Fatal aluminium phosphide poisoning

Abstract

surface required for assembly of the platelet-bound coagulation enzymes, and the production of enough thrombin to cause substantial fibrin formation. Plateletderived micro-particles such as P-selectin, which are formed during the process provide a mechanistic route for amplifying thrombus formation on a thrombogenic surface [4,7].Leukocyte activation (CD11b upregulation) also occurs within minutes leading to adhesion while tissue factor expression occurs over hours. Complement activation occurs at all these time scales [3].Researchers should be aware that the choice of the storage tube can influence TEG s variables. The advice is that reference intervals for TEG s variables be established, and this is likely to be specific for the nature of the tube used. The values for r and MA obtained during this study fell within the references ranges for our own analyser for citrated samples.Our results suggest that glass is a more potent surface for activation of the coagulation cascade than plastic. This is reflected in lower r values and greater MA values for glass tubes when compared to plastic tubes.In conclusion, both glass and plastic tubes show no significant effect between 45 min and 4 h. Glass tubes are associated with shorter r values and higher MA when compared with plastic tubes. References 1. Willschke H, Bräunlich P, Zimpfer M, Varady S, Kozek S. Prevention of storage-induced clot strength reductions. Eur J Anaesthesiol 2001; A207. 2. Camenzind V, Bombeli T, Seifert B et al. Citrate storage affects Thromboelastograph s Analysis. Anesthesiology 2000; 92: 1242-1249. 3. Gorbet M, Sefton M. Biomaterial-associated thrombosis: roles of coagulation factors, complement, platelets and leukocytes. Biomaterials 2004; 25(26): 5681-5703. 4. Siedlecki CA, Wang IW, Higashi JM, Kottke-Marchant K, Marchant RE. Platelet-derived microparticles on synthetic surfaces observed by atomic force microscopy and fluorescence microscopy. Biomaterials 1999; 20(16): 1521-1529. 5. Otto M, Franzen A, Hansen T, Kirkpatrick CJ. Modification of human platelet adhesion on biomaterial surfaces by protein preadsorption under static and flow conditions. J Mater Sci -Mater Med 2004; 15(1): 35-42. 6. Gemmell CH. Assessment of material-induced procoagulant activity by a modified viper venom coagulation time test.EDITOR: Aluminium phosphide is used to control rodents and pests in grain-storage facilities. When aluminium phosphide comes into contact with water, it releases large quantities of phosphine (PH 3 ), a very toxic gas and a mitochondrial poison. We present a case report of suspected inhalation exposure to phosphine gas in a manufacturing facility for aluminium phosphide fumigants. Case reportA 45-yr-old male was admitted to the hospital with a history of severe diarrhoea, nausea and vomiting for 3 days. He was treated with intravenous saline without improvement and his clinical picture deteriorated with the appearance of dyspnoea. His symptoms had started soon after he had used an insecticide (Fosguard which contains phosphine) to clean a smal...

A Systematic Review of Aluminium Phosphide Poisoning

“…Jaundice can even be a manifestation of another disturbances such as intravascular haemolysis (29). A more common fi nding is transient elevation of serum aspartate and alanine aminotransferase (40)(41)(42)(43). The main histopathological fi ndings in the liver at autopsy of fatal phosphine poisoning include cytoplasmic vacuolisation of hepatocytes and sinusoidal congestion.…”

Phosphine inhalation, case series of domestic unintentional poisoning commonly used as anti-bed bug chemical from a low income country

“…15,16 The initial toxicity of phosphine poisoning may be nonspecific and transient; however in severe exposure patients develop metabolic acidosis, cardiovascular collapse, oliguria, and proteinuria eventually leading to anuria, which may require hemodialysis. 7 Phosphine (Aluminum phosphide) in low doses has the potential to cause headache, dizziness, numbness, general fatigue, breathing difficulties (tightness around the chest, pain in the region of the diaphragm and cough) and gastrointestinal disturbances (pain, nausea, vomiting and diarrhea) while victims of chronic exposure exhibit lung irritation, persistent coughing, tremors and convulsions eventually leading to pulmonary edema, myocardial injury, kidney damage and coma. The cause of death varies from usually within the first few hours to up to two weeks in the case of liver failure or cardiovascular failure.…”

Aluminium Phosphide Poisoning

“…Recurring locations include ships holds (Gregorakos, et al, 2002, Hansen & Pedersen, 2001, Vohra, et al, 2006, rail wagons (Perotta, et al 1994, Vohra, et al, 2006, grain elevators (Abder-Rahman, et al, 2000), grain stores (Brautbar & Howard, 2002, Misra, et al, 1988, and even stores in homes (Abder-Rahman, et al, 2000). Potentially lethal concentrations of the gas may develop in the head-spaces of unventilated or poorly ventilated storage containers and domestic premises (Memis, et al, 2007). Phosphine may be released during the illicit manufacture of methamphetamine (Burgess, 2001, Willers-Russo, 1999; deaths have resulted (Willers-Russo, 1999).…”

“…Transient elevations of alanine aminotransferase and aspartate aminotransferase activities are not infrequent after ingestion of metal phosphides (Frangides & Pneumatikos, 2002;Memis, et al, 2007) but jaundice secondary to liver damage (Chugh, et al, 1998) is much less common. It was present in 12 out of 92 cases and was said to be common in another series of 15 patients (Singh, et al, 1985) but confirmatory laboratory data were not provided.…”

“…Two others had no history to suggest this possible predisposing disorder Lakshmi, 2002) and in the remaining four the issue was not addressed . Intravascular hemolysis was associated with renal failure and severe metabolic acidosis to which 3 days of vomiting and diarrhea may have partly contributed (Memis, et al, 2007). In addition to hemolysis one man was found to have methemoglobinaemia of 17% 32 h post-ingestion (Lakshmi, 2002) while another developed Heinz bodies (Srinivas, et al, 2007), a further indicator of damage to hemoglobin.…”