- highly toxic herbicide
- common agent in suicide in 3rd world, especially Asia (lethal in small amounts, cheap, available)
- leading single agent causing death from pesticide poisoning in many countries including Sri Lanka
- occurs sporadically elsewhere
- >50% case fatality rate
- Paraquat is rapidly but incompletely absorbed and then largely eliminated unchanged in urine within 12–24h
- volume of distribution of 1.2–1.6 l kg−1
- Kinetics of distribution into target tissues can be described by a two-compartment model with time-dependent elimination from the central compartment. The lungs may be considered a third compartment from which elimination is very slow.
- Paraquat generates reactive oxygen species which cause cellular damage via lipid peroxidation, activation of NF-κB, mitochondrial damage and apoptosis in many organs.
- actively taken up against a concentration gradient into lung tissue leading to pneumonitis and lung fibrosis.
- Paraquat also causes renal and liver injury.
- Ingestion of large amounts of liquid concentrate (>50–100 ml of 20% ion w/v) results in fulminant organ failure and death (hours to days)
- Ingestion of smaller quantities usually leads to toxicity in the two key target organs (kidneys and lungs) developing over the next 2–6 days (still >50% mortality)
- ulceration of the mucous membranes (paraquat tongue), esophageal perforation
- pulmonary oedema
- cardiovascular collapse
- renal failure (early)
- liver dysfunction with abnormal LFTs
- acute alveolitis over 1–3 days followed by a secondary fibrosis (3-7 days) with death at up to 5 weeks
- paraquat assay
- sodium dithionite test on urine (if changes colour to blue -> confirms urine paraquat concentration >1 mg l−1, indicates a very poor prognosis)
- FBC, UEC, LFTs, lipase, coags (multi-organ dysfunction)
- CT Chest
- Fullers earth (non-plastic clay): 30%, 250mL Q 4 hourly -> until comes out in stools
- early NGT recommended (due to mucosal injury)
- avoid gastric lavage (caustic injury, and unlikely to provide any benefit)
- titrate O2 (can worsening pulmonary fibrosis, mild hypoxia is acceptable e.g. SpO2 >88%)
- immediate plasma exchange or haemofiltration (not likely to change outcome – distribution to the lungs occurs <2h)
- immune suppression with cyclophosphamide, MESNA, methylprednisolone and dexamethasone to dampen inflammatory reaction (unproven)
- Antioxidants such as acetylcysteine and salicylate might be beneficial through free radical scavenging, anti-inflammatory and NF-κB inhibitory actions (no evidence)
- patients in extremis should be palliated