|Year : 2018 | Volume
| Issue : 3 | Page : 816-821
Metal phosphide poisoning in Menoufia University Hospitals
Samy M Badawi1, Amira M Alseidy1, Ahmed K Alfeki1, Magda Mansour2, Amira Abd El-Hamid1
1 Department of Forensic Medicine and Clinical Toxicology, Faculty of Medicine, Menoufia University, Shebeen El-Kom, Egypt
2 Department of Histology, Faculty of Medicine, Menoufia University, Shebeen El-Kom, Egypt
|Date of Submission||14-Jan-2018|
|Date of Acceptance||03-Mar-2018|
|Date of Web Publication||31-Dec-2018|
Amira Abd El-Hamid
Source of Support: None, Conflict of Interest: None
To assess the pattern, severity, and outcome of metal phosphide poisoning cases admitted to Menoufia University Poison and Dependence Control Center (MPCC).
Over the past years, the consumption of metal phosphide rodenticide has been increasing, causing severe morbidity and elevated mortality. It was the first cause of death in poisoning cases admitted to MPCC during the past 2 years. On phosphides contact with moisture or acids, liberation of phosphine gas leads to widespread organ damage. Phosphine blocks the enzyme cytochrome C oxidase, as a result of which mitochondrial oxidative phosphorylation is inhibited. It also denatures many enzymes involved in cellular respiration and metabolism.
Patients and methods
A prospective study was conducted on 80 patients with acute zinc and aluminum phosphide (ALP) poisoning who were admitted to MPCC, during the period from the first of September 2015 to the end of February 2016.
A significant relation was found between zinc phosphide, time passed since exposure, and complaint on arrival (P = 0.04), and a nonsignificant relation between ALP, time passed since exposure, and complaint on arrival was detected (P = 0.1). Highly significant relation was noticed between type of phosphide and both echocardiography and poison severity score (P < 0.001). Relation between type of phosphide and outcome of cases was highly significant.
Metal phosphide compounds cause very serious manifestations to exposed humans with high mortality, which is especially pronounced in ALP poisoned cases.
Keywords: blood pressure, echocardiography, metal phosphide, phosphine gas
|How to cite this article:|
Badawi SM, Alseidy AM, Alfeki AK, Mansour M, Abd El-Hamid A. Metal phosphide poisoning in Menoufia University Hospitals. Menoufia Med J 2018;31:816-21
|How to cite this URL:|
Badawi SM, Alseidy AM, Alfeki AK, Mansour M, Abd El-Hamid A. Metal phosphide poisoning in Menoufia University Hospitals. Menoufia Med J [serial online] 2018 [cited 2019 Jan 20];31:816-21. Available from: http://www.mmj.eg.net/text.asp?2018/31/3/816/248711
| Introduction|| |
Consumption of metal phosphides in the form of rodenticide, insecticide, and fumigant has been increasing over the past years. Morbidity and mortality rates of these compounds are elevated. It is preferred because it does not affect seed viability, is cost effective, and leaves little residue in the food. Phosphide poisoning was one of the most common causes of acute poisoning cases presented to Menoufia University Poison and Dependence Control Center (MPCC) during the past 2 years and the first cause of death in poisoning cases. Aluminum phosphide (ALP), calcium phosphide, magnesium phosphide, and zinc phosphide are the types available. ALP is present in the form of tablets, whereas zinc phosphide is a black powder. Upon phosphides contact with moisture or acids, liberation of phosphine gas leads to widespread organ damage. Phosphine blocks the enzyme cytochrome C oxidase as a result of which mitochondrial oxidative phosphorylation is inhibited. It also denatures many enzymes involved in cellular respiration and metabolism. Moreover, phosphine converts oxyhemoglobin to methemoglobin and hemi-chrome species, so oxyhemoglobin level in blood declines. Metal phosphides and phosphine gas have corrosive effects. They lead to free radical formation and acceleration of lipid peroxidation, which result in damage of cell membrane, disruption of ionic barrier, nucleic acid damage, and finally cell death. The manifestations of toxicity depend on type of phosphide, the dose, route of entry, and time elapsed since exposure. Garlic odor in mouth or breath, nausea, and vomiting may appear within few minutes. Cardiac arrhythmias, hypotension, and refractory hypovolemic shock are also present owing to massive intravascular fluid loss because of insufficient vascular wall integrity. Pulmonary edema, coma, metabolic acidosis, and electrolyte disturbance are frequently found. The mortality rates of acute ALP poisoning vary from 40 to 80%, whereas zinc phosphide mortality rates vary from 3 to 25%. The most common cause of death in phosphide poisoning is cardiogenic shock. Diagnosis of cases can be achieved by history of exposure to metal phosphides, manifestations, investigations like silver nitrate test, and routine investigations. Treatment may be approached according to the stability of the case and manifestations.
The aim of this study was to assess the pattern, severity, and outcome of metal phosphide poisoning cases admitted to MPCC.
| Patients and Methods|| |
The study was approved by Menoufia University Ethical Committee. It is a prospective clinical study that was carried on 80 cases with acute zinc or ALP poisoning of both sexes and of different age groups who were admitted to MPCC during the period from the first of September 2015 to the end of February 2016. Informed valid consent was taken before the study. Exclusion criteria were cases having cardiovascular, renal, and hepatic diseases and concomitant exposure to another poison. Special sheet was designed to be fulfilled for every patient, which includes sociodemographic data; intoxication data that include type of phosphide poison, amount taken, and time elapsed since intake; data regarding clinical assessment; and clinical poison severity score according to the method described by Person et al.. Investigations like measurement of cholinesterase activity in serum and silver nitrate test in gastric content were done for all studied cases. ECG and echocardiography (Echo) were done when indicated. Moreover, data related to outcome were recorded.
The statistical analysis of data was done using Excel and statistical package for the social science programs (SPSS, version 19) from IBM Company (New York, New York, USA), on personal computer. The description of the data was done in the form of mean and SD for quantitative data, whereas frequency distribution and percentage for qualitative data. Analysis of the data was done to test statistical significance difference between groups. Moreover, χ2-test was used for categorical variables. P value less than 0.05 was considered statistically significant.
| Results|| |
The total number of studied cases was 80 patients. Age stratification showed that the age group 11–20 years old had the highest incidence at 45% among all patients followed by age group 21–30, which represented 28.75%. Among the studied cases, 33 (41.25%) were males and 47 (58.75%) were females, with male to female ratio of 1: 1.42. More than three-quarters (77.5%) of cases were from rural areas. Regarding the marital status, 56.25% of cases were single and 28.75% were married, whereas children represented 15%. Civil employees topped the list, representing 42.5%, followed by nonworkers (18.75%) and students (15%). Secondary education was found in 42.5% of cases followed by those who had higher education (18.75%) and illiterates (15%) [Table 1].
|Table 1: Distribution of phosphide poisoning cases regarding sex, age, residence, marital status, occupation, and education (n=80)|
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Spontaneous vomiting represented 37.5% of cases, whereas 27.5% of cases had no manifestations. Induced vomiting represented 18.75% of cases, and cases experiencing spontaneous vomiting and abdominal pain constituted 17.5%. Relation between poison severity score (PSS) and complaint at arrival was significant (P = 0.03) [Table 2].
|Table 2: Relation between poison severity score and clinical manifestations of studied cases (n=80)|
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The results illustrated that 66.7% of ALP arrived between 2 and 6 h and had experienced spontaneous vomiting, no manifestations, and spontaneous vomiting and abdominal pain, representing 26.6, 20, and 20%, respectively. The rest of the patients (33.3%) arrived in less than 2 h and complained of spontaneous vomiting and spontaneous vomiting and abdominal pain. Meanwhile, 13.8% of zinc phosphide cases that came in less than 2 h had no manifestations followed by 7.7% who experienced spontaneous vomiting. Regarding cases that came between 2 and 6 h, 15.5% had no manifestations, followed by 6.2% who had induced vomiting. All patients who arrived after 6 h had manifestations divided between spontaneous vomiting and spontaneous vomiting and abdominal pain, representing 23 and 4.7%, respectively. Relation between type of phosphide, time passed since exposure, and manifestations on arrival was nonsignificant (P = 0.1) in ALP poisoning and significant (P = 0.04) in zinc phosphide poisoning [Table 3].
|Table 3: Relation between the time elapsed since intake of phosphides and type of phosphide regarding the clinical manifestations on arrival (n=80)|
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The results revealed that severe grade of PSS was 62.5% in cases of ALP toxicity, whereas zinc phosphide cases represented the highest percent in minor grade PSS, which was 89.4%. Moderate grade of PSS was the same in both types of phosphide poisoning. Relation between type of phosphide and PSS was highly significant (P < 0.001). Echo was performed in all cases of ALP and in zinc phosphide patients when indicated. The results showed that 90% of patients who had hypokinesia and decreased ejection fraction were poisoned by ALP. A highly significant relation between type of phosphide and Echo changes was found, with P value less than 0.001 [Table 4].
|Table 4: Relation of type of phosphide to poison severity score and echocardiography changes|
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Suicidal mode in this study was the most prevalent (71.25%), followed by accidental cases that represented 28.75%. Suicidal ingestion was the most common mode in all age groups except age group 0–10 which was accidental. The highest percentage of suicide incidents (35%) was in age group 11–20 years old, whereas accidental mode was the most common (13.75%) in age group 0–10 years old, and relation between age and mode of phosphides poisoning was significant (P = 0.03).
Suicidal mode was higher in females, representing 46.25% of cases, whereas accidental mode was higher in males (16.25%). The relation between sex and mode of poisoning was highly significant (P < 0.001). Suicidal mode was the most common mode of poisoning in either rural (56.25%) or urban (15%) areas. Relation between mode of poisoning and residence was significant (P = 0.02). Cases that had family troubles or emotional troubles had the highest suicidal mode, representing 61.25% each [Figure 1].
|Figure 1: Column chart showing relation between mode of phosphide poisoning and age, sex, residence, family, and emotional troubles.|
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Zinc phosphide poisoning represented ∼81.25% of cases, whereas ALP poisoning was present in 18.75% of poisoned cases. Relation between the type of phosphide and the outcome was highly significant (P < 0.001). The total number of dead cases was eight patients: five were poisoned with ALP and three had zinc phosphide toxicity. ALP poisoning was found to be more associated with death as 62.5% of dead patients were poisoned by ALP, meanwhile 84.4% of improved cases were poisoned with zinc phosphide [Figure 2].
| Discussion|| |
Many studies in different parts of the world had been done on phosphide poisoning. In Egypt, Halawa et al. mentioned that ∼0.01% of cases in Poison Control Center, Ain Shams University Hospitals, in 2012 were zinc phosphide poisoning.
The present study showed that age groups 11–20 years old and 21–30 years old were more affected, as they are more susceptible to socioeconomic stress and depression, so become more vulnerable to commit suicide. They also may have conflict with other family members or friends and emotional problems. In a study conducted in Iran, it was found that distribution of age group, sex, and mode of exposure results were coincident with the present study results. The high percent of suicide could be explained on the ground of sex tendency and socioeconomic factors as well as availability of ALP in the household. However, these do not coincide with the results of Kanchan and Ritesh who found that male: female was 2.8: 1 in India. The present study illustrated that percent of patients in secondary education was high, and this can be explained by their age, as they face more stress owing to learning difficulties, conflicts with family members and friends, and love affairs, so become more vulnerable to commit suicide. These results coincide with the results of Shokrzadeh et al. who found that 51.55 and 20.95% of cases were in secondary and preparatory schools, respectively. Metal phosphides are a double-edged weapon: ignorance about its toxicity leads to improper handling and accidental ingestion, whereas knowing its lethal action leads to its use in suicidal attempts. This agreed with a 10-year retrospective study in India which found that suicidal mode was the most common. Another retrospective study done in Thailand on phosphide poisoned patients reveled that suicidal attempts were present in 84.4% of cases, accidental exposure accounted for 15.4% of cases, and occupational exposure was seen in only 0.2%.
This high rate of suicide can be explained by illiteracy, frustration, depression, failure in examination, disputes in the family, inability to find suitable avenues of income, and easy availability of ALP in the household.
In a study in Tanta by Sagah et al., it was found that 65% of patients came from rural areas owing to easy availability and low cost of metal phosphides. This was different from the results reported by El Masry and Tawfik in Ain Shams University Hospitals in Cairo, which is an urban governorate. Regarding marital status, Sagah et al. found that 65% were single, and this can be explained by the higher stress and psychic burden that amounts in single individuals owing to higher susceptibility to depression and lack of feeling of interest from others. The study showed that employee represented the highest percent among cases, and this can be explained by the stress of work and responsibility that employees face. This result does not coincide with the results of Maharani and Vijayakumari who found that 18.66% of patients were laborers followed by students (16.66%) and farmers (13.33%) in India. Regarding clinical manifestations, phosphides decompose into highly toxic phosphine gas by the action of dilute hydrochloric acid content of the stomach and by the action of moisture. Phosphine gas cause gastrointestinal tract irritation and also it has corrosive effect, so most patients present vomiting and abdominal pain. The present study results agreed with the results of a study in Thailand which showed that nausea and vomiting was the most prevalent complaint, representing 49.9%, whereas 9% experienced abdominal pain.
The difference in manifestations in relation to type of phosphide and time elapsed since exposure can be explained by the fact that ALP is unstable metal phosphides so manifestations of systemic toxicity occur within a short time interval, whereas zinc phosphide is an intermediate compound that forms phosphonium, which is reduced in the intestine, and phosphine is formed and absorbed, leading to some delay in appearance of manifestations. Moreover, zinc phosphide requires acidic conditions for appreciable hydrolysis and subsequent formation of phosphine, whereas ALP and magnesium phosphide will hydrolyze to form phosphine in neutral pH.
Toxicity by ALP is more dangerous to life. ALP had higher severity score and hence high mortality than zinc phosphide in the present study, which could be owing to low LD50 of ALP compared with zinc phosphide. Mortality was more associated with ALP cases, as LD50 of ALP is 20 mg/kg and toxic dose is 0.5 g whereas zinc phosphide toxic dose is 4–5 g. Moreover, ALP is in tablet form of 3 g (56% active ingredient), and patients usually ingest the entire tablet, whereas zinc phosphide is in powder form in 5 g sachet (80% active ingredient).
These coincided with the results of Kalawat et al. which showed that mortality rate of ALP poisoned patients was 38%. Another study done in Thailand by Trakulsrichai et al. found that mortality rate among zinc phosphide poisoned patients was 7%.
Echo was done for 20 cases. It was performed in all cases of ALP and in zinc phosphide patients when indicated. Overall, 90% of cases who had hypokinesia and decreased ejection fraction were ALP.
Phosphine gas acts as general protoplasmic poison interfering with the enzyme system, inhibiting incorporation of amino acids into myocardial proteins causing cardiac dysfunction. It has direct toxic effect on myocardium contractility, and also has a role in inhibiting cytochrome oxidase in the mitochondria and causing myocarditis. So deterioration in Echo reflects the magnitude of toxicity. This coincided with the results of Kalawat et al. who performed Echo in 30 ALP poisoned cases and found hypokinesia in 20 cases, decreased ejection fraction in four cases, and normal Echo in six cases. Relation between Echo changes and type of phosphide was highly significant.
| Conclusion|| |
Metal phosphide compounds cause very serious manifestations to exposed humans, with high mortality, being especially pronounced in ALP poisoned cases. The heart is the commonly affected organ by this poisoning, and cardiovascular collapse was the most prevalent cause of death among patients.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Bumbarh GS, Krishan K, Kanchan T, Sharma M, Sodhi GS. Phosphide poisoning. A review of literature. Forensic Sci Int 2012; 214
Proudfoot AT. Aluminum and zinc phosphide poisoning. Clin Toxicol 2009; 47
Zanaty AW. Prospective study on acute poison related death in Menoufia Poison and Dependence Control Center (MPCC). Ain Shams J Forensic Med Clin Toxicol 2017; 29
Nekooghadam S, Haghighatkhah H, Vaezi F, Taheri MS, Moharamzad Y. Zinc phosphide poisoning with unusual radiologic findings. Clin Case Rep 2017; 5
Mehrpour O, Singh S. Rice tablet poisoning.a major concern in Iranian population. Hum Exp Toxicol 2010; 29
Marashi SM, Nasri-Nasrabadi Z. Can sodium bicarbonate really help in treating metabolic acidosis caused by aluminum phosphide poisoning? Arh Hig Rada Toksikol 2015; 66
Ashu M, Madhurita SB. A cute aluminum phosphide poisoning. Can we predict mortality? Indian J Anaesth 2010; 54
Ahmed HA. Determination of zinc phosphide and related heavy metals in biological samples. A case report. Asian J Chem 2017; 29
Person HE, Sjoberg GK, Haines JA, Pronczuk de GJ. Poisoning severity score. Grading of acute poisoning. J Toxicol Clin Toxicol 1998; 6
Reddy VP. Organofluorine compounds in biology and medicine
ed. Newnes: Elsevier; 2015.
Halawa HM, Nageeb S, El Guindi MK. Annual report of the poison control. Ain Shams University Hospitals 2012. Ain Shams Forensic Med Clin Toxicol 2013; 21
Alinejad S, Zamani N, Abdollahi M, Mehrpour O. A narrative review of acute adult poisoning in Iran. Iran J Med Sci 2017; 42
Chang B, Gitlin D, Patel R. The depressed patient and suicidal patient in the emergency department. Evidence-based management and treatment strategies. Emerg Med Pract 2011; 13
Shokrzadeh M, Hoseinpoor R, Hajimohammadi A, Delaram A, Pahlavani M, Rezaei M, et al
. Pattern of deliberate self-poisoning in Gorgan North of Iran. Int J Med Toxicol Forensic Med 2017; 7
Kanchan T, Ritesh G. Suicidal poisoning in Southern India. Gender differences. J Forensic Leg Med 2008; 15
Anand R, Binukumar BK, Kiran DG. Aluminum phosphide poisoning: an unsolved riddle. J Appl Toxicol 2011; 31
Trakulsrichai S, Kosanyawat N, Atiksawedparit P, Sriapha C, Tongpoo A, Udomsubpayakul U, et al
. Clinical characteristics of zinc phosphide poisoning in Thailand. Ther Clin Risk Manag 2017; 13
Kalawat S, Thakur V, Thakur A, Punjabi ND. Cardiovascular profile of aluminum phosphide poisoning and its clinical significance. Int J Adv Med 2016; 3
Sagah GA, Oreby MM, El-Gharbawy RM, Fathy AS. Evaluation of potential oxidative stress in Egyptian patients with acute zinc phosphide poisoning and the role of vitamin C. Int J Health Sci 2015; 9
El Masry MK, Tawfik HM. 2011 Annual Report of the Poison Control Centre of Ain Shams University Hospital, Cairo, Egypt. Ain Shams J Forensic Med Clin Toxicol 2013; 20
Maharani B, Vijayakumari N. Profile of poisoning cases in a tertiary care hospital, Tamil Nadu. India J App Pharm Sci 2013; 3
Marashi SM. What really happens after zinc phosphide ingestion? a debate against the current proposed mechanism of phosphine liberation in zinc phosphide poisoning. Eur Rev Med Pharmacol Sci 2015; 19
Knight MW. Zinc phosphide. In: Peterson ME, Talcott PA, editors. Small animal toxicology
ed. St Louis, USA: Elsevier Saunders; 2006. pp. 1101–1118.
[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3], [Table 4]