Acute pesticide poisoning amongst adolescent girls and women in northern Tanzania.

BACKGROUND: Acute pesticide poisoning (APP) is reported to affect community health worldwide but its burden in Tanzania is unknown particularly in women. This study examines APP involving adult females and adolescent girls 10 to 19 years in 3 regions of Tanzania which are famous for coffee and vegetable production. METHODS: Over the period of 12 months, health facility-based surveillance for cases of APP was implemented in 10 Tanzanian healthcare facilities in 2006. RESULTS: The study identified 108 APP cases of whom 31 (28.7%) occurred amongst adolescent girls. Suicide was the leading poisoning circumstances (60.2%) and the most vulnerable women were 20-29 years old who comprised 38.4% of all cases with suicide as circumstance. Organophosphates (OPs), zinc phosphide, paraquat and endosulfan were common amongst known reported poisoning agents. The annual APP incidence, mortality and Case Fatality Rate for women were 5.1/100,000, 0.2/100,000 and 3.7/100, respectively. CONCLUSION: APP amongst women in Tanzania is common and this call for diverse preventive interventions to reduce poisoning incidents.

Suicidal Zinc Phosphide Poisoning Unmasking Brugada Syndrome and Triggering Near Fatal Ventricular Arrhythmia.

Brugada syndrome (BrS) is an inherited channelopathy associated with increased incidence of ventricular arrhythmias and has many acquired triggers. Zinc phosphide (ZnP) is a rodenticide and is commonly implicated in suicidal poison ingestion. ZnP poisoning can cause myocardial toxicity and death. We report a case of ZnP poisoning that triggered a type I Brugada pattern and ventricular fibrillation in a 67-year-old male. He had no other features of toxicity and recovered later. As metal phosphide is the commonest toxin involved in suicidal poisoning in India and BrS being endemic here, this case highlights an important clinical problem.

[Case Report: Zinc phosphide poisoning after ingestion of a rodentizide in suicidal intention]. / Kasuistik - Suizidale Einnahme von Wühlmausköder (Zinkphosphid).

Zinc phosphide normally serves as a rodenticide but is occasionally ingested for suicide, potentially causing multiorgan failure. Phosphine gas is commonly in use for fumigation of grain silos and shipping containers.We describe a suicide attempt of a 54 year old female, the clinical symptoms, the treatment, the chemical and biochemical background and we give information on the potential occurrence of zinc phosphide and phosphine gas.

Plain abdominal radiography: a powerful tool to prognosticate outcome in patients with zinc phosphide poisoning.

AIM: To evaluate the clinical features of zinc phosphide poisoning and to investigate whether outcome could be prognosticated based on abdominal radiography on presentation. MATERIALS AND METHODS: All zinc phosphide-poisoned patients who were referred to Loghman-Hakim Hospital between March 2011 and September 2013 were retrospectively reviewed. Data regarding patients' demographic characteristics, characteristics of the poisoning, abdominal radiography results, and patients' outcome were recorded. RESULTS: In 102 patients, the most common presenting signs/symptoms were nausea and vomiting (60%). Four patients died and another seven had developed complications during their hospitalization (metabolic acidosis, liver abnormalities, or acute renal failure). Nineteen patients had radio-opaque abdominal radiographs, nine of whom had died or developed complications (p = 0.001). Plain abdominal radiography had a sensitivity and specificity of 81% and 89% in predicting the patients' death or further development of complications. The positive and negative predictive values were 47% and 97%, respectively. CONCLUSION: Plain abdominal radiography is a very good tool for prognostication in patients with zinc phosphide poisoning. Immediate abdominal radiography can help stratify patients into high- or low-risk groups and determine treatment strategies.

Abdominal imaging in zinc phosphide poisoning.

Radiography has been proved to be a good diagnostic tool in visualization of many radiopaque xenobiotics in clinical toxicology. Zinc is a potentially radiopaque material which is a constituent of the zinc phosphide (ZN2P3) rodenticide. We report two cases of zinc phosphide poisoning with positive abdominal X-rays in whom the diagnosis was confirmed by abdominal imaging. Positive abdominal imaging was an indication for aggressive management; however, aggressive treatment was not lifesaving in one of them. We aim to emphasize the diagnostic value of abdominal X-rays in zinc phosphide-poisoned patients. We also would like to suggest that zinc phosphide (ZP)-poisoned patients with positive X-rays have more chance to become unstable even if they are symptom free on presentation and should be more aggressively managed.

Sudden Cardiac Arrest in an Asymptomatic Zinc Phosphide-Poisoned Patient: A Case Report.

Zinc phosphide is a gray to black powder mainly used as a rodenticide. In contact with gastric fluid, it releases phosphine which is the main toxic material of this compound. Phosphine interferes with oxidative respiratory cycle of the cells, but is generally expected to manifest its toxicity with prodromal signs and symptoms including abdominal pain, nausea and vomiting, metabolic acidosis, and increased liver function tests. A 64-year-old man was referred to our center with the history of ingestion of three full table spoons of zinc phosphide powder with only a mild GI discomfort. Abdominal X-ray revealed radiopaque material in epigastric and abdominal right upper quadrant. Despite treatment with polyethylene glycol and completely normal vital signs and lab tests, he experienced sudden cardiac arrest 19 h after admission. Autopsy showed clues of focal myopathy and fibrosis with evidences of ischemia and congestion in cardiac tissue, pulmonary edema, shrunken bilateral kidneys, and nutmeg yellow liver. Toxicology panel confirmed the presence of phosphine and zinc phosphide in the gastric fluid. The patient deteriorated suddenly despite being completely symptom-free during the hours preceding cardiovascular arrest. Since the cardiopulmonary injury is the most rampant cause of early death, checking of the cardiac enzymes and cardiac monitoring could be beneficial for early detection and efficient management of these patients.

Mortality and factors associated with phosphide poisoning: prospective cohort study / Mortalidad y factores asociados con intoxicación por fosfuros: estudio de cohorte prospectiva

Background: Aluminum and zinc phosphides are solid fumigants for pest control. Metal phosphide poisoning (PP) is common in suicide and suicide attempts. In Mexico, zinc phosphide is easily available, and is a common agent in poisonings. Objective: To identify mortality in PP, and associated factors in a poison control center. Material and methods: Prospective cohort study. The starting point was the exposure (PP) and it was made a follow-up on the outcome (mortality and non-mortality). Main factors associated to PP outcome were assessed (e.g.: personal and clinical factors, duration of poisoning, detoxification, and radiographic evidence of poisoning). It was used relative risk (RR) as a risk estimator with 95% CI, as well as chi-squared with Fisher's exact test, Kaplan-Meier survival curves, and Log- Rank test as a comparative mean. Results: 44 exposed patients, and 88 non-exposed were followed up. Mortality rate in PP was of 16% in acute phase patients; there were no deaths in either subacute or chronic phases. Mortality risk was 14 (95% CI, 2 110). Main factors associated with increased mortality were: time of first medical assistance > 6 hours, RR = 15 (95% CI, 1.7-128); dose of poison ≥ 1 bottle or 1 tablet, RR = 14 (95% CI, 1.8-108); radiographic evidence of poisoning, RR = 10 (95% CI, 1.3 77). Conclusion: Metal PP has a high mortality rate and is associated to long periods of exposure to the toxic chemical due to ineffective detoxification.

Introducción: los fosfuros de aluminio y zinc son fumigantes sólidos para controlar plagas. La intoxicación por fosfuros (IpF) es un método común en suicidios o intentos de suicidio. En México los fosfuros son de fácil distribución y son un agente común en las intoxicaciones. Objetivo: identificar la mortalidad en la IpF y los factores asociados en un centro de toxicología. Material y métodos: estudio de cohorte prospectiva. Se partió de la exposición (IpF) y se siguió el desenlace (mortalidad y no mortalidad). Se evaluaron los principales factores asociados al desenlace de IpF (por ejemplo: clínicos, personales, tiempo de la intoxicación, descontaminación y evidencia radiográfica). Para estimar el riesgo se empleó el riesgo relativo (RR), con IC al 95%, chi cuadrada con prueba exacta de Fisher, curvas de supervivencia de Kaplan-Meier y su comparación por medio de Log-Rank. Resultados: se siguieron 44 pacientes expuestos y 88 no expuestos. La mortalidad por fosfuros fue del 16% de los pacientes intoxicados en la fase aguda; no hubo mortalidad en la fase subaguda y crónica. El riesgo de mortalidad fue de 14 (IC 95%: 2-110). Los factores de mayor magnitud asociados a la mortalidad en la IpF fueron: tiempo de primera atención > 6 horas, RR = 15 (IC 95% 1.7 128); dosis del tóxico ≥ 1 frasco o 1 pastilla, RR = 14 (IC 95%: 1.8 108); evidencia radiográfica del tóxico RR = 10, (IC 95%: 1.3 77). Conclusiones: la intoxicación por fosfuros metálicos tiene alta mortalidad y está asociada a estados prolongados de exposición al tóxico por descontaminación inadecuada.

Zinc as a marker in viscera of suspected metal phosphide poisoning: a study by neutron activation analysis.

Zinc as a marker element in the viscera of suspected metal phosphide poisoning has been studied during the present work. Neutron activation analysis (NAA) has been employed to detect and quantify the concentration of zinc in the viscera/stomach portion. The methodology has been developed on simulated and real life viscera samples to quantify the amount of zinc using NAA. The results obtained by NAA for real-life samples have been validated using a complementary analytical technique (viz. differential pulse anodic stripping voltammetry), and the values obtained were in good agreement, within +/- 5-8%. This exercise could be useful in medico-legal field for framing a definitive opinion about zinc phosphide poisoning.

Acute hepatic steatosis: a helpful diagnostic feature in metallic phosphide-poisoned horses.

Metal phosphides, particularly zinc and aluminum phosphide, occasionally poison horses and other equids following their use as rodenticides and insecticides. Grain-based aluminum phosphide baits are used to control rodents such as prairie dogs. The clinical course in intoxicated horses is short (<24-48 h), and animals may be found dead. Hepatic lesions caused by phosphine poisoning are not well described. Laboratory confirmation depends on detecting phosphine gas in gastric contents. Eight horses and a mule were exposed to zinc phosphide used to control prairie dogs on a Wyoming ranch. Three of 9 exposed equids developed some combination of sweating, ataxia, anxiety, and colic; 2 died acutely, and 1 recovered. A diagnosis of zinc phosphide was made by detecting phosphine in stomach contents from a horse and a mule. The liver was pale and swollen in the affected horse, which died after a clinical course of ~12 h. Other changes were generalized congestion and edema, pulmonary edema, and acute cerebrocortical edema. There was diffuse hepatocellular microvesicular steatosis. Similar histologic lesions were present in 7 equine livers from 2 previously published episodes of metallic phosphide poisoning. Older lesions (>24 h of clinical signs) had centrilobular hepatic necrosis with congestion and a mixture of microvesicular and macrovesicular steatosis. Phosphine poisoning should be considered in horses that die acutely and are found to have steatosis, either with or without hepatocellular necrosis.

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

BACKGROUND: Run 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 PRESENTATION: A 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. CONCLUSION: Run 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.

The toxicology of zinc chloride smoke producing bombs and screens.

CONTEXT: Zinc chloride (ZnCl2)-based smoke bombs and screens are in use since the Second World War (1939-1945). Many case descriptions on ZnCl2 smoke inhalation incidents appeared since 1945. OBJECTIVE: We provide a comprehensive overview of the clinical symptoms and underlying pathophysiology due to exposure to fumes from ZnCl2 smoke producing bombs. In addition, we give a historical overview of treatment regimens and their outcomes. METHODOLOGY: We performed a literature search on Medline, Scopus and Google Scholar databases using combinations of the following search terms "smoke bomb", "smoke screen", "ZnCl2", "intoxication", "poisoning", "case report", "HE smoke", "hexachloroethane smoke", "smoke inhalation" and "white smoke". We retrieved additional reports based on the primary hits. We collected 30 case reports from the last seven decades encompassing 376 patients, 23 of whom died. Of all the patient descriptions, 31 were of sufficient detail for prudent analysis. RESULTS AND CONCLUSIONS: Intoxication with clinical signs mainly took place in war situations and in military and fire emergency training sessions in enclosed spaces. Symptoms follow a biphasic course mainly characterised by dyspnoea, coughing and lacrimation, related to irritation of the airways in the first six hours, followed by reappearance of early signs complemented with inflammation related signs and tachycardia from 24 h onwards. Acute respiratory stress syndrome developed in severely affected individuals. Chest radiographs did not always correspond with clinical symptoms. Common therapy comprises corticosteroids, antibiotics and supplemental oxygen or positive pressure ventilation in 64% of the cases. Of the 31 patients included, eight died, three had permanent lung damage and 15 showed complete recovery, whereas in five patients outcome was not reported. Early signs likely relate to caustic reactions in the airway lining, whereas inhaled ZnCl2 particles may trigger an inflammatory response and associated delayed fibrotic lung damage. Smoke bomb poisoning is a potentially lethal condition that can occur in large cohorts of victims simultaneously.

[Zinc phosphide poisoning in pediatric patients from a Toxicology Center at Mexico City]. / Intoxicación con fosfuro de zinc en el paciente pediátrico en un centro toxicológico de la Ciudad de México.

BACKGROUND: Zinc phosphide is a chemical compound that is frequently used as a rodenticide; it is a highly toxic product that is widely used, among other spaces, at home. Given that it is a highly commercialized pesticide and that there is no antidote, it is mandatory to establish favorably the clinical manifestations of the intoxication. The aim was to describe the epidemiological and clinical profile of children intoxicated with zinc phosphide attended in a toxicological center of a tertiary referral hospital. METHODS: Cross-sectional, retrospective and observational study based on the medical records of 36 pediatric patients attended from 2005 to 2015 at the Centro de Información y Atención Toxicológica from Hospital General "Dr. Gaudencio González Garza", which belongs to the Instituto Mexicano del Seguro Social. RESULTS: The study didn't show a prevalence of gender; 66% of patients were children between ages 1 and 2. 96% of patients were healthy and three adolescents used the product with suicidal purposes. Zinc phosphide exposure occurred at home. Toxicity was characterized by hypotension, hypoglycemia, metabolic acidosis, abdominal pain, nausea, and vomiting; none of the patients died. In addition, neither required mechanical ventilation nor hemodialysis. CONCLUSION: The lack of knowledge of the potential toxicity of zinc phosphide and the fact that is easily reached at home allow the exposure to this product; it is an absolutely preventable risk.

Introducción: el fosfuro de zinc es usado para exterminar roedores; es un producto altamente tóxico, no crea resistencias y es de uso popular. Debido a que es un plaguicida altamente comercializado de elevada toxicidad que no cuenta con un antídoto disponible, es imperativo precisar e identificar con oportunidad las manifestaciones clínicas de la intoxicación. El objetivo fue describir el perfil epidemiológico y clínico de los niños intoxicados con fosfuro de zinc atendidos en un centro toxicológico de tercer nivel de atención. Métodos: estudio retrospectivo, observacional y trasversal del 2005 al 2015, con 36 registros de pacientes pediátricos atendidos en el Centro de Información y Atención Toxicológica del Hospital General "Dr. Gaudencio González Garza" del Centro Médico Nacional La Raza del Instituto Mexicano del Seguro Social. Resultados: el estudio no demostró predominio de algún género. El 66% de los pacientes se encontraba entre 1 y 2 años de edad. El 96% de los pacientes eran sanos y tres adolescentes utilizaron el producto con fines suicidas. La exposición ocurrió en el hogar. La toxicidad se caracterizó por hipotensión arterial, hipoglucemia, acidosis metabólica, dolor abdominal, náuseas, vómitos; ninguno de los pacientes falleció ni requirió de asistencia ventilatoria ni de hemodiálisis. Conclusión: la falta de conocimiento del potencial tóxico y la accesibilidad al producto en el interior del domicilio de los pacientes facilita su exposición; se trata de un riesgo 100% prevenible.

An autopsy case of zinc chloride poisoning.

Ingestion of large amounts of zinc chloride causes corrosive gastroenteritis with vomiting, abdominal pain, and diarrhea. Some individuals experience shock after ingesting large amounts of zinc chloride, resulting in fatality. Here, we present the results of an administrative autopsy performed on a 70-year-old man who ingested zinc chloride solution and died. After drinking the solution, he developed vomiting, abdominal pain, and diarrhea, and called for an ambulance. Except for tachycardia, his vital signs were stable at presentation. However, he developed hypotension and severe metabolic acidosis and died. The patient's blood zinc concentration on arrival was high at 3030µg/dL. Liver cirrhosis with cloudy yellow ascites was observed, however, there were no clear findings of gastrointestinal perforation. The gastric mucosa was gray-brown, with sclerosis present in all gastric wall layers. Zinc staining was strongly positive in all layers. There was almost no postmortem degeneration of the gastric mucosal epithelium, and hypercontracture of the smooth muscle layer was observed. Measurement of the zinc concentration in the organs revealed the highest concentration in the gastric mucosa, followed by the pancreas and spleen. Clinically, corrosive gastroenteritis was the cause of death. However, although autopsy revealed solidification in the esophagus and gastric mucosa, there were no findings in the small or large intestine. Therefore, metabolic acidosis resulting from organ damage was the direct cause of death.

Zinc chloride (smoke bomb) inhalation lung injury: clinical presentations, high-resolution CT findings, and pulmonary function test results.

STUDY OBJECTIVES: Zinc chloride smoke inhalation injury (ZCSII) is uncommon and has been rarely described in previous studies. We hypothesized that structural changes of the lung might correlate with pulmonary function. To answer this question, we correlated findings from high-resolution CT (HRCT) scan and the results of pulmonary function tests (PFTs) in patients with ZCSII. DESIGN: Retrospective cohort study. SETTING: University hospital. PATIENTS: Twenty patients who had been hospitalized with ZCSII-related conditions. MEASUREMENTS: The study included HRCT scan scores (0 to 100), static and dynamic lung volumes, and diffusing capacity of the lung for carbon monoxide (D(LCO)). RESULTS: HRCT scans and PFTs were performed initially after injury (range, 3 to 21 days) in all patients and during the follow-up period (range, 27 to 66 days) in 10 patients. The predominant CT scan findings were patchy or diffuse ground-glass opacities with or without consolidation. The majority of patients showed a significant reduction of FVC, FEV1, total lung capacity, and D(LCO), but normal FEV1/FVC ratio values. Changes of functional parameters correlated well with HRCT scan scores. Substantial improvements in CT scan abnormalities and pulmonary function were observed at follow-up. CONCLUSIONS: The majority of our patients with ZCSII presented with a predominant parenchymal injury of the lung that was consistent with a restrictive type of functional impairment and a reduction in Dlco rather than with obstructive disease. Our results suggest that HRCT scanning and pulmonary function testing may reliably predict the severity of ZCSII.

Diagnosis of zinc phosphide poisoning in chickens using a new analytical approach.

Approximately 200 chickens were found dead after the flooring of a slat-and-litter house was breached. No clinical signs of illness were observed in the surviving birds. During necropsy, rolled oats were found in the chickens' crops and gizzards, and the contents had a petroleum-like odor. Histopathologic examination revealed severe pulmonary edema and congestion of the chickens' lungs, hearts, livers, and kidneys. Based on the history and necropsy findings, zinc phosphide exposure was suspected. Diagnosis of zinc phosphide poisoning has previously been based on history of exposure, identification of the bait material in the gastrointestinal tract, and chemical detection of phosphine gas. However, currently available diagnostic methods are nonconfirmatory, and may produce false positive results. The objective of this case report was to determine whether the sudden death described in these chickens was caused by the ingestion of zinc phosphide, by developing a sensitive and highly specific gas chromatography/mass spectrometry (GC/MS) methodology for analysis of the gastrointestinal samples submitted to the laboratory. It was also found that the determination of zinc concentrations in liver or kidney tissue or stomach contents is not a reliable indicator of zinc phosphide poisoning.

Zinc phosphide intoxication of wild turkeys (Meleagris gallopavo).

Zinc phosphide (Zn3P2) is a rodenticide used to control a variety of small mammal species. It is available over-the-counter or as a restricted-use pesticide depending on how it is to be applied. The toxicity of Zn3P2 is dependent on the species exposed, whether the animal is able to vomit or not, and whether it is ingested on a full or empty stomach. Nontarget species can be exposed through inadvertent or intentional product misapplication. In this article we describe four mortality events in which wild turkeys (Meleagris gallopavo) were believed to have been intoxicated following the ingestion of baits containing Zn3P2.

Acute liver failure due to zinc phosphide containing rodenticide poisoning: Clinical features and prognostic indicators of need for liver transplantation.

Zinc phosphide (ZnP) containing rodenticide poisoning is a recognized cause of acute liver failure (ALF) in India. When standard conservative measures fail, the sole option is liver transplantation. Records of 41 patients admitted to a single centre with ZnP-induced ALF were reviewed to identify prognostic indicators for requirement of liver transplantation. Patients were analyzed in two groups: group I (n = 22) consisted of patients who either underwent a liver transplant (n = 14) or died without a transplant (n = 8); group II (n = 19) comprised those who survived without liver transplantation. International normalized ratio (INR) in group I was 9 compared to 3 in group II (p < 0.001). Encephalopathy occurred only in group I. Model for End-Stage Liver Disease (MELD) score in group I was 41 compared to 24 in group II (p < 0.001). MELD score of 36 (sensitivity of 86.7 %, specificity of 90 %) or a combination of INR of 6 and encephalopathy (sensitivity of 100 %, specificity of 83 %) were the best indicators of mortality. Such patients should undergo urgent liver transplantation.