Paraquat Poisoning: Symptoms, Types, Causes and Treatment

Paraquat is a widely used herbicide, but its high toxicity has made it a significant concern for both accidental and intentional poisonings. Understanding the symptoms, types, causes, and current treatment options is crucial for healthcare providers, affected individuals, and the general public. This comprehensive guide breaks down the latest knowledge and clinical experience related to paraquat poisoning, drawing on research and real-world case reports.

Symptoms of Paraquat Poisoning

Paraquat poisoning presents a unique set of clinical features that can range from mild gastrointestinal discomfort to life-threatening multi-organ failure. Early recognition of these symptoms is critical for timely intervention and improving outcomes.

Symptom	Severity	Clinical Feature	Source
Nausea/Vomiting	Early	Almost universal sign	2 4 5 10
Oral Ulcers	Moderate	"Paraquat tongue", mouth/esophageal ulcers	2 3 4 5
Abdominal Pain	Mild-Moderate	Upper GI pain, heartburn	3 4
Respiratory Distress	Severe	Dyspnea, ARDS, pulmonary fibrosis	1 4 5 8 10
Renal Failure	Severe	Oliguria, ARF	1 4 10
Multi-Organ Failure	Severe	Liver, kidney, heart affected	1 5 10
Jaundice	Severe	Hepatic involvement	4 10

Table 1: Key Symptoms of Paraquat Poisoning

Early Symptoms

After ingestion or significant exposure to paraquat, symptoms typically begin with gastrointestinal (GI) irritation. Nearly all patients experience nausea and vomiting, often within hours of exposure. Oral and esophageal ulcers are common, sometimes referred to as "paraquat tongue," where the lining of the mouth and throat becomes eroded and painful 2 4 5. Abdominal pain and heartburn may also occur at this stage 3 4.

Progressive and Severe Symptoms

As paraquat is absorbed and distributed, more severe systemic effects develop:

• Respiratory distress is a hallmark of moderate to severe poisoning. Paraquat accumulates in the lungs, causing inflammation, pneumonitis, and eventually pulmonary fibrosis. Shortness of breath and hypoxia may progress rapidly 1 4 5 8 10.
• Renal failure frequently develops, reflected by oliguria (reduced urine output) and, in severe cases, acute renal failure (ARF) 1 4 10. The kidneys are particularly vulnerable to paraquat’s oxidative damage.
• Hepatic involvement may lead to jaundice and impaired liver function in advanced cases 4 10.
• Multi-organ failure is the most serious consequence, involving the heart, adrenal glands, pancreas, and nervous system, often resulting in death within hours to days if exposure is massive 1 5 10.

Unique Manifestations

Some patients develop rare complications such as esophagitis dissecans superficialis (EDS), characterized by sloughing of the esophageal lining, causing severe pain and difficulty swallowing 3. Skin contact, especially over broken skin, can cause severe local corrosion and contribute to systemic toxicity 6.

Types of Paraquat Poisoning

The outcome and clinical presentation of paraquat poisoning largely depend on the dose and route of exposure. Categorizing the poisoning type helps guide prognosis and management.

Type	Dose/Route	Main Features	Source
Mild	<20 mg/kg, ingestion	GI symptoms, full recovery	1 2 4
Moderate	20–40 mg/kg, ingestion	GI + systemic (renal/lung) involvement	1 2 4
Fulminant	>40 mg/kg, ingestion	Rapid multi-organ failure, fatal	1 5 10
Dermal	Skin exposure	Local corrosion, risk of systemic toxicity if skin is broken	1 4 6
Inhalational	Rare	Mild respiratory symptoms, rarely severe	4 6
Injection	Rare	Severe, rapid systemic toxicity	1

Table 2: Types of Paraquat Poisoning

Mild Poisoning

• Characterized by ingestion of small quantities (less than 20 mg/kg).
• Symptoms are limited to the GI tract: nausea, vomiting, and oral ulcers.
• Patients typically recover fully with supportive care 1 2 4.

Moderate to Severe Poisoning

• Ingestion of 20–40 mg/kg results in systemic symptoms.
• Local GI symptoms are followed by renal failure and pulmonary fibrosis—these may not appear until days or even weeks after exposure.
• Most cases result in delayed death (2–3 weeks), primarily due to lung and kidney failure 1 2 4.

Acute Fulminant Poisoning

• Ingestion of large amounts (>40 mg/kg) leads to overwhelming toxicity.
• Multi-organ failure develops rapidly, involving the heart, lungs, liver, kidneys, and other organs. Death may occur within hours to a few days 1 5 10.

Non-Oral Routes

• Dermal exposure can cause local tissue injury and, if the skin is broken, systemic toxicity 1 4 6.
• Inhalational exposure is uncommon but may cause mild respiratory symptoms.
• Injection (subcutaneous, intravenous, intraperitoneal) is rare and can lead to rapid, severe systemic toxicity 1.

Causes of Paraquat Poisoning

Understanding why and how paraquat poisoning occurs aids in both prevention and early intervention. The circumstances of exposure vary across the globe.

Cause	Frequency	Population Affected	Source
Deliberate Ingestion	Most common	Adults, suicidal intent	1 2 4 10
Accidental Ingestion	Occasional	Children, workers	1 4
Occupational Exposure	Less common	Agricultural workers	1 4 6
Skin/Mucosal Contact	Rare	Workers, accidental	4 6
Inhalation	Rare	Sprayers	4 6

Table 3: Causes of Paraquat Poisoning

Deliberate Self-Poisoning

The majority of paraquat poisonings today are due to intentional ingestion, often with suicidal intent. Studies from Asia and developing countries report that over 90% of cases are deliberate, reflecting both the accessibility of paraquat and its notoriety as a lethal agent 1 2 4 10.

Accidental Exposure

Accidental ingestion can occur, especially in children or when paraquat is stored in unlabelled containers. Such cases, though less common, highlight the dangers of improper storage and handling 1 4.

Occupational and Environmental Exposure

People working with paraquat, especially in agriculture, are at risk of poisoning through careless handling, lack of protective equipment, or accidental spills. Skin contact, particularly over damaged skin, can lead to significant absorption and toxicity 1 4 6.

Other Routes

Rare cases involve inhalation (breathing in spray mist) or injection. These usually occur in the context of occupational accidents or unusual circumstances 1 4 6.

Treatment of Paraquat Poisoning

Managing paraquat poisoning is one of the most challenging tasks in clinical toxicology due to the herbicide’s high lethality and lack of a proven antidote. However, early and aggressive supportive interventions can sometimes improve outcomes.

Treatment	Purpose	Evidence/Effectiveness	Source
Gastric Lavage	Decontamination	Early use, but not always recommended	2 7 13
Activated Charcoal/Fuller’s Earth	Adsorption	Routinely given, limited proof	7 12
Haemoperfusion	Toxin removal	May improve survival if given early	7 13
Antioxidants (N-acetylcysteine, salicylate)	Reduce oxidative damage	Possible benefit, limited evidence	2 7 9
Immunosuppression (steroids, cyclophosphamide)	Reduce inflammation	Widely used, weak evidence	2 7
Symptomatic/Supportive Care	Organ support	Essential, mainstay of therapy	1 2 4 5 7
Experimental Antidote (CB7)	Inhibit absorption	Effective in animal studies	12

Table 4: Treatment Approaches for Paraquat Poisoning

Early Decontamination

• Gastric lavage may be considered soon after ingestion, though some guidelines advise against it due to the risk of GI perforation from ulceration 2 7.
• Activated charcoal or Fuller's earth is routinely administered to bind paraquat in the gut and reduce absorption, though the benefit is unproven 7 12.
• Experimental antidote: A synthetic receptor, cucurbit7uril (CB7), has shown strong efficacy in animal models by tightly binding paraquat and inhibiting its absorption. However, this is not yet available for human use 12.

Enhancing Elimination

• Haemoperfusion (blood purification): Some studies suggest that early haemoperfusion (within 6 hours) may improve survival in severe cases by removing paraquat from the blood 13.
• Haemodialysis has not shown clear benefits for outcome improvement 7.

Limiting Oxidative Injury

• Antioxidants, such as N-acetylcysteine and salicylates, are used to scavenge free radicals and reduce cellular damage. There is some benefit suggested, but robust clinical trials are lacking 2 7 9.

Immunosuppressive Therapy

• Steroids (methylprednisolone, dexamethasone) and cyclophosphamide are widely used to suppress the inflammatory response and limit pulmonary fibrosis, but strong evidence for efficacy is lacking 2 7.

Supportive and Symptomatic Care

• Treatment of organ failure (renal, hepatic, respiratory) with intensive supportive care is essential. This may include mechanical ventilation, renal replacement therapy, and intravenous fluids 1 2 4 5 7.
• Pain management and nutritional support are important, especially for those with severe oral and esophageal ulceration 1 3 5.

Prognosis and Limitations

Despite aggressive management, the prognosis remains poor in severe cases, particularly when multi-organ failure develops. There is currently no specific antidote available for clinical use, though research into agents like CB7 holds future promise 12.

Conclusion

Paraquat poisoning is a grave medical emergency with a high fatality rate, predominantly due to its widespread use, lack of an effective antidote, and the rapid progression of multi-organ damage.

Key Points:

• Symptoms progress from GI irritation and oral ulcers to potentially fatal pulmonary, renal, and hepatic failure.
• Types of poisoning depend on dose and route, ranging from mild (fully recoverable) to fulminant (rapidly fatal).
• Causes are chiefly intentional (suicidal), but accidental exposures occur, especially among agricultural workers and children.
• Treatment is largely supportive, with early decontamination and haemoperfusion offering some benefit. Antioxidants and immunosuppressants are used, but with limited evidence. There is no approved antidote, though promising research is ongoing.

Takeaway:
Raising awareness, improving safe handling practices, and restricting access are crucial for prevention. For those exposed, swift medical intervention remains the best hope for survival while research into specific antidotes continues.