CELPHOS POISONING PDF

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Aluminum phosphide (ALP) is a cheap, easily available agricultural pesticide which causes lethal poisoning by liberation of phosphine and. Aluminium Phosphide Poisoning: Management and Prevention of AlP poisoning, mediated by phosphine and mechanism of action have not been established. Aluminium phosphide (AlP) is a cheap solid fumigant and a highly toxic pesticide that is commonly used for grain preservation. AlP has currently generated.

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Celphos poisoning is one the most common and lethal poisonings with no antidote available till now. To evaluate the effectiveness of new treatment regimens and interventions in reduction of mortality from the fatal effects of celphos poisoning. A profile of 33 patients, who got admitted in Intensive Care Unit ICU of our institute with alleged intake of celphos pellets, poieoning studied.

In all the 33 patients with alleged celphos poisoning, extensive gastric lavage was done with a mixture of coconut oil and sodium bicarbonate solution. Majority of the poioning out of the total 33 were young with mean age of The mean stay of the patients in ICU was 5.

Aluminum phosphide AlP is used to preserve grains all over the world. It is also known as celphos and is one of the most dreaded poisons one can ever encounter in toxicology. The salt is usually available in tablet and pellet forms. AlP poisoning is common in all parts of the world, but is found more commonly in developing countries like India and is often implicated in accidental and suicidal poisonings in India.

Many lives have been lost in the last three decades, especially poislning the young rural population of northern India. It is not just limited to the agricultural society, but the incidence is increasing in the urban families also. Previously, the laws and legislations were not that strict and it was easily available on the counter; but in the last few years stricter norms have reduced its easy availability, even though they are still not enough to reduce the suicidal rate due to its consumption, which traumatizes so many families.

Patients remain mentally clear till cerebral anoxia due to shock supervenes resulting in drowsiness, delirium and coma. Reversible myocardial injury has also been reported. The breath of patients who have ingested AlP has a characteristic garlic-like odor. Conformation of diagnosis is based on the patient’s history and a positive result blackening on tests of the patient’s breath poisoniny paper moistened with fresh silver nitrate solution or by chemical analysis of blood or gastric acid for phosphine.

The literature is full of different drugs and trials to counter its irreversible toxic effects, but hardly with any concrete success. Keeping all these facts and figures in consideration, we undertook a retrospective analysis at the Intensive Care Unit ICU of our institute, whereby we tried to treat the patients with mixture of coconut oil and sodium bicarbonate used for gastric lavage, mixed in equal proportions, to make lavage solution of ml.

Management of celphos poisoning with a novel intervention: A ray of hope in the darkest of clouds

The main aim was to find whether the regimen we devised is of any help in saving the precious lives of the people who in a rage and fury consume this deadly poison, the antidote for which is still not in the sight. The objective was to see the effectiveness of this medication combo to decrease the very high the mortality and morbidity as result of consumption of this poison. The approval celhos Ethics Committee of the institute had already been taken for all poisoning cases and especially for the treatment of celphos poisoning.

Thirty-three patients got admitted to ICU of our institute over the last 3. Most of the patients were young and either unmarried or newly married.

Most of them had features of cardiogenic shock, hypotension and arrhythmias, while few got admitted with respiratory distress and rest of them had multitude of symptoms related to different celphoz systems. Poisonong intubation was done with appropriate size cuffed endotracheal tube and patients were put on mechanical ventilation.

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Gastric lavage was initiated with aliquots of 50 ml of coconut oil and 50 ml of sodium bicarbonate solution and continued for the next half an hour, with simultaneous aspiration being done after every 2—3 minutes through Ryle’s tube. Coconut oil was just heated to lukewarm temperature so as to make a miscible solution with sodium bicarbonate.

Aluminium phosphide poisoning

The procedure of gastric lavage was usually done posioning times in the first hour. Initial 30 ml lavage was sent to forensic laboratory for toxicological analysis. An intravenous access through internal jugular vein was established for central venous pressure monitoring as well as for guiding the fluid therapy in majority of patients who had presented with cardiovascular instability, respiratory distress and renal failure.

Symptomatic treatment was initiated on a patient to patient basis. Magnesium sulfate, dopamine, dobutamine, amiodarone infusions and other appropriate intravenous drugs were given depending on the patient’s clinical presentation and symptomatology, as well as arrhythmias and blood pressure variations. Urine output was monitored through Foley’s catheter attached to urobag. Patients who required mechanical ventilation were kept sedated with injection midazolam and paralyzed with injection vecuronium.

During this period, strict and vigil monitoring xelphos all vital parameters was done and treatment regimens were titrated according to the clinical condition of the patients. Gastric lavage was again performed after 1 hour of admission with the same solution for next half an hour.

Managing aluminum phosphide poisonings

After admission in the ICU, all the baseline routine and specific investigations were carried out including regular arterial blood gas analysis ABG. Soda bicarbonate was given empirically to all patients in a dose of 1—1.

At the end of the study period, all the data were arranged systematically and were subjected to statistical analysis using non-parametric tests.

In the last 3. The demographic poisonihg of these patients is shown in Table 1. The age of 33 patients who got admitted in ICU ranged from 18 to 48 years, with a mean and standard deviation of There was not much significant difference ceplhos the gender basis as 19 males and 14 females were admitted with poizoning consumption.

The incidence was more in the families of moderate income, especially among the unmarried young members, which was statistically significant on analysis.

Rest of the patients got admitted with other symptoms such as GI bleed or altered sensorium [ Table 3 ].

The mean stay in ICU varied from 2 to 11 days, with a mean stay of 5. Celphos is formulated as a greenish gray tablet of 3 g, which in the presence of moisture or HCl, releases phosphine:. AlP, when ingested, liberates a lot of phosphine PH 3 gas in the poisoming, which has a very pungent smell. Phosphine gas is rapidly absorbed from the gastric mucosa and, once it gains access to bloodstream, it reaches various tissues and at cellular level inhibits the mitochondrial respiratory chain and hence leads to cell necrosis and death.

It has been suggested that phosphine celpos to non-competitive inhibition of the cytochrome oxidase of mitochondria, blocking the electron transfer chain and oxidative phosphorylation, producing an energy crisis in the cells. This has been suggested to inhibit myocardial cellular metabolism and necrosis of the cardiac tissue, resulting in the piosoning of reactive oxygen intermediates.

Vascular changes may lead to marked low blood pressure that does not respond well to pressor agents. Histopathology shows myocytolysis, multiple areas of necrosis and congestion. Majority of our patients were young, unmarried with male gender predominance, and poisoning was quite prevalent in the educated community, both from the rural and urban population, in almost equal proportion.

The incidence was equal among working and the non-working population, highlighting the fact that the employment stress is not the only factor but rather it is the social and family factors which drive these people to commit suicide. Toxicity that occurs after inhalation is characterized by chest tightness, cough and shortness of breath. Severe exposure can cause accumulation of fluid in the lungs, which may have a delayed onset of 72 hours or more after exposure.

Children may be more vulnerable because of relatively increased minute ventilation per kilogram and failure to evacuate an area promptly, when exposed.

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Furthermore, this phosphine gas is eliminated through the lungs; hence, due to high concentration in the respiratory alveoli, it is responsible for direct alveolar damage. Ventilator was unable to deliver the oxygen due to very high pressures in the pulmonary alveoli.

We continued the manual ventilation till the correction of hypoxemia, which almost took 2—3 hours in all the five patients. Acute respiratory distress syndrome ARDS and exudative pleural poisning can develop. Studies in the past have shown increased levels of inflammatory markers cytokines and interleukins in ARDS, which increase the capillary permeability.

This combined effect of increase in capillary permeability xelphos to global hypoxia and ARDS could be responsible for the exudative effusion seen predominantly in the pleural cavity and not in other serous cavities.

GI symptoms are usually the first to occur after exposure. Symptoms may include nausea, vomiting, abdominal pain and diarrhea. One of our patients, who consumed six tablets of celphos, developed severe gastric bleeding which could not be controlled and ultimately led to the death of the patient within 1 hour.

Death due to acute hepatocellular toxicity and fulminant hepatic failure has also been reported in acute poisoning. Blood and protein in the urine, and acute kidney failure due to shock can occur. Analysis of blood gases may reveal combined respiratory and metabolic acidosis. Also, there poisojing been reports of significant hypomagnesemia and hypermagnesemia associated with massive focal myocardial damage. Chronic exposures to very low concentrations may result in anemia, bronchitis, GI disturbances, and visual, speech, and motor disturbances.

Gastric lavage is important in the initial stage. The management principles aim to sustain life with appropriate resuscitation measures until phosphine is excreted from the body. If phosphides have been ingested, do not induce emesis.

Gastric lavage with saline or sodium bicarbonate or potassium permanganate 1: As the poison itself causes a lot of gastric mucosal damage, it exposes a lot of raw area for phosphine absorption.

The mechanism by which coconut oil reduces the toxicity of phosphides is unknown but most probably it forms a protective layer around the gastric mucosa, thereby preventing the absorption of phosphine gas. Secondly, it helps in diluting the HCl and again inhibiting the breakdown of phosphide from the pellet. Soda bicarbonate mainly neutralizes the HCl and thus diminishing the catalytic reaction of phosphide with HCl, thereby inhibiting the release of phosphine.

Certain specific measures can be adopted to reduce the fatal episodes of AlP. These include the following. Antidotes for various fatal poisons have been developed over the last three decades, but even now cflphos poison is killing the poisoninh. Although few lives have been saved here and there, doubt still remains about the nature of poison consumed, the amount of poison consumed, the time interval between consumption and resuscitation and so on.

Four of our patients consumed three or more than three tablets of the celphos poison, while five of the patients were brought to the hospital almost more than 4 hours of ingestion of the celphos pellet which we believe led to the increase of mortality rate among our patients.

We recommend the use of this regimen by all the intensivists and physicians so as to possibly save the lives of so many patients from this hopeless situation. National Center for Biotechnology InformationU. Journal List Anesth Essays Res v. Author information Copyright and License information Disclaimer. Sukhminder Bajwa, House No. This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3. This article poisonning been cited by other articles in PMC.

Aluminum phosphide, celphos, coconut oil, magnesium sulfate, phosphide poisoning.

Table 1 Demographic opisoning and the patient characteristics. Open in a separate window. Table 2 Clinical presentation of the patients in ICU. Table 3 Treatment pattern in ICU.

Table 4 Number of organ systems affected.