Paraquat (1,1′-Dimethyl-4,4′-bipyridinium dichloride) has the ability to generate highly reactive oxygen and nitrite species which cause cellular damage and apoptosis in many organs [3]. The clinical manifestations depend upon the quantity ingested. Ingestion of large amounts of liquid concentrate (> 50–100 ml of 20% w/v) results in fulminant multi-organ failure and death within several hours to a few days [3]. Ingestion of smaller quantities usually leads to toxicity to two key target organs, kidneys and lungs, developing over days to weeks [3, 4].
An ingestion of 10–15 ml of 20% w/v Paraquat solution is considered lethal [4]. The estimated amount taken by our patient was 30 ml of 20 SL solution, which was quite high. Following ingestion, the herbicide induces a burning sensation of the mouth and throat, gastrointestinal irritation, abdominal pain, nausea, vomiting, and diarrhea [3]. In our patient, all the initial symptoms were due to erosion and irritation. Activated charcoal or Fuller’s earth was not used due to unavailability.
Irrespective of its route of administration, it is rapidly distributed in most tissues, with the highest concentration found in the lungs and kidneys [3, 4]. It is actively taken up by the type II pneumocytes against a concentration gradient. Lung damage occurs in two phases, initially from destructive alveolitis over one to three days followed by proliferative phase leading to fibrosis [3, 4]. Excretion of Paraquat is biphasic, owing to lung accumulation and occurs largely in the urine [4, 5]. In our patient, renal failure was evident by a rise of serum creatinine to 4.32 mg/dl on day 1, which subsequently normalized by day 30 with conservative treatment. Respiratory symptoms appeared at the end of 2nd week and features of lung fibrosis became evident within 1 month, consistent with hallmark lung findings of Paraquat poisoning [6].
This case posed a number of diagnostic challenges to the medical team. Paraquat poisoning is an emerging problem of Bangladesh and never been reported from this region [7]. Therefore, there was considerable confusion regarding the identity of the pesticide ingested. This patient got gastric lavage (which made his condition worse) and test doses of atropine initially and might have looked upon as OP poisoning. Later he was confirmed as a case of Paraquat poisoning after examining the container. Secondly, the initial clinical features were nonspecific. Initial symptoms of vomiting and mucosal ulceration mislead to other corrosive agents. Thirdly, failure to anticipate the complications led to an early discharge of the patient. Subsequently, he developed overt lung fibrosis within 30 days. Methylprednisolone and cyclophosphamide therapy was not given initially (started later), which was a major pitfall in the management of our patient. Early initiation of these therapies might reduce the accumulation into lung [3].
Up to date, 38 countries have issued a ban on Paraquat including the European Union, Sri Lanka, Vietnam and South Korea [8,9,10,11]. Bans of W.H.O class I pesticides is proved to significantly lower the suicide rates in Bangladesh [1]. Therefore it is the high time to implement such regulation on Paraquat also.
Paraquat poisoning can lead to death and fatal long-term consequences. Unfortunately, there is no available antidote, which makes it more hazardous. All cases, regardless of symptoms, must be hospitalized and observed for early detection of complications. We recommend the government should look into the problem at large and issue a ban on Paraquat which will effectively lower the poisoning death-rates.