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Precipitating events in ACLF.
Source publication
Zinc phosphide is an inorganic compound that is used as a rodenticide. A case of a young female is described who developed acute on chronic liver failure (ACLF) precipitated by deliberate self-harm (DSH) with zinc phosphide. She had underlying cirrhosis due to surreptitious alcohol intake. She recovered propitiously following meticulous intensive c...
Context in source publication
Context 1
... acute insult precipitating ACLF (Table 1) are quite distinct in different parts of the world. Infections are the predominant acute insult in East although hepato toxins (as in our case) and herbal indigenous medicines are important etiologies for liver failure in the Asian countries. ...
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AIM
To validate prognostic scores for acute decompensation of cirrhosis and acute-on-chronic liver failure in Brazilian patients.
METHODS
This is a prospective cohort study designed to assess the prognostic performance of the chronic liver failure-consortium (CLIF-C) acute decompensation score (CLIF-C AD) and CLIF-C acute-on-chronic liver failure...
Background & aims:
Infections are life threatening to patients with acute decompensation and acute-on-chronic liver failure (AD/ACLF). Patients with AD/ACLF have prostaglandin E2-mediated immune suppression, which can be reversed by administration of albumin; infusion of 20% human albumin solution (HAS) might improve outcomes of infections. We per...
Methods:
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Citations
... ALF caused by drug-induced hepatitis is a leading cause of death and disability among adult individuals. ZnP can cause liver failure and serious damage [5]. ...
... Literature on ZnP poisoning and its associated symptoms has been published in Asian countries, although reports of its association with acute or chronic liver failure are rare [1,[5][6][7][8]. Common signs of ZnP poisoning include nausea, vomiting, abdominal pain, shortness of breath, low blood pressure, rapid heart rate, abnormal heart rhythms, agitation, hallucinations, depression, and coma [9,10]. ...
The use of rodenticides such as zinc phosphate is common in tropical countries. However, it has a toxic effect on humans when consumed or absorbed accidentally or deliberately. Although the adverse effects often only last for a short period, acute or fulminant liver failure can occur in few patients. Because the chemicals can create a wide variety of symptoms, it is essential to investigate the progression of symptoms from mild to severe so that treatment protocols can be understood and patients can receive appropriate care. In this report, we detail a case of rodenticide poisoning in a middle-aged man who, initially, had only minor symptoms but ultimately developed fulminant liver failure.
In this example, we discuss the case of a 40-year-old man who intentionally consumed 10 gm of rat poison (zinc phosphide (ZnP)) and reported to our department with a complaint of nausea and three episodes of vomiting. A neurological evaluation showed that the patient had a Glasgow Coma Scale score of 9/15 (Eye(E): 2; Motor(M): 4; Verbal(V): 3). Doll’s eyes were present, and the patient’s pupils were semi-dilated, sluggishly reacting to light. The plantars were bilateral extensor. In the subsequent four hours, the patient developed a deep coma. The patient’s lack of awareness, coagulopathy, and abnormal liver enzyme values all pointed to acute fulminant liver failure. His condition improved with supportive therapy over a period of three weeks.
... It is a gray-to-black inorganic chemical compound that is available in different forms, such as paste, bait, granules, dust, and tracking powder formulations. [1][2][3] ZnP is also potentially toxic for mammals in acute exposure, even for humans, accidentally or intentionally through suicidal or homicidal uses. 1,2,4 No existing specific antidote for ZnP poisoning leads to a high mortality rate of 37-100%, and only supportive care is considered. ...
... It takes 30 min to manifest acute toxicity, and death could occur within the first 6 h after ingestion. [2][3][4] Most patients with PH 3 intoxication are referred to hospital with common signs and symptoms, including N/V, retrosternal burning, metabolic acidosis, hypotension, hypoglycemia, delirium, and tonic-clonic seizures, which can lead to severe clinical findings such as circulatory collapse, dysrhythmias, congestive heart failure, pulmonary edema, acute liver, and renal failure that can cause early death. 8,11 Our patient was presented to the hospital with N/V, hypotension, and sinus tachycardia on ECG. ...
In the patients with a history of intentional or unintentional consumption of rodenticide compounds, especially ZnP, it is necessary to assess ABG and abdominal radiography. image
... 40 Cases of hepatic failure and hepatic encephalopathy have also been reported. 41,42 ...
Introduction:
Toxicity from rodenticides such as metal phosphides is common worldwide, particularly in developing countries where consumers have access to unlabeled and uncontrolled insecticides and pesticides.
Case report:
We present the first documentation of a metal phosphide exposure in Lebanon. A middle-aged woman presented to the emergency department following the ingestion of an unknown rodenticide. Spectroscopy analysis of the sample brought by the patient was used and helped identify zinc phosphide. The patient developed mild gastrointestinal symptoms and was admitted to the intensive care unit for observation without further complications.
Review:
We subsequently conducted a literature review to understand the diagnosis, pathophysiology, clinical presentation, and management of metal phosphide toxicity. Multiple searches were conducted on MEDLINE and PubMed, and articles related to the topics under discussion were included in the review. Metal phosphide is associated with significant morbidity and mortality involving all body systems. Patients presenting with metal phosphide intoxication need extensive workup including blood testing, electrocardiogram, and chest radiography. To date there is no antidote for metal phosphide toxicity, and management is mostly supportive. Many treatment modalities have been investigated to improve outcomes in patients presenting with metal phosphide toxicities.
Conclusion:
Emergency physicians and toxicologists in developing countries need to consider zinc and aluminum phosphides on their differential when dealing with unlabeled rodenticide ingestion. Treatment is mostly supportive with close monitoring for sick patients. Further research is needed to better understand metal phosphide toxicity and to develop better treatment options.
... 2. Phosphine and hydrogen peroxide bind to create a radical compound which is the main mechanism of cell death by lipid peroxidation and disrupting cell structure [13]. 3. Phosphine exerts anti choline-esterase effects and also causes deterioration in oxyhemoglobin molecules [14]. ...
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.
... It inhibits protein synthesis and enzymatic activity 9. It has anti-choline esterase effects and also causes denaturation of oxy-haemoglobin molecules [12]. ...
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.
