Esophageal Complications Following Aluminium Phosphide Ingestion: An Emerging Issue Among Survivors of Poisoning

Jain, Rajendra K.; Gouda, Narendra B.; Sharma, Virendra K.; Dubey, T. N.; Shende, Atul; Malik, Rajesh; Tiwari, Gurudutt

doi:10.1007/s00455-009-9251-y

Cited by 12 publications

(7 citation statements)

References 14 publications

(20 reference statements)

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“…[3747–53] In follow-up among survivors, one-third of the patients had dysphagia due to esophageal complications, including esophageal stricture or tracheo-esophageal fistula. [54]…”

Section: Clinical Featuresmentioning

confidence: 99%

Managing aluminum phosphide poisonings

Gurjar

Baronia

Azim

et al. 2011

J Emerg Trauma Shock

145

125

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Aluminum phosphide (AlP) is a cheap, effective and commonly used pesticide. However, unfortunately, it is now one of the most common causes of poisoning among agricultural pesticides. It liberates lethal phosphine gas when it comes in contact either with atmospheric moisture or with hydrochloric acid in the stomach. The mechanism of toxicity includes cellular hypoxia due to the effect on mitochondria, inhibition of cytochrome C oxidase and formation of highly reactive hydroxyl radicals. The signs and symptoms are nonspecific and instantaneous. The toxicity of AlP particularly affects the cardiac and vascular tissues, which manifest as profound and refractory hypotension, congestive heart failure and electrocardiographic abnormalities. The diagnosis of AlP usually depends on clinical suspicion or history, but can be made easily by the simple silver nitrate test on gastric content or on breath. Due to no known specific antidote, management remains primarily supportive care. Early arrival, resuscitation, diagnosis, decrease the exposure of poison (by gastric lavage with KMnO4, coconut oil), intensive monitoring and supportive therapy may result in good outcome. Prompt and adequate cardiovascular support is important and core in the management to attain adequate tissue perfusion, oxygenation and physiologic metabolic milieu compatible with life until the tissue poison levels are reduced and spontaneous circulation is restored. In most of the studies, poor prognostic factors were presence of acidosis and shock. The overall outcome improved in the last decade due to better and advanced intensive care management.

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“…[3747–53] In follow-up among survivors, one-third of the patients had dysphagia due to esophageal complications, including esophageal stricture or tracheo-esophageal fistula. [54]…”

Section: Clinical Featuresmentioning

confidence: 99%

Managing aluminum phosphide poisonings

Gurjar

Baronia

Azim

et al. 2011

J Emerg Trauma Shock

145

125

View full text Add to dashboard Cite

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“…Several patients have gone on to develop esophageal strictures (Nijhawan et al, 2006). A few cases have been reported with trachea-esophageal fistulae (Agrawal et al, 2010;Jain et al, 2010).…”

Section: Gastrointestinal Toxicitymentioning

confidence: 99%

Aluminum phosphide poisoning: an unsolved riddle

Anand

Binukumar

Gill

2011

J of Applied Toxicology

102

107

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Aluminum phosphide (ALP), a widely used insecticide and rodenticide, is also infamous for the mortality and morbidity it causes in ALP-poisoned individuals. The toxicity of metal phosphides is due to phosphine liberated when ingested phosphides come into contact with gut fluids. ALP poisoning is lethal, having a mortality rate in excess of 70%. Circulatory failure and severe hypotension are common features of ALP poisoning and frequent cause of death. Severe poisoning also has the potential to induce multi-organ failure. The exact site or mechanism of its action has not been proved in humans. Rather than targeting a single organ to cause gross damage, ALP seems to work at the cellular level, resulting in widespread damage leading to multiorgan dysfunction (MOD) and death. There has been proof in vitro that phosphine inhibits cytochrome c oxidase. However, it is unlikely that this interaction is the primary cause of its toxicity. Mitochondria could be the possible site of maximum damage in ALP poisoning, resulting in low ATP production followed by metabolic shutdown and MOD; also, owing to impairment in electron flow, there could be free radical generation and damage, again producing MOD. Evidence of reactive oxygen species-induced toxicity owing to ALP has been observed in insects and rats. A similar mechanism could also play a role in humans and contribute to the missing link in the pathogenesis of ALP toxicity. There is no specific antidote for ALP poisoning and supportive measures are all that are currently available.

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“…In another report (39), dysphagia was observed in 38.87 % of survivors after a mean interval of 38.6 days from the day of AlP poisoning. Oesophageal strictures were seen in 32.2 % of the survivors.…”

Section: Gastrointestinal Toxicitymentioning

confidence: 99%

“…The neurological symptoms continued for 1.5 years post AlP exposure. Jain et al (39) reported dysphagia, oesophageal strictures, and tracheoesophageal fi stula in survivors a month after AlP exposure.…”

Section: Sequelae In Survivors?mentioning

confidence: 99%

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A Systematic Review of Aluminium Phosphide Poisoning

Mehrpour¹,

Jafarzadeh

Abdollahi

2012

Archives of Industrial Hygiene and Toxicology

160

214

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Every year, about 300,000 people die because of pesticide poisoning worldwide. The most common pesticide agents are organophosphates and phosphides, aluminium phosphide (AlP) in particular. AlP is known as a suicide poison that can easily be bought and has no effective antidote. Its toxicity results from the release of phosphine gas as the tablet gets into contact with moisture. Phosphine gas primarily affects the heart, lungs, gastrointestinal tract, and kidneys. Poisoning signs and symptoms include nausea, vomiting, restlessness, abdominal pain, palpitation, refractory shock, cardiac arrhythmias, pulmonary oedema, dyspnoea, cyanosis, and sensory alterations. Diagnosis is based on clinical suspicion, positive silver nitrate paper test to phosphine, and gastric aspirate and viscera biochemistry. Treatment includes early gastric lavage with potassium permanganate or a combination with coconut oil and sodium bicarbonate, administration of charcoal, and palliative care. Specifi c therapy includes intravenous magnesium sulphate and oral coconut oil. Moreover, acidosis can be treated with early intravenous administration of sodium bicarbonate, cardiogenic shock with fl uid, vasopresor, and refractory cardiogenic shock with intra-aortic baloon pump or digoxin. Trimetazidine may also have a useful role in the treatment, because it can stop ventricular ectopic beats and bigeminy and preserve oxidative metabolism. This article reviews the epidemiological, toxicological, and clinical/pathological aspects of AlP poisoning and its management.

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Esophageal Complications Following Aluminium Phosphide Ingestion: An Emerging Issue Among Survivors of Poisoning

Cited by 12 publications

References 14 publications

Managing aluminum phosphide poisonings

Managing aluminum phosphide poisonings

Aluminum phosphide poisoning: an unsolved riddle

A Systematic Review of Aluminium Phosphide Poisoning

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