Zinc Phosphide Poisoning

Doğan, Erdal; Güzel, Abdulmenap; Çiftçi, Taner; Aycan, İlker Öngüç; Çelik, Feyzi; Çetin, Bedri; Kavak, Gönül Ölmez

doi:10.1155/2014/589712

Cited by 23 publications

(35 citation statements)

References 12 publications

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“…Mostly the victims succumbed despite of fluid resuscitation, inotropic support, renal replacement or bicarbonate therapy [3]. Ozgur et al, had reported another 22 year old patient who expired following severe refractory acute pulmonary oedema with renal as well as liver impairment, myopericarditis leading to refractory acidosis and respiratory arrest.…”

Section: Discussionmentioning

confidence: 99%

A case report of zinc phosphide poisoning: complicated by acute renal failure and tubulo interstitial nephritis

Yogendranathan

Herath

Sivasundaram

et al. 2017

BMC Pharmacol Toxicol

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BackgroundRun Rat® is a rodenticide widely used against small mammals. It comprises of a minimum of 32% zinc phosphide which is highly toxic in acute exposures to humans. It may be consumed accidentally or intentionally. It enters the body via skin, respiratory and gastrointestinal tracts. Zinc phosphide is hydrolyzed by the gastric acid and is transformed into phosphine gas. Phosphine is a respiratory toxin that inhibits cytochrome C oxidase system resulting in renal failure and liver failure.Case presentationA 35 year old Sri Lankan female presented following ingestion of 2.5 g of Run Rat®, which is a branded preparation of zinc phosphide, resulting in 61 mg/kg poison load. She developed severe acute kidney injury with acute tubular necrosis, subnephrotic ranged proteinuria and tubulointerstitial nephritis for which she underwent haemodialysis three times along with other measures of resuscitation. She also developed elevated liver enzymes with hyperblirubinaemia, hypoalbuminaemia, acute pancreatitis and mild myocarditis. She improved with supportive therapy over a period of 3 weeks.ConclusionRun Rat® is a commonly used rodenticide and the toxic effects are mediated through conversion of phosphide to phosphine gas. The majority of the deaths had occurred in the first 12 to 24 h and the main causes identified are refractory hypotension and arrhythmias. The late deaths (beyond 24 h) had been commonly due to adult respiratory distress syndrome, liver and renal failure. The outcome is poorer with delayed presentation, development of coagulopathy, hyperglycaemia and multiorgan failure with elevated liver enzymes. In our patient, Zinc phosphide poisoning caused severe acute kidney injury, abnormal liver profile, pancreatitis and possible myocarditis. The patient improved with repeated haemodialysis. The renal biopsy revealed acute tubulointerstitial nephritis with acute tubular necrosis.In tropical countries, the rural population engaged in agriculture has easier access to the compound, as it is available at a lower cost. Furthermore, the lack of an antidote and advanced resuscitative measures such as inotropic supportive therapy and renal replacement facilities at most of the peripheral hospitals pose a major challenge in providing timely interventions to prevent deaths.

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Section: Discussionmentioning

confidence: 99%

A case report of zinc phosphide poisoning: complicated by acute renal failure and tubulo interstitial nephritis

Yogendranathan

Herath

Sivasundaram

et al. 2017

BMC Pharmacol Toxicol

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“…Phosphine mainly affects the cardiovascular, respiratory, gastrointestinal (GI), hepatobiliary, and hematologic systems and causes electrolyte and metabolic abnormalities 1,2. The severe clinical symptoms in patients with phosphine poisoning include circulatory collapse, hypotension, pulmonary edema, congestive heart failure, cardiac arrhythmia, and acute renal failure 1,3,4. No specific antidote has been identified; therefore, the main treatment is supportive care.…”

Section: Introductionmentioning

confidence: 99%

Clinical characteristics of zinc phosphide poisoning in Thailand

Trakulsrichai¹,

Kosanyawat²,

Sriapha

et al. 2017

TCRM

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ObjectiveThe objectives of this study were to describe the clinical characteristics and outcomes of poisoning by zinc phosphide, a common rodenticide in Thailand, and to evaluate whether these outcomes can be prognosticated by the clinical presentation.Materials and methodsA 3-year retrospective cohort study was performed using data from the Ramathibodi Poison Center Toxic Exposure Surveillance System.ResultsIn total, 455 poisonings were identified. Most were males (60.5%) and from the central region of Thailand (71.0%). The mean age was 39.91±19.15 years. The most common route of exposure was oral (99.3%). Most patients showed normal vital signs, oxygen saturation, and consciousness at the first presentation. The three most common clinical presentations were gastrointestinal (GI; 68.8%), cardiovascular (22.0%), and respiratory (13.8%) signs and symptoms. Most patients had normal blood chemistry laboratory results and chest X-ray findings at presentation. The median hospital stay was 2 days, and the mortality rate was 7%. Approximately 70% of patients underwent GI decontamination, including gastric lavage and a single dose of activated charcoal. In all, 31 patients were intubated and required ventilator support. Inotropic drugs were given to 4.2% of patients. Four moribund patients also received hyperinsulinemia–euglycemia therapy and intravenous hydrocortisone; however, all died. Patients who survived and died showed significant differences in age, duration from taking zinc phosphide to hospital presentation, abnormal vital signs at presentation (tachycardia, low blood pressure, and tachypnea), acidosis, hypernatremia, hyperkalemia, in-hospital acute kidney injury, in-hospital hypoglycemia, endotracheal tube intubation, and inotropic requirement during hospitalization (P<0.05).ConclusionZinc phosphide poisoning causes fatalities. Most patients have mild symptoms, and GI symptoms are the most common. Patients who present with abnormal vital signs or electrolytes might have more severe poisoning and should be closely monitored and aggressively treated. All patients should be observed in the hospital for 2 days and followed up for cardiovascular and respiratory symptoms, electrolyte balances, kidney function, and blood glucose.

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“…Zinc phosphide (Zn 3 P 2 /ZnP) is used as a highly effective rodenticide to protect grain from rodents and is usually produced as a dark gray powder [1]. When ingested by accident, through suicidal or homicidal attempts, in the presence of water and acid in the stomach, it transforms into phosphine gas (PH 3 ) and affects different parts of the body especially the heart, liver, and lungs.…”

Section: Introductionmentioning

confidence: 99%

“…When ingested by accident, through suicidal or homicidal attempts, in the presence of water and acid in the stomach, it transforms into phosphine gas (PH 3 ) and affects different parts of the body especially the heart, liver, and lungs. Till date, there is no known specific antidote [1]. The estimated mortality rate of ZnP poisoning is around 37-100% [2].…”

Section: Introductionmentioning

confidence: 99%

Hepatotoxicity due to zinc phosphide poisoning in two patients: role of N‐acetylcysteine

Oghabian

Afshar

Rahimi

2016

Clinical Case Reports

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Key Clinical MessageZinc phosphide (Zn3P2/ZnP) is used as a rodenticide. The most common signs of toxicity are nausea, vomiting, hypotension, and metabolic acidosis; patients presenting such signs are referred to the emergency department (ED) of the hospitals. Therefore, this study aimed to report two cases of hepatotoxicity following accidental and intentional ZnP poisoning and successful management with N‐acetylcysteine (NAC).

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Zinc Phosphide Poisoning

Cited by 23 publications

References 12 publications

A case report of zinc phosphide poisoning: complicated by acute renal failure and tubulo interstitial nephritis

A case report of zinc phosphide poisoning: complicated by acute renal failure and tubulo interstitial nephritis

Clinical characteristics of zinc phosphide poisoning in Thailand

Hepatotoxicity due to zinc phosphide poisoning in two patients: role of N‐acetylcysteine

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