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      Thoughts on the current management of acute aluminum phosphide toxicity and proposals for therapy: An Evidence-based review

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          Abstract

          The majority of aluminum phosphide (ALP) toxicity cases are suicidal attempts. Despite advances in critical care medicine, the mortality rate of ALP remains very high. Unfortunately, knowledge on the toxicokinetics of ALP is very low. An obsolete idea was proposed that inhibition of complex IV of cytochrome C oxidase is responsible for multiorgan dysfunction. However, based on human studies, this effect might be insignificant. Thus, a novel idea proposes that the main mechanism might be vascular wall integrity disruption. The low frequency of acute toxicity and unanswered questions about the toxicokinetics and toxicodynamics has led to leaden advances of novel treatments. The aim of this review was to evaluate problems regarding current treatment protocols and propose new ideas based on updated information. For this purpose, we reviewed all available articles on the management of ALP poisoning published to date. Considering failure of conventional therapies on maintaining systolic blood pressure, correcting acid-base disturbances, and support cardiac function, the previous treatment protocols have been overruled. However, repudiate of conventional treatments in this deadly condition is not without penalties for the health-care provider. The introduction of new therapies including refuse of gastric lavage with water-soluble compounds, administration of a high molecular weight colloidal solution for fluid resuscitation and termination using sodium bicarbonate, and vasoactive agents has been prospected to improve patient survival. This protocol is in early clinical evaluation; nevertheless, it appears to improve patient's survival; hence, future randomized trials should be performed to support their effectiveness.

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          Most cited references 77

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          Aluminium and zinc phosphide poisoning.

          Aluminium and zinc phosphides are highly effective insecticides and rodenticides and are used widely to protect grain in stores and during its transportation. Acute poisoning with these compounds may be direct due to ingestion of the salts or indirect from accidental inhalation of phosphine generated during their approved use. Both forms of poisoning are mediated by phosphine which has been thought to be toxic because it inhibits cytochrome c oxidase. While phosphine does inhibit cytochrome C oxidase in vitro, the inhibition is much less in vivo. It has been shown recently in nematodes that phosphine rapidly perturbs mitochondrial morphology, inhibits oxidative respiration by 70%, and causes a severe drop in mitochondrial membrane potential. This failure of cellular respiration is likely to be due to a mechanism other than inhibition of cytochrome C oxidase. In addition, phosphine and hydrogen peroxide can interact to form the highly reactive hydroxyl radical and phosphine also inhibits catalase and peroxidase; both mechanisms result in hydroxyl radical associated damage such as lipid peroxidation. The major lethal consequence of phosphide ingestion, profound circulatory collapse, is secondary to factors including direct effects on cardiac myocytes, fluid loss, and adrenal gland damage. In addition, phosphine and phosphides have corrosive actions. There is usually only a short interval between ingestion of phosphides and the appearance of systemic toxicity. Phosphine-induced impairment of myocardial contractility and fluid loss leads to circulatory failure, and critically, pulmonary edema supervenes, though whether this is a cardiogenic or non-cardiogenic is not always clear. Metabolic acidosis, or mixed metabolic acidosis and respiratory alkalosis, and acute renal failure are frequent. Other features include disseminated intravascular coagulation, hepatic necrosis and renal failure. There is conflicting evidence on the occurrence of magnesium disturbances. There is no antidote to phosphine or metal phosphide poisoning and many patients die despite intensive care. Supportive measures are all that can be offered and should be implemented as required.
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            A systematic review of aluminium phosphide poisoning.

            Every year, about 300,000 people die because of pesticide poisoning worldwide. The most common pesticide agents are organophosphates and phosphides, aluminium phosphide (AlP) in particular. AlP is known as a suicide poison that can easily be bought and has no effective antidote. Its toxicity results from the release of phosphine gas as the tablet gets into contact with moisture. Phosphine gas primarily affects the heart, lungs, gastrointestinal tract, and kidneys. Poisoning signs and symptoms include nausea, vomiting, restlessness, abdominal pain, palpitation, refractory shock, cardiac arrhythmias, pulmonary oedema, dyspnoea, cyanosis, and sensory alterations. Diagnosis is based on clinical suspicion, positive silver nitrate paper test to phosphine, and gastric aspirate and viscera biochemistry. Treatment includes early gastric lavage with potassium permanganate or a combination with coconut oil and sodium bicarbonate, administration of charcoal, and palliative care. Specific therapy includes intravenous magnesium sulphate and oral coconut oil. Moreover, acidosis can be treated with early intravenous administration of sodium bicarbonate, cardiogenic shock with fluid, vasopresor, and refractory cardiogenic shock with intra-aortic baloon pump or digoxin. Trimetazidine may also have a useful role in the treatment, because it can stop ventricular ectopic beats and bigeminy and preserve oxidative metabolism. This article reviews the epidemiological, toxicological, and clinical/pathological aspects of AlP poisoning and its management.
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              Successful treatment of acute aluminium phosphide poisoning: possible benefit of coconut oil.

              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.
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                Author and article information

                Journal
                Indian J Crit Care Med
                Indian J Crit Care Med
                IJCCM
                Indian Journal of Critical Care Medicine : Peer-reviewed, Official Publication of Indian Society of Critical Care Medicine
                Medknow Publications & Media Pvt Ltd (India )
                0972-5229
                1998-359X
                December 2016
                : 20
                : 12
                : 724-730
                Affiliations
                From: Department of Forensic Medicine and Clinical Toxicology, AJA Medical School, AJA University of Medical Sciences, Tehran, Iran
                [1 ]Department of Forensic Medicine, Sabzevar University of Medical Sciences, Sabzevar, Iran
                [2 ]Department of Forensic Medicine and Clinical Toxicology, Shiraz University of Medical Sciences, Shiraz, Iran
                Author notes
                Correspondence: Dr. Sayed Mahdi Marashi, Trauma Research Center, Emergency Room, Division of Medical Toxicology, Hazrat Ali Asghar (p) Hospital, Meshkinfam Street, Shiraz 7143918796, Iran. E-mail: marashi@ 123456sums.ac.ir
                Article
                IJCCM-20-724
                10.4103/0972-5229.195712
                5225774
                Copyright: © Indian Journal of Critical Care Medicine

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

                Categories
                Review Article

                Emergency medicine & Trauma

                toxicity, phosphine, new therapies, aluminum phosphide

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