12 Nov, 09 | by BMJ Group
The night before last, one of the other doctors admitted a 22 year old male who had ingested concentrated paraquat whilst intoxicated. At the time of admission he was 24 hours post ingestion and his presenting complaint was pain in his mouth and throat due to chemical burns. The night shift doctor handed over the case, along with a wealth of information regarding paraquat accumulated from internet searching and ringing the poisons helpline in the United States. The outlook from all this data was bleak, especially given our lack of facilities to deal with multi-organ failure. I have no experience with paraquat poisoning, but from published case reviews it appears that paraquat ingestion anywhere in the world is a one-way road.
For those unfamiliar with paraquat (1,1′-dimethyl-4,4′-bipyridylium dichloride), it is a herbicide used to prepare land or control weeds in major food crops. Although banned in many countries, including the entire EU, it is still one of the most widely used herbicides in the world. It is highly toxic to humans, with a particular penchant for destruction of lung tissue, but becomes inactive shortly after contact with soil or water.
Death occurs through a variety of complications between 1 day to several weeks later. Acute fulminant poisoning results in death within 3 days from a combination of acute pulmonary oedema, oliguric renal failure and hepatocellular and adrenal necrosis. Mediastinitis and adrenal failure can cause death within 10 days and it can take up to several weeks for pulmonary fibrosis to peak and cause death by respiratory failure.
Cavalli et al report a survival rate of just 13% with no treatment with ingestion of just 7-8ml of concentrated paraquat. However long it takes, and by whichever mode, ingestion of as little as two teaspoons of concentrated paraquat is frequently fatal with mortality rates of both accidental and intentional poisoning varying from 30%-96% worldwide.
In 1978 Fitzgerald et al reviewed international literature regarding paraquat poisoning, and reported three series of patients based on quantity and concentration of paraquat ingested. There were 3 deaths out of 7 patients who ingested between 10-20ml of paraquat, 6 deaths out of 8 who had ingested between 20-30ml, and 34 deaths out of the 34 patients who had ingested above 30ml.
That equates to 100% mortality associated with the equivalent of a little over a shot of tequila.
Since seeing this patient, I’ve been doing a little digging into the deep, dark and dirty world of paraquat. It is difficult to get to the bottom of it. I’ve established this much: while paraquat is now illegal to use in Britain, a large proportion of the world’s paraquat is produced in Huddersfield and exported primarily to developing countries. An FAQ I found on one manufacturer’s website is ‘why is paraquat attractive to those trying to commit suicide?’
The actual answer is because it is so very good at it, and easily, and cheaply available in developing countries. I asked around, and was directed to a shop in the market, where a 6 year old girl was ready and waiting, among bottles of toxic substances, to take my order.
I found some interesting research from Samoa which showed that between 1979 and 2001, paraquat was the agent used in 70% of successful suicides. More so, up until 1972, when paraquat became available, the number of suicides was less than 10 a year. This number rose by 367% in 1981; paraquat ingestion accounted for 40 of these 49 suicides. Within 3 years of government control of paraquat, the suicide rate had fallen again, with just 6 suicides in 1984.
While I don’t believe that the availability of paraquat encouraged suicide as some opposition groups suggest, I do think that if such a toxic agent were available in the UK, a huge number of the ‘I didn’t mean it’ impulse overdoses could end up as successful suicide statistics.
Our patient was systemically well, with no abdominal or respiratory symptoms, and stable vital signs. He was, however, unable to swallow or speak due to oral pharynx burns extending as far down the throat as could be seen on examination.
He claimed he had not taken the paraquat as a suicide attempt but that he had been inebriated, and had drunk from the bottle of herbicide mistaking it for beer. He had no idea how much he had swallowed, but the family brought in the bottle which was empty. Accidents happen, but having now smelt the noxious fumes from an empty bottle, I believe it would be impossible, however intoxicated, to let it anywhere near your lips, let alone to swallow it, without realising it wasn’t beer.
On the advice of 2 doctors in the States who were contacted during the night, the doctor on call started IV fluids to force diuresis and high dose steroids to help prevent lung damage. Clear instruction to avoid oxygen was also given to the nurses.
One of the US doctors contacted explained that he had seen 4 or 5 cases of paraquat poisoning in the number of times he had worked in this region over the past few years. Some had been treated at city hospitals, some had refused treatment, and all had died. He recommended we keep the patient comfortable with ice for the burns, and explain as gently as possible the most likely prognosis. We had the option to keep him at the hospitalito and treat as aggressively as we could with fluid and steroids or to transfer to a public hospital (a costly option for the family given the uncertainty of what could happen and the unlikely availability of aggressive treatment).
Although literature and available resources stated the outcome of paraquat poisoning is fairly predictable, it was incredibly difficult explaining it to the patient’s family when trying to help them reach a decision. Given his inability to swallow, the outcome without basic treatment was entirely predictable.
His parents, brothers and wife were called in, as all decisions are made by the family. One brother kept saying, “He has burns to his mouth; I don’t know why you keep saying that he might not survive.” I doubted myself, and of course with no idea of how much he had ingested, I had to agree that it was possible he could recover. Even with my accumulated knowledge of paraquat poisoning, it was hard to equate the well patient with his predicted bleak prognosis.
While he looked so well, the family wanted to take the patient home rather than pay for treatment here or a transfer. They struggled to comprehend how the situation was going to change. I found myself explaining that in England, or the United States, most people who ingest paraquat die, despite hasty and aggressive treatment to clean the blood and remove the toxin. I wanted to make sure they knew that if they took him home he would surely die, if not from the direct effect of paraquat then simply from dehydration. They of course wanted reassurance that if they paid for the treatment or transfer he wouldn’t die. I found myself saying, “There is no cure for this, there is no antidote. Back home, where we have extensive facilities, still many people die.”
Despite knowing he would surely die from dehydration alone, they decided to take him home, and we have heard nothing since. He had capacity and signed his form. He decided that if we could not guarantee his survival, he would rather be at home with his family.
I understand that developing countries are in need of boosted food production and crop protection, so I’m not going to jump straight on the anti-paraquat bandwagon. However given that the EU has banned this substance due to its phenomenal toxicity, should we not also insist that its distribution and use in developing countries be controlled too? In the USA paraquat is for use on a limited basis by trained and certified individuals only, which seems sensible and also applicable internationally.
Any success stories with paraquat poisoning to cheer us?
Is there anyway of predicting volume consumed and outcomes without urine or plasma analysis, dare I say it, for the next time?
Louise Kenny has completed F2 year in the Northern Deanery and is now working in Guatemala.
The patient’s consent was obtained for this blog.