsy findings of the present case which rarely defined in classical literature will be guide for aluminum phosphide poisoning to medico-legal examiners.

Diagnosis of aluminum phosphide poisoning using a new analytical approach: forensic application to a lethal intoxication.

Aluminum phosphide (AlP) is an effective and cheap pesticide that is commonly used worldwide, but it is also a common cause of human poisoning and carries a high mortality rate. AlP reacts with moisture in air, water, and hydrochloric acid in the stomach to produce phosphine (PH3) gas. Two routes of exposure are ingestion of AlP and inhalation of phosphine generated by the action of moisture on AlP. Absorbed phosphine is rapidly metabolized into phosphite and hypophosphite. A method is described for the analysis of the phosphine metabolites in various biological matrices. The method involves reacting the sample with zinc and aqueous H2SO4 in a volatile organic analysis vial. The metabolites were transformed into phosphine gas and then analyzed by headspace gas chromatography coupled with mass spectrometry (HS-GC-MS). This method is capable of detecting quantities of PH3 as low as 0.2μg/mL in a sample. After validation, the method was applied to animal experiments and a real case of human AlP intoxication. This approach has the advantage of detecting metabolites of PH3, in case the PH3 was converted, and can be considered a useful additional tool for the diagnosis of AlP poisoning in forensic science.

Therapeutic effects of oral liothyronine on aluminum phosphide poisoning as an adjuvant therapy: A clinical trial.

In aluminum phosphide (AlP) poisoning, death is mainly due to cardiovascular failure and refractory acute heart failure. There is a lot of evidence showing thyroid hormones have cardioprotective effects. The purpose of this study was to evaluate the effect of oral liothyronine in the treatment of AlP poisoning. Twenty-four patients from intensive care unit of Baharloo Hospital, Tehran, Iran, were included based on the inclusion and exclusion criteria. They were randomly divided into two parallel groups of 12 cases and 12 controls. Intervention in the case group was administration of 50 µg liothyronine via nasogastric tube after gastric lavage, in the first 6 h of poisoning. In both groups, the routine treatment of AlP poisoning was performed. Blood samples were prepared at the beginning of the study and after 12 h. Patients were followed up till discharge from the hospital or death. The findings demonstrated that oral liothyronine was able to significantly improve systolic blood pressure, arterial blood pH, and total thiol molecules and also could decrease lipid peroxidation, increase catalase activity, and prevent further decline in total antioxidant capacity. Liothyronine administration is effective in controlling AlP poisoning and can improve patients' outcome.

The convergence of considerations in aluminum phosphide poisoning: The occurrence of injuries beyond the metabolic manifestations.

The convergence of considerations in aluminum phosphide poisoning: The occurrence of injuries beyond the metabolic manifestations.

Trend of blood lactate level in acute aluminum phosphide poisoning.

Aluminum phosphide (AlP) poisoning is common in the developing countries. There is no specific antidote for the treatment of acute AlP poisoning. Early diagnosis of poisoning and outcome predictors may facilitate treatment decisions. The objective of this study was to determine the trend of blood lactate level in acute AlP poisoning to evaluate its role as a prognostic factor. This was a prospective study on acute AlP intoxicated patients during one year. Demographic data, clinical and laboratory data on admission, and outcome were recorded in a self-made questionnaire. Blood lactate levels were analyzed every two hours for 24 hours. Thirty-nine (27 male, 12 female) patients were included in the study. The mortality rate was 38.5%. The mean blood pressure, pulse rate, blood pH and serum bicarbonate level were significantly different between the survivors and non-survivors groups. Blood lactate level was significantly higher in the non-survivors group during 8 to 16 hours post ingestion. Blood lactate level could be used as an index of severity of acute AlP poisoning.

N-acetylcysteine as an Adjuvant in The Treatment of Acute Aluminum Phosphide Poisoning: A Randomized Clinical Trial

Aluminum phosphide (ALP) is a common pesticide used for agricultural and non-agricultural purposes. Being cheap, widely available and highly toxic, it is responsible for many cases of poisoning. Aluminum phosphide poisoning has no specific antidote, therefore, based on role of oxidative stress in ALP poisoning, N-acetylcysteine (NAC) was suggested as adjuvant therapy in acute ALP poisoning.This study is a randomized clinical trial. It was conducted in Poison Control Center (Emergency Hospital, Tanta University). Thirty acute ALP intoxicated patients were randomly allocated into two equal groups A and B using the sequentially numbered, opaque sealed envelopes method. Group Areceived NAC 140 mg/Kg IV infusion as a loading dose followed by 70 mg/KgIV infusion every 4 hours up to 17 doses in addition to the routine treatment. Group B received only the routine treatment. Complete physical examination, routine laboratory investigations and oxidative stress markers; Malondialdehyde (MDA) and total antioxidant capacity (TAC) were performed for each patient.Results of the current study revealed no statistical significant difference between group A and group B patients regarding sociodemographic, toxicologicaland clinical data as well as routine laboratory investigation. On admission, MDA and TAC serum levels showed no statistical significant difference between group A and B. After treatment a statistical significant difference was observed in serum MDA and TAC levels between group A and B. Also, significant differenceswere noticed between group A and group B patients concerning mortality, dose of dopamine and hospitalization time.The study concluded that NAC might be a promising adjuvant therapy in treatment of acute ALP toxicity.

Effect of vitamin E supplementation on superoxide and malondialdehyde generation in acute celphos poisoning

Introduction: Aluminum phosphide is one of the most commonly used grain fumigants and aluminum phosphide poisoning (ALP) has been reported as the most common cause of acute poisoning in India. Aluminum toxicity has been reported to increase the rate of lipid peroxidation and free radical formation. Materials and Methods: The present study was designed to investigate the role of vitamin E supplementation on free radical generation and lipid peroxidation in acute aluminium phosphide poisoning in rats. Thirty disease free albino rats were taken to study the effect of acute aluminium phosphide poisoning (ALP poisoning) were further divided into 3 subgroups of ten rats each: A, B and C. Group A: given vehicle (Ginni Oil) only. Group B: given 5 ml 'celphos mixture' (or 0.3mg/g body wt.). Group C: rats with acute Celphos poisoning along with vitamin E (1.5 mg vitamin E/g body weight of rat. The MDA levels and superoxide levels (Nitroblue tetrazolium (NBT) reduction) were estimated. Results: MDA levels were significantly higher in the group B as compared to Group A. In group C, administration of vitamin E resulted in decreased MDA level compared to group B. MDA levels in group C still remained significantly higher as compared to group A. NBT reduction was significantly increased in group B as compared to group A. Administration of vitamin E to rats of group C resulted in significant decrease of NBT reduction. Conclusion: Findings of the present study showed that vitamin E via its antioxidant action and anti-inflammatory effects has protective effect on phosphine-induced toxicity in rats.

Criminal Poisoning with Aluminium Phosphide

Aluminium Phosphide poisoning is one of the leading causes of suicidal deaths in India. Death may also occur due to accidental exposure to Aluminium Phosphide/Phosphine. A number of deaths due to Aluminium Phosphide poisoning are reported all over India. Here in this article, we have discussed about its passage through placenta and subsequently fatal effect on the fetus.

Antioxidant therapy in patients with severe aluminum phosphide poisoning: A pilot study

Background:N-acetyl cysteine (NAC) is a powerful antioxidant and has been used extensively in the treatment of paracetamol overdose with great success. Aluminum phosphide (ALP) ingestion results in significant oxidative stress. In this study, we evaluated the effects of NAC on mortality in patients with severe ALP poisoning.Subjects and Methods:This prospective intervention study was carried out in the emergency medical unit attached to the Nehru Hospital at PGIMER, Chandigarh, over a period of 1 year. All the patients presenting with severe ALP poisoning were randomized into two group. The treatment group received NAC in the dose of 150 mg/kg intravenous over 1 h, followed by 50 mg/kg over 4 h, followed by 100 mg/kg 16 h in 5% dextrose. The placebo group received 5% dextrose. The primary end point was mortality.Results:A total of 50 patients were recruited. The baseline parameters were comparable in both groups. The survivors in the treatment group received 19 g of NAC, but the nonsurvivors received only 12.15 g of NAC. The overall mortality in the study group was 88% with 87.5% mortality in the treatment group and 88.5% in the placebo group.Conclusions:Antioxidant therapy in the form of NAC in severe ALP poisoning did not confer any survival benefit.

Cardiogenic Shock: The Main Cause of Mortality in Acute Aluminum Phosphide Poisoning.

Cardiogenic Shock: The Main Cause of Mortality in Acute Aluminum Phosphide Poisoning.

Sophism in the Management of Acute Aluminum Phosphide Poisoning may Cause Patient Harm.

Sophism in the Management of Acute Aluminum Phosphide Poisoning may Cause Patient Harm.

Vitamin E as a novel therapy in the treatment of acute aluminum phosphide poisoning.

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. 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. 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 (SAPSII) 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). Vitamin E along with supportive treatment could have a therapeutic effect in acute AlP poisoning.

A Case of Acute Aluminum Phosphide Poisoning Leading to Demyelinating Optic Neuropathy

Aluminum phosphide has been known, to be a major cause of non-accidental poisoning all over the world. The most common clinical manifestations being gastrointestinal and cardiovascular. Ocular manifestations have not been documented in the literature. We report a unique and rare presentation of aluminum phosphide poisoning. A 16 year old girl was brought with alleged ingestion of aluminum phosphide tablet and, developed redness and decreased vision in both the eyes. Visually Evoked Potential was suggestive of demyelinating optic neuropathy. She was treated with eye padding and eye drops to prevent dryness. Recovery and improvement in vision was seen after 5-6 days of ingestion. Aluminum phosphide poisoning may cause demyelinating optic neuropathy as a rare complication. In the presence of ocular symptoms, further ophthalmological and neurological evaluation is recommended. It is a diagnosis of exclusion and other possible etiologies must be ruled out before making the diagnosis.

Gastric decontamination in aluminium phosphide poisoning: a case against the use of water-based solutions.

Gastric decontamination in aluminium phosphide poisoning: a case against the use of water-based solutions.

Raised Red Cell Distribution Width as a Prognostic Tool for Acute Aluminium Phosphide Poisoning (AALPP) Patients

Objectives & Aims: Identify the acute aluminium phosphide poisoning. Identify the acute aluminium phosphide poisoning induced changes in hematological parameters .Raised red cell distribution used as a prognostic tool for acute aluminium phosphide poisoning . The changed hematological parameter used as a survival index of acute aluminium phosphide poisoning patients. Material & Methods: Blood was collected in a sterile EDTA containing tube and processed following our established ISO certified hospital laboratory protocol .A complete blood counting including HB%,PCV, Red cell indices ,platelet count and total white cell count and differential was done by Automated blood cell counter with peripheral blood smear examination and further confirmed by manual oil immersion smear study method. Peripheral smears study was done with field A and B stain and leishman stain. Conclusion: Aluminium phosphide poisoning caused changes in size of peripheral red blood cell due to lipid per oxidation and oxidative stress of cell membrane. These oxidative stress and lipid per oxidations lead to damage the cell membrane of RBC. These damage directly related with severity of exposer of the Aluminium phosphide. This type of damages decided the outcome survival of patients. So variable size of RBC occurs in peripheral blood used as a prognostic tool for severity of toxicity, monitoring of patients ,follow-up and outcome survival in the form of RDW .The RDW is a hematological parameter is easily generated by all type of hematological cell counters used as a good prognostic tool for acute aluminium phosphide poisoning Keyword: aluminium phosphide poisoning, Red cell distribution width. Material & Methods Study area and designThis present study was conducted at the Department of Pathology curewell hospital Pvt Ltd Indore MP. The study was designed as a observational hospital based study over a period of time from 2011 to 2016 years. Ethical ConsiderationBlood was collected in a sterile EDTA containing tube and processed following our established laboratory protocol then generate the report of each patient. Take informed consent was obtained from all study participant for use of your blood sample for medical research after doing physician request investigating and generate the report. Patient’s Selection CriteriaThe study target all the acute aluminium phosphide poisoning toxicity patients on the basis of clinical signs, www.jmscr.igmpublication.org Impact Factor 5.244 Index Copernicus Value: 83.27 ISSN (e)-2347-176x ISSN (p) 2455-0450 DOI: http://dx.doi.org/10.18535/jmscr/v4i10.28

A review of aluminium phosphide poisoning and a flowchart to treat it.

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.

N-acetylcysteine, ascorbic acid, and methylene blue for the treatment of aluminium phosphide poisoning: Still beneficial?

N-acetylcysteine, ascorbic acid, and methylene blue for the treatment of aluminium phosphide poisoning: Still beneficial?

Treatment of Aluminium Phosphide Poisoning with a Combination of Intravenous Glucagon, Digoxin and Antioxidant Agents.

Aluminium phosphide (AlP) is used to protect stored grains from rodents. It produces phosphine gas (PH3), a mitochondrial poison thought to cause toxicity by blocking the cytochrome c oxidase enzyme and inhibiting oxidative phosphorylation, which results in cell death. AlP poisoning has a high mortality rate among humans due to the rapid onset of cardiogenic shock and metabolic acidosis, despite aggressive treatment. We report a 21-year-old male who was referred to the Afzalipour Hospital, Kerman, Iran, in 2015 after having intentionally ingested a 3 g AlP tablet. He was successfully treated with crystalloid fluids, vasopressors, sodium bicarbonate, digoxin, glucagon and antioxidant agents and was discharged from the hospital six days after admission in good clinical condition. For the treatment of AlP poisoning, the combination of glucagon and digoxin with antioxidant agents should be considered. However, evaluation of further cases is necessary to optimise treatment protocols.

Chemical Reaction between Boric Acid and Phosphine Indicates Boric Acid as an Antidote for Aluminium Phosphide Poisoning.

Aluminium phosphide (AlP) is a fumigant pesticide which protects stored grains from insects and rodents. When it comes into contact with moisture, AlP releases phosphine (PH3), a highly toxic gas. No efficient antidote has been found for AlP poisoning so far and most people who are poisoned do not survive. Boric acid is a Lewis acid with an empty p orbital which accepts electrons. This study aimed to investigate the neutralisation of PH3 gas with boric acid. This study was carried out at the Baharlou Hospital, Tehran University of Medical Sciences, Tehran, Iran, between December 2013 and February 2014. The volume of released gas, rate of gas evolution and changes in pH were measured during reactions of AlP tablets with water, acidified water, saturated boric acid solution, acidified saturated boric acid solution, activated charcoal and acidified activated charcoal. Infrared spectroscopy was used to study the resulting probable adduct between PH3 and boric acid. Activated charcoal significantly reduced the volume of released gas (P <0.01). Although boric acid did not significantly reduce the volume of released gas, it significantly reduced the rate of gas evolution (P <0.01). A gaseous adduct was formed in the reaction between pure AlP and boric acid. These findings indicate that boric acid may be an efficient and non-toxic antidote for PH3 poisoning.