Intravascular haemolysis due to glucose-6-phosphate dehydrogenase deficiency in a patient with aluminium phosphide poisoning

Srinivas, Radhika; Agarwal, Ritesh; Jairam, A; Sakhuja, Vinay

doi:10.1136/emj.2006.040097

Cited by 15 publications

(11 citation statements)

References 3 publications

(5 reference statements)

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“…This case raised our attention to the possibility of the development of disseminated intravascular coagulopathy (DIC) as recorded in previous studies [39,42,46,[50][51][52]. Proudfoot in 2009 [39] attributed its occurrence to the highly toxic phosphine gas not to the metal phosphides.…”

Section: Discussionmentioning

confidence: 60%

Zinc phosphide toxicity with a trial of tranexamic acid in its management

Naggar

Mahdy

2011

Journal of Advanced Research

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Zinc phosphide is a highly effective rodenticide used widely to protect grain in stores and domestically to kill rodents. Acute poisoning may be direct by ingestion or indirect through accidental inhalation of phosphine gas generated during its use. This study aims to identify the patterns of intoxication with zinc phosphide among Egyptian patients admitted to the National Egyptian Center of Clinical and Environmental Toxicological Research (NECTR); to study the role of antifibrinolytics in management of zinc phosphide toxicity; and to publish the results of the study, which include recommendations for action towards planning prevention and education programs. The study provides descriptive data and analysis of 188 cases admitted to the NECTR with acute zinc phosphide poisoning over a period of 22 months. Results show that poisoning is more common among females (60.6% of cases) than males (39.4%); the mean age is nearly 21 years old. The most common cause of poisoning is suicidal attempts (83.6%) followed by accidental exposure (16.4%). The most common causative factors that lead to self-poisoning are marital disharmony, economic hardship, social problems and scolding from other family members. Signs and symptoms of toxicity include gastrointestinal disturbances, respiratory compromise and changes in mental status. Other features include disseminated intravascular coagulation, hepatic and renal impairment. Metabolic disturbances had been reported. Death can result immediately due to pulmonary edema or delayed due to cardiotoxicity. Patients must be admitted to hospital and observed for at least 3 days. Symptomatic and supportive care is the mainstay of therapy. Zinc phosphide poisoning requires gastric lavage with excessive sodium bicarbonate solution. Tranexamic acid -an antifibrinolytic

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Section: Discussionmentioning

confidence: 60%

Zinc phosphide toxicity with a trial of tranexamic acid in its management

Naggar

Mahdy

2011

Journal of Advanced Research

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“…Recurrent vomiting and epigastric distress, cardiac arrhythmias, and electrocardiographic abnormalities, acute respiratory failure, hepatic damage, bleeding diathesis, acute tubular necrosis, and acute pericarditis are the main manifestations of AlP intoxication [8]. Although it is not common, intravascular hemolysis following AlP intoxication has been reported in the setting of glucose-6-phosphate dehydrogenase (G-6-PD) deficiency [11,12] as well as individuals with normal level of G-6-PD [8] which indicates oxidizing properties of AlP. In fact, the agent can oxidize hemoglobin protein, precipitate the oxidized protein as Heinz bodies, and finally result in intravascular hemolysis [7].…”

Section: Discussionmentioning

confidence: 99%

Blood Levels of Methemoglobin in Patients with Aluminum Phosphide Poisoning and its Correlation with Patient’s Outcome

et al. 2010

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“…Uncommon and rare complications of phosphide poisoning include gastroduodenitis, hepatitis, delayed esophageal stricture, acute tubular necrosis, methemoglobinemia and hemolysis (Lakshmi, 2002;. To the best of recent knowledge, only few cases of phosphide poisoning presented with intravascular hemolysis; two of them had glucose 6 phosphate dehydrogenase (G-6-PD) enzyme deficiency (Sood et al, 1997;Srinivas et al, 2007) and the other were with normal G-6-PD enzyme level (Aggarwal et al, 1999;Lakshmi, 2002;. In addition, methemoglobinemia was recorded in only few cases of phosphide poisoning (Lakshmi, 2002;Lall et al, 2000;Soltaninejad et al, 2011)and there is only one study regarding blood level of methemoglobin (Met-Hb) after phosphide poisoning (Mostafazadeh et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Methemoglobinemia and Intravascular Hemolysis; Unusual Presentations of Metal Phosphides Poisoning

Wahdan

Elmadah

2016

Ain Shams Journal of Forensic Medicine and Clinical Toxicology

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Introduction: Metal phosphides are highly effective insecticides and rodenticide. They are used as a cheap and effective rodenticide in developing countries. Hemolysis and methemoglobinemia are rare but reported complications of phosphide poisoning Aim of the work: The aim of this study was to detect the incidence of methemoglobinemia and intravascular hemolysis in some cases of acute phosphide poisoning. Patients and methods: A cross sectional study was conducted on 50 cases suffering from acute metal phosphide poisoning admitted to Tanta toxicology unit, from the start of October 2014 till the end of March 2015. For each case, the following were done: history taking, physical examination and laboratory investigations (including measurement of methemoglobin (Met-Hb) level, arterial blood gas analysis, routine investigations, lactate dehydrogenase enzyme and complete blood picture with reticulocytic count). Results: Eight cases (16%) had combined methemoglobinemia and hemolysis. Aluminum phosphide was the toxic agent in seven of them and zinc phosphide in only one. Three cases (6%) had methemoglobinemia alone; one of them was poisoned by aluminum phosphide and the other two by zinc phospide. Another three cases had hemolysis alone; one of them was due to aluminum phosphide toxicity and the other two were due to zinc phospidetoxicity. So the present study included a total of eleven cases (22%) of methemoglobinemia. Their median age was 27 years old, while it was 24 years for patients with normal Met-Hb level. The median delay time was 4 hours for them and 2 hours for cases with normal Met-Hb level with significant statistical differences between both. The mean Met-Hb level was 14.45 ± 9.32% and1.63 ± 0.45% in cases with high and normal Met-Hb level respectively, with a significant statistical difference between both. Furthermore, the mean oxygen saturation showed a significant statistical difference between both. In addition, the present study included a total of eleven cases (22%) of hemolysis. Their median age was 27 years old, while it was 24 years for patients with no hemolysis. The median delay time was 3 hours in them and 2 hours in cases with no hemolysis. Conclusion: It was concluded that methemoglobinemia and hemolysis can complicate the course of acute phosphide poisoning. Recommendations: Further studies on a large scale of cases of acute phosphide poisoning with assessment of the outcome of cases presented with methemoglobinemia and hemolysis and the efficacy of the available treatment for such cases are recommended. Furthermore, it is important that health care professionals be aware of these rare presentations of phosphide poisoning.

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Intravascular haemolysis due to glucose-6-phosphate dehydrogenase deficiency in a patient with aluminium phosphide poisoning

Cited by 15 publications

References 3 publications

Zinc phosphide toxicity with a trial of tranexamic acid in its management

Zinc phosphide toxicity with a trial of tranexamic acid in its management

Blood Levels of Methemoglobin in Patients with Aluminum Phosphide Poisoning and its Correlation with Patient’s Outcome

Methemoglobinemia and Intravascular Hemolysis; Unusual Presentations of Metal Phosphides Poisoning

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