Methemoglobinemia in aluminum phosphide poisoning

2010 ◽  
Vol 30 (3) ◽  
pp. 250-253 ◽  
Author(s):  
Shahin Shadnia ◽  
Kambiz Soltaninejad ◽  
Hossein Hassan ian-Moghadam ◽  
Anahaita Sadeghi ◽  
Hormat Rahimzadeh ◽  
...  

Introduction. Acute aluminum phosphide (AlP) poisoning is one of the most common causes of acute pesticide poisoning in Iran. Hydrogen phosphide or phosphine gas is produced following reaction of AlP with water even at ambient humidity. Methemoglobinemia is a rare finding following phosphine poisoning. In this paper, two cases of fatal AlP poisoning complicated by methemoglobinemia are reported. Case Report. Two patients presented following suicidal ingestion of AlP tablets. In the Emergency Department (ED), they received gastric lavage with sodium bicarbonate and potassium permanganate. Both of them received supportive care. In each case, hematuria and hemolysis were significant events. The patients also showed a decrease in O2 saturation in spite of high FIO2. Methemoglobin levels of 40% and 30% were detected by co-oximetry. Neither patient responded to treatment (ascorbic acid in one case, methylene blue in the other). Both patients died due to systemic effects of phosphine poisoning. Discussion and conclusion. Hemolysis and methemoglobinemia may complicate the course of phosphine poisoning that seems resistant to methylene blue and ascorbic acid. Therefore, other treatments including hyperbaric oxygen therapy and exchange blood transfusion should be considered.

2017 ◽  
Vol 37 (2) ◽  
pp. 107-117 ◽  
Author(s):  
MH Goharbari ◽  
F Taghaddosinejad ◽  
M Arefi ◽  
M Sharifzadeh ◽  
M Mojtahedzadeh ◽  
...  

Background: 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. Objective: The purpose of this study was to evaluate the effect of oral liothyronine in the treatment of AlP poisoning. Methods: 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. Results: 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. Conclusion: Liothyronine administration is effective in controlling AlP poisoning and can improve patients’ outcome.


2013 ◽  
Vol 20 (06) ◽  
pp. 855-863
Author(s):  
MUHAMMAD A. GHAZI,

Purpose: The number of deaths due to wheat pill poisoning is enormous and despite aggressive management only a fewpatients survive the fatal effects of the wheat pill poison. Despite the growing number of patients appearing in the emergency departmentswith this easily available poison in the market, very little effort has been put forth to study the subject scientifically and to prevent theongoing loss of precious lives. This is a narrative review of the wheat pill poisoning, highlighting the important steps in diagnosis andmanagement. Methods: Data sources include Pubmed, Scopus, Medline (1996 to date), Cochrane library and Google scholar. Weincluded all clinical trials, systematic reviews and ongoing cohort studies. Conclusions: Wheat pill (Aluminum Phosphide) poisoning is alethal toxin and its effective treatment requires prompt diagnosis and early, time-efficient management. Early transfer to a healthcarefacility, good resuscitation, diagnosis, monitoring, gastric lavage and supportive therapy are the hallmarks of management and may resultin improved outcomes. The governmental and legislative authorities must take appropriate steps towards limiting its availability at thegrass-roots level. Aluminum Phosphide poisoning must be a part of the medical students’ curriculum and long-term, well-designedcomprehensive research studies are required to discover new modalities of treatment.


2016 ◽  
Vol 5 (11) ◽  
pp. 5041
Author(s):  
Farkhondeh Jamshidi ◽  
Ahmad Ghorbani ◽  
Sina Darvishi*

The abuse of some pesticides especially to suicide is one of the current problems of pesticides. Aluminum phosphide induced poisoning usually happens to suicide and sometimes it is due to accidental occupational exposure and in a few cases it has some criminal intensions. This study is conducted to evaluate patients poisoned with aluminum phosphide. In the present study the medical records of cases of poisoning with rice tablets (aluminum phosphide) hospitalized in Ahvaz Razi hospital is studied. Accordingly, a checklist is prepared that included demographic information of patients (age, gender) and information on patient records (information on poisoning) are completed using the patients’ medical records. The analysis of data is done by SPSS V22. 18 patients poisoned with rice tablet (aluminum phosphide) are studied. Results of the study show that 11 patients are male and seven are female. The mean patient age is 27.06 ±8.04 years that is 28 ±9 and 25 ±6.02 in men and women respectively. Statistical tests show no statistically significant difference in mean age in both genders (P> 0.05). Among patients, 11 subjects took aluminum phosphide to attempt suicide and 3 cases took it unintentionally and of course the reason is not mentioned in four cases. Among the patients who tried to commit suicide by taking aluminum phosphide, 6 cases are male and 5 cases are female that no statistically significant difference is observed between the genders in this respect (P> 0.05). In addition to the study of the complications caused by this poisoning and its mortality, it is recommended to responsible authorities to provide the necessary educations and treatments to prevent this type of poisoning.


Author(s):  
Deepak Yadav ◽  
Rajasri Bhattacharyya ◽  
Dibyajyoti Banerjee

2018 ◽  
Vol 5 ◽  
pp. 1053-1059 ◽  
Author(s):  
Asieh Karimani ◽  
Amir Hooshang Mohammadpour ◽  
Mohammad Reza Zirak ◽  
Ramin Rezaee ◽  
Bruno Megarbane ◽  
...  

1994 ◽  
Vol 28 (5) ◽  
pp. 643-649 ◽  
Author(s):  
Luis F. Rodriguez ◽  
Lynn M. Smolik ◽  
Alicia J. Zbehlik

OBJECTIVE: To report a case of benzocaine-induced inethemoglobinemia and present a review of the related literature. CASE REPORT: An 83-year-old man received benzocaine topical anesthesia 600 mg prior to intubation for resection of a thyroid adenoma. The patient became severely cyanotic after induction of anesthesia. After a negative workup for common causes of cyanosis, blood co-oximetry analysis revealed a methemoglobin concentration of 54.1 percent. Intravenous methylene blue reversed the methemoglobinemia, although delayed recurrence 20 h later necessitated readministration of intravenous methylene blue. The patient developed cardiovascular instability and severe neurologic depression requiring prolonged ventilatory support. DISCUSSION: Methemoglobinemia can result from exposure to a number of drugs including benzocaine. Cyanosis, neurological and cardiac dysfunction may result when methemoglobin concentrations exceed 30 percent. Clinical diagnosis is made on the presentation of cyanosis unresponsive to oxygen administration and a distinctive arterial blood brown color; laboratory confirmation is by co-oximetry. Treatment of symptomatic methemoglobinemia is by intravenous methylene blue (1–2 mg/kg) administration. Fifty-four cases of benzocaine-induced methemoglobinemia have been reported in the literature. Intubation, endoscopy/bronchoscopy, and ingestion were the most common procedures in which benzocaine administration produced methemoglobinemia. Infants and the elderly were more likely to develop toxic methemoglobinemia after benzocaine exposure. Other risk factors included genetic reductase deficiencies, exposure to high doses of anesthetic, and presence of denuded skin and mucous membranes. CONCLUSIONS: Because of the potential for severe complications, methemoglobinemia should be corrected promptly in compromised patients and those with toxic benzocaine concentrations. The possibility of masking symptoms during general anesthesia carries special risk of use of this agent in the preanesthesia setting.


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