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Diquat Toxicity: Multi-Organ Failure from Herbicide Ingestion
Description
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A6902 - Diquat Toxicity: Multi-Organ Failure from Herbicide Ingestion
Author Block: E. Rayyan1, S. Savajiyani1, S. Uppalapu2; 1The University of Arizona College of Medicine-Phoenix, Phoenix, AZ, United States, 2Banner University Medical Center Phoenix, Phoenix, AZ, United States.
Background:
Diquat is a non-selective contact herbicide that has been commercially available since the 1950s. It is a potent redox cycler and its effects relate to its mechanism of creating highly reactive superoxide radicals, causing local and systemic reactions. Most cases of diquat poisoning have been as a result of intentional ingestion, and between 1968-1999 only 30 cases of diquat poisoning were reported in detail in literature-13 of which were fatal.
Case Summary:
The patient is a 25 year old male, working as a landscaper, who presented after accidently ingesting a then-unidentified liquid while at work. Concerned that he had ingested a toxin, he induced vomiting and sought medical care. It was found that the chemical in question was “Tribune”, containing 37.3% of diquat dibromide. Activated charcoal was given immediately and the patient underwent an emergency qualitative testing (NaOH and Sodium dithionite urine testing), which was positive. Efforts for management were directed at addressing the oxidant stress from oxygen free radical formation, and thus the patient was started on continuous hemodialysis and was loaded with Deforaximine and n-acetylcysteine. During his hospital course the patient developed mucosal sloughing, mucositis and bleeding esophageal erosions requiring intubation. Additionally he developed cardiogenic shock requiring inotropic support, anuric renal failure requiring hemodialysis and CRRT, propofol induced hypertriglyceridemia requiring plasmapheresis, as well as ARDs. His ARDs was complicated by the concern for precipitating oxygen free radical complications with supplemental oxygen, and the patient was eventually started on systemic corticosteroids and underwent a tracheostomy placement. With the above interventions the patient survived his ingestion, was liberated from the ventilator, and was discharged on day 31 of his hospital course. At that time he had failed to achieve renal recovery and was dependent on hemodialysis.
Discussion:
Most diquat toxicity involves accidental or deliberate ingestion of the chemical. Confirmation of the diagnosis can be made rapidly and qualitatively by the addition of sodium dithionite to the patient’s urine. It is a highly toxic compound with a fatality rate as high as 80% because of lack of a specific antidote. Diquat has been shown to cause significant damage to multiple organs including the lungs, myocardium, liver, kidneys and GI mucosa. After confirmation of ingestion, efforts are threefold: First, to try to decrease systemic absorption via activated charcoal; second, to try to decrease potential for oxidative damage; thirdly, to anticipate affected organ systems and cater supportive care to likely complications.
Author Block: E. Rayyan1, S. Savajiyani1, S. Uppalapu2; 1The University of Arizona College of Medicine-Phoenix, Phoenix, AZ, United States, 2Banner University Medical Center Phoenix, Phoenix, AZ, United States.
Background:
Diquat is a non-selective contact herbicide that has been commercially available since the 1950s. It is a potent redox cycler and its effects relate to its mechanism of creating highly reactive superoxide radicals, causing local and systemic reactions. Most cases of diquat poisoning have been as a result of intentional ingestion, and between 1968-1999 only 30 cases of diquat poisoning were reported in detail in literature-13 of which were fatal.
Case Summary:
The patient is a 25 year old male, working as a landscaper, who presented after accidently ingesting a then-unidentified liquid while at work. Concerned that he had ingested a toxin, he induced vomiting and sought medical care. It was found that the chemical in question was “Tribune”, containing 37.3% of diquat dibromide. Activated charcoal was given immediately and the patient underwent an emergency qualitative testing (NaOH and Sodium dithionite urine testing), which was positive. Efforts for management were directed at addressing the oxidant stress from oxygen free radical formation, and thus the patient was started on continuous hemodialysis and was loaded with Deforaximine and n-acetylcysteine. During his hospital course the patient developed mucosal sloughing, mucositis and bleeding esophageal erosions requiring intubation. Additionally he developed cardiogenic shock requiring inotropic support, anuric renal failure requiring hemodialysis and CRRT, propofol induced hypertriglyceridemia requiring plasmapheresis, as well as ARDs. His ARDs was complicated by the concern for precipitating oxygen free radical complications with supplemental oxygen, and the patient was eventually started on systemic corticosteroids and underwent a tracheostomy placement. With the above interventions the patient survived his ingestion, was liberated from the ventilator, and was discharged on day 31 of his hospital course. At that time he had failed to achieve renal recovery and was dependent on hemodialysis.
Discussion:
Most diquat toxicity involves accidental or deliberate ingestion of the chemical. Confirmation of the diagnosis can be made rapidly and qualitatively by the addition of sodium dithionite to the patient’s urine. It is a highly toxic compound with a fatality rate as high as 80% because of lack of a specific antidote. Diquat has been shown to cause significant damage to multiple organs including the lungs, myocardium, liver, kidneys and GI mucosa. After confirmation of ingestion, efforts are threefold: First, to try to decrease systemic absorption via activated charcoal; second, to try to decrease potential for oxidative damage; thirdly, to anticipate affected organ systems and cater supportive care to likely complications.
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