Abbas Aghabiklooei, Shahin Shadnia, Hossein Hassanian-Moghaddam and Nasim Zamani
Acute respiratory distress syndrome (ARDS) due to methadone (MTD) toxicity is a known but rather uncommon phenomenon. In most of the previously reported cases of MTD-related ARDS, MTD was ingested orally in the form of tablets in high or unknown amounts. Despite the findings from the available literature, this case report is aimed at demonstrating that even small amounts of MTD syrup can cause ARDS earlier than it is usually expected. We present a non-addicted MTD-overdosed patient who developed ARDS after ingesting a very small amount of MTD syrup. We suggest close monitoring of MTD-overdosed patients from at least 48 h to 72 h for possible respiratory complications such as pulmonary oedema.
Omid Mehrpour, Mostafa Jafarzadeh and Mohammad Abdollahi
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.
Fumonisin B1 (FB1) is a mycotoxin produced by Fusarium spp. moulds that contaminate crop, predominantly maize, all around the world. More than 15 types of fumonisins have been indentified so far, but FB1 is the most abundant and toxicologically the most significant one. FB1 has a wide range of toxic effects, depending on animal species. In horses FB1 causes equine leukoencephalomalacia (ELEM), in pigs pulmonary oedema and in experimental rodents nephrotoxicity and hepatotoxicity. In humans exposure to FB1 is linked with higher incidence of primary liver cancer and oesophageal cancer, which are frequent in certain regions of the world (such as Transkei region in South Africa) where maize is staple food. The occurrence of neural tube defect in children in some countries of Central America (such as Mexico and Honduras) is connected with the consumption of FB1-contaminated maize-based food. However, possible involvement of FB1 in the development of human diseases is not clear. Nevertheless, the International Agency for Research on Cancer (IARC) has classified FB1 as a possible carcinogen to humans (group 2B).
FB1 is a causative agent of ELEM, a brain disorder in equines, indicating that brain is a target organ of FB1 toxicity. Several studies on experimental animals or on cell cultures of neural origin have established that FB1 has a neurodegenerative potential, although the mechanism of its neurotoxicity is still vague. The aim of this article is to give an overview of available literature on FB1 neurotoxicity and involved mechanisms, and to offer a new perspective for future studies.