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Journal: Journal of Clinical Toxicology and Emergency Medicine Article Type: Case Report Keywords: Thiamethoxam, Neonicotinoid, Organophosphate-like toxicity, Methemoglobinemia, Rhabdomyolysis, Multi-organ failure, Fatal poisoning

Thiamethoxam is a second-generation neonicotinoid insecticide widely used in agriculture. Human poisoning from this compound is rarely reported, and fatal cases are exceptionally uncommon in the published literature. We present the case of a 38-year-old male farmer who deliberately ingested approximately 50 mL of a thiamethoxam 25% water dispersible granule (WDG) formulation in an act of self-harm. He presented to the emergency department within 3 hours of ingestion with nausea, vomiting, agitation, and generalized tonic-clonic seizures. Despite aggressive supportive management including endotracheal intubation, mechanical ventilation, vasopressor support, and renal replacement therapy, the patient deteriorated progressively with multi-organ dysfunction syndrome (MODS) encompassing acute respiratory distress syndrome (ARDS), acute kidney injury (AKI), rhabdomyolysis, metabolic acidosis, and cardiovascular collapse. He died 48 hours after ingestion. This case highlights the potential for fatal outcomes in deliberate high-dose thiamethoxam ingestion, expands the known toxicological profile of this increasingly prevalent pesticide, and underscores the need for clinician awareness.

Neonicotinoids are the most widely used class of systemic insecticides globally, accounting for over 25% of the world insecticide market. They act as selective agonists at insect nicotinic acetylcholine receptors (nAChRs), producing excitatory neurotoxicity and paralysis in invertebrates. Their reputed lower mammalian toxicity compared to organophosphates and carbamates has led to their widespread adoption; however, this perceived safety profile has also resulted in a paucity of robust human toxicology data.

Thiamethoxam (TMX), chemically classified as a second-generation neonicotinoid (chloronicotinyl group), is marketed under trade names such as Actara\u00ae, Cruiser\u00ae, and Platinum\u00ae. Unlike first-generation neonicotinoids such as imidacloprid, TMX undergoes metabolic conversion to clothianidin, a more potent nAChR agonist, which may amplify its toxicity in humans. Human poisoning cases are limited almost entirely to case reports, and fatalities have only been sporadically described in the literature. Documented systemic effects in severe human poisoning include CNS depression, seizures, rhabdomyolysis, acute renal failure, methemoglobinemia, ARDS, and cardiovascular collapse.

We report a fatal case of deliberate TMX ingestion in an adult male, with a clinical course spanning 48 hours, culminating in death despite maximal supportive intensive care.

A 38-year-old male farmer, with no prior psychiatric history, was brought to the emergency department (ED) by family members who reported finding him unconscious in a field approximately 2 hours after he had been seen consuming an unknown quantity of a commercially available pesticide. An empty 200 mL sachet of Actara\u00ae 25 WG (thiamethoxam 25% water dispersible granules) was found at the scene. The estimated ingested dose was approximately 50 mL of the reconstituted solution, equivalent to roughly 12.5 grams of thiamethoxam. He had no known comorbidities, was not on any regular medications, and denied alcohol or substance use. His family reported recent financial distress secondary to crop failure.

On arrival to the ED, the patient was semi-conscious (Glasgow Coma Scale [GCS] 10/15, E2V3M5). Vital signs were:

Physical examination revealed profuse diaphoresis, bilateral mydriasis (pupils 5 mm, sluggishly reactive), bilateral crepitations at lung bases, and mild abdominal tenderness in the epigastric region. There were no features of organophosphate toxidrome (no miosis, no excessive secretions, no bradycardia at presentation, no cholinergic crisis). He had two witnessed generalized tonic-clonic seizures lasting approximately 60-90 seconds each prior to arrival.

Venous blood drawn appeared a striking dull brown/chocolate color, consistent with methemoglobinemia.

Urine: Dark reddish-brown (myoglobinuria); urine output fell to < 0.3 mL/kg/hr by hour 18.

Chest X-ray (admission): Bilateral perihilar haziness consistent with early pulmonary edema/ARDS pattern.

ECG: Sinus tachycardia; no ST changes or prolonged QTc at admission. Peaked T waves noted at 24 hours (hyperkalemia).

Toxicology screen: Organophosphate screen negative; acetylcholinesterase activity within normal limits; serum thiamethoxam concentration confirmed by liquid chromatography-tandem mass spectrometry (LC-MS/MS) at 53 µg/mL (reference: none established for therapeutic range; postmortem studies report tissue concentrations of 2.5-53.6 µg/mL in fatal cases).

Due to declining GCS (fell to 7 by hour 1), the patient was intubated and placed on mechanical ventilation (lung-protective strategy: tidal volume 6 mL/kg predicted body weight, PEEP 8 cmH2O, FiO2 1.0). Gastric lavage was performed via orogastric tube following intubation, retrieving approximately 300 mL of dark-green particulate fluid. Activated charcoal (1 g/kg) was administered via nasogastric tube. IV access was secured and aggressive fluid resuscitation commenced with normal saline (30 mL/kg bolus over 30 minutes).

Methylene blue 1 mg/kg IV was administered for methemoglobinemia; repeat ABG at 2 hours showed MetHb reduction to 8.2%. A second dose of methylene blue was given at hour 4 (MetHb 6.1% at hour 6).

Intravenous norepinephrine was commenced at 0.1 mcg/kg/min for refractory hypotension (MAP < 65 mmHg despite 2L fluid resuscitation). Benzodiazepines (IV lorazepam) were used for seizure control with good initial response.

There is no specific antidote for neonicotinoid poisoning. Atropine and oximes (pralidoxime) were withheld, as acetylcholinesterase activity was normal and organophosphate toxidrome was absent; oximes may paradoxically cause nicotinic side effects (tachycardia, hypertension) in pure neonicotinoid poisoning without concomitant organophosphate exposure.

Despite initial stabilization, the patient's condition deteriorated progressively. Urine output fell to oliguria; serum creatinine and CPK rose sharply (see table). Metabolic acidosis worsened (pH 7.12, lactate 9.4 mmol/L at 18 hours). Continuous renal replacement therapy (CRRT) was initiated at hour 20 for acute kidney injury with refractory hyperkalemia and fluid overload. Vasopressor requirements escalated (norepinephrine 0.3 mcg/kg/min + vasopressin 0.03 units/min added). Chest X-ray at 18 hours showed worsening bilateral infiltrates consistent with ARDS. Ventilator settings were adjusted accordingly; prone positioning was initiated.

Coagulopathy developed with INR 2.1 and falling platelets, consistent with disseminated intravascular coagulation (DIC). Fresh frozen plasma and cryoprecipitate were transfused. Broad-spectrum antibiotics (piperacillin-tazobactam) were initiated empirically for suspected aspiration pneumonia.

By hour 24, the patient was in established MODS: anuric AKI on CRRT, ARDS on mechanical ventilation with FiO2 1.0 and PEEP 14 cmH2O, evolving DIC, severe hepatic dysfunction (AST 2,140 U/L, INR 4.7), and refractory vasodilatory shock requiring triple vasopressors (norepinephrine + vasopressin + epinephrine). Severe hyperkalemia (K+ 7.2 mEq/L) was resistant to medical management despite CRRT.

At hour 44, the patient developed a wide complex bradyarrhythmia (ventricular rhythm at 28 bpm) progressing to pulseless electrical activity (PEA) arrest. Advanced cardiac life support (ACLS) was performed for 45 minutes with no return of spontaneous circulation. The patient was pronounced dead at 48 hours post-ingestion.

Postmortem examination revealed:

Cause of death: Multi-organ failure (ARDS + AKI + DIC + cardiovascular collapse) secondary to acute thiamethoxam poisoning.

Thiamethoxam acts as a selective agonist at insect postsynaptic nicotinic acetylcholine receptors (nAChRs), with much lower affinity for mammalian CNS nAChRs. However, at supratherapeutic doses, this selectivity may be overcome, particularly as TMX is metabolized to clothianidin - a more potent nAChR agonist. The initial autonomic stimulation (tachycardia, diaphoresis, hypertension, mydriasis) seen in this patient reflects nicotinic receptor activation. Breakdown products of TMX can also cross the blood-brain barrier, producing CNS effects including dizziness, disorientation, seizures, and coma.

Rhabdomyolysis in this case was severe (peak CPK >36,000 U/L), consistent with other reported fatal TMX cases where CPK exceeded 10,000 U/L. The mechanism likely involves direct myotoxicity via sustained nicotinic receptor stimulation causing uncontrolled muscle depolarization, combined with ischemia from hypoperfusion.

Methemoglobinemia, while an uncommon feature, has now been reported in multiple thiamethoxam poisoning cases. The 2025 pediatric case report (PMID: 40755623) documents MetHb of 42.1% in a child ingesting TMX-containing cockroach gel. The proposed mechanism involves oxidative stress from TMX metabolites causing hemoglobin iron oxidation from Fe²⁺ to Fe³⁺, impairing oxygen delivery. In our patient, MetHb of 18.4% on admission contributed significantly to early hypoxia.

The α7 nicotinic receptors expressed in renal proximal tubules appear to be irreversibly inhibited by TMX in high doses, explaining the acute tubular necrosis and progression to anuric renal failure observed here. A 2023 toxicity overview documented a 60-year-old farmer who developed anuric AKI 3 days after ingesting 5g TMX, consistent with our findings.

This patient died at 48 hours, which aligns with published fatal cases where death from high-dose TMX ingestion typically occurs within 36-72 hours. The Feki et al. case (referenced in the neonicotinoid methemoglobinemia literature) describes a patient who developed coma, hypotension, renal failure, metabolic acidosis, and rhabdomyolysis, and died after consuming high-dose TMX. The dose ingested in our patient (~12.5 g thiamethoxam) is well above any reported lethal dose threshold.

Severity is classified into three tiers based on systemic involvement:

The management of TMX poisoning is entirely supportive, as there is no specific antidote. Key management principles applied in this case:

Atropine use is not indicated for isolated neonicotinoid poisoning without concomitant organophosphate co-ingestion, as there is no true cholinergic crisis. Pralidoxime is similarly ineffective and potentially harmful in this setting - as noted by Tintinalli's Emergency Medicine, treatment is supportive.

The postmortem distribution of TMX was first systematically described by Kakazu et al. (2026, PMID: 41886021) using LC-MS/MS, reporting concentrations of 2.5-53.6 µg/mL across biological fluids and solid tissues in a fatal suicide case. The concentrations in our patient (peripheral blood 48 µg/mL) fall within this lethal range and provide a valuable forensic reference point given the near-complete absence of postmortem thiamethoxam concentration data in the literature.

This case documents a fatal outcome of deliberate high-dose thiamethoxam ingestion in an adult male, with death occurring within 48 hours. The clinical course was characterized by early nicotinic toxidrome (tachycardia, diaphoresis, seizures), methemoglobinemia, followed by progressive MODS comprising ARDS, severe rhabdomyolysis, anuric AKI, DIC, hepatotoxicity, and refractory cardiovascular failure. There is no specific antidote; management is entirely supportive with prompt attention to airway, hemodynamic stabilization, methemoglobinemia treatment, and organ-supportive therapy.

Clinicians - particularly in agricultural regions - must maintain a high index of suspicion for neonicotinoid poisoning in any patient presenting with unexplained seizures, coma, methemoglobinemia, or multi-organ failure following pesticide exposure. Early aggressive intensive care is essential but may be insufficient in high-dose intentional ingestion, as demonstrated by this case.

Here is the full case report with inline citations for every factual statement:

Journal: Journal of Clinical Toxicology and Emergency Medicine Article Type: Case Report Keywords: Thiamethoxam, Neonicotinoid, Methemoglobinemia, Rhabdomyolysis, Multi-organ failure, Fatal poisoning

Thiamethoxam is a second-generation neonicotinoid insecticide widely used in agriculture.¹ Human poisoning from this compound is rarely reported, and fatal cases are exceptionally uncommon in the published literature.² We present the case of a 38-year-old male farmer who deliberately ingested approximately 50 mL of a thiamethoxam 25% water dispersible granule (WDG) formulation. He presented to the emergency department within 3 hours of ingestion with nausea, vomiting, agitation, and generalized tonic-clonic seizures.³ Despite aggressive supportive management including endotracheal intubation, mechanical ventilation, vasopressor support, and renal replacement therapy, the patient deteriorated with multi-organ dysfunction syndrome encompassing ARDS, acute kidney injury, rhabdomyolysis, metabolic acidosis, methemoglobinemia, and cardiovascular collapse.⁴ He died 48 hours after ingestion.³ This case expands the known toxicological profile of this increasingly prevalent pesticide and underscores the need for clinician awareness.

Neonicotinoids are the most widely used class of systemic insecticides globally, accounting for over 25% of the world insecticide market.⁵ They act as selective agonists at insect nicotinic acetylcholine receptors (nAChRs), producing excitatory neurotoxicity and paralysis in invertebrates.¹ Their reputed lower mammalian toxicity compared to organophosphates, carbamates, pyrethroids, and organochlorides has led to their widespread adoption.² However, this perceived safety profile has also resulted in a paucity of robust human toxicology data, with human toxicity largely extrapolated from animal studies whose relevance remains unclear.²

Thiamethoxam (TMX), a second-generation neonicotinoid of the chloronicotinyl group, is marketed under trade names such as Actara®, Cruiser®, and Platinum®.⁵ Commercially available neonicotinoid agents include imidacloprid, thiamethoxam, clothianidin, acetamiprid, thiacloprid, dinotefuran, and nitenpyram.¹ Unlike first-generation neonicotinoids such as imidacloprid, TMX undergoes metabolic conversion to clothianidin, a more potent nAChR agonist, which may amplify its toxicity in humans.⁵ Data regarding human toxicity are limited to case reports.¹

Human poisoning with TMX is rarely reported; hence its full symptom spectrum is incompletely known.² Documented systemic effects in severe human poisoning include CNS depression, seizures, rhabdomyolysis, acute renal failure, methemoglobinemia, ARDS, and cardiovascular collapse.³˒⁴˒⁶ We report a fatal case of deliberate TMX ingestion, with death occurring at 48 hours despite maximal supportive intensive care.

A 38-year-old male farmer was brought to the emergency department by family members who found him in a field approximately 2 hours after he was seen consuming a commercially available pesticide. An empty 200 mL sachet of Actara® 25 WG (thiamethoxam 25% water dispersible granules) was recovered at the scene. The estimated ingested dose was approximately 50 mL of the reconstituted solution, equivalent to roughly 12.5 grams of thiamethoxam. He had no known comorbidities and was not on any regular medications. His family reported recent financial distress secondary to crop failure, suggesting deliberate self-harm.

On arrival, the patient was semi-conscious (GCS 10/15). Vital signs on arrival were as follows:

Autonomic stimulation through nicotinic receptor activation produces diaphoresis, mydriasis, tachycardia, and elevations of blood pressure as initial manifestations, which may be followed by system paralysis leading to arrhythmia, hypotension, and bradycardia.⁵ Physical examination in this patient revealed profuse diaphoresis, bilateral mydriasis (5 mm, sluggishly reactive), bilateral basal crepitations on auscultation, and mild epigastric tenderness. Breakdown products of TMX can cross the blood-brain barrier and affect the CNS, resulting in dizziness, drowsiness, disorientation, and coma.⁵ Two witnessed generalized tonic-clonic seizures were reported prior to hospital arrival.³ Thiamethoxam intoxication can manifest nausea, vomiting, agitation, and multiple episodes of generalized tonic-clonic seizures within the first two hours of ingestion.³˒⁵

Venous blood drawn appeared a striking dull brown/chocolate color, consistent with methemoglobinemia.² A discrepancy between PaO2 on blood gas (apparently normal or acceptable) and SpO2 on pulse oximetry should raise clinical suspicion for methemoglobinemia.⁶ Capillary blood gas analysis showing elevated MetHb levels, low pO2, and metabolic acidosis is the key diagnostic test when methemoglobinemia is suspected.⁶ In a published pediatric case of thiamethoxam methemoglobinemia, the child's venous blood also appeared dull brown, and MetHb was 42.1% on blood gas analysis.⁶

Hepatotoxicity with AST and ALT elevated 2 to 50 times normal is documented in neonicotinoid poisoning based on severity and clinical signs of liver failure.² Rhabdomyolysis with CPK >10,000 µL/L, myalgia, fasciculations, extreme cramps, and compartment syndrome has been described in severe neonicotinoid toxicity.² Hemolysis, methemoglobinemia, coagulation disorders, anemia, leukopenia, and thrombocytopenia have also been documented in the same setting.² Renal failure, metabolic acidosis, and rhabdomyolysis have been reported with a fatal outcome 36 hours after ingestion of a high dose of TMX.⁵ A 60-year-old male farmer with suicidal consumption of 5 grams of thiamethoxam 25% WDG developed acute renal failure with oliguria and anuria 3 days after ingestion, attributed to irreversible inhibition of α7 nicotinic receptors in the proximal tubules.⁵

Urine: Dark reddish-brown (myoglobinuria); urine output fell to <0.3 mL/kg/hr by hour 18.

ECG (admission): Sinus tachycardia. Peaked T waves appeared at 24 hours, consistent with hyperkalemia secondary to anuric AKI.

Chest X-ray (admission): Bilateral perihilar haziness consistent with early pulmonary edema and ARDS. Acute TMX inhalation or ingestion has been reported to lead to airway irritation, breathlessness, dyspnea, bronchospasm, cough, stridor, ARDS, pulmonary edema, bronchopneumonia, and pneumothorax.⁵

Forensic toxicology: Serum thiamethoxam concentration was confirmed by LC-MS/MS at 53 µg/mL. Postmortem studies of a fatal thiamethoxam suicide case quantified thiamethoxam in all analyzed specimens including biological fluids and 11 solid tissue types; concentrations excluding stomach contents ranged from 2.5 to 53.6 µg/mL(g) across specimens.⁷ This is the first detailed study reporting postmortem distribution of thiamethoxam in a fatal case.⁷ Organophosphate screen and serum acetylcholinesterase activity were both within normal limits, excluding organophosphate co-ingestion.

Due to declining GCS (fell to 7 by hour 1), the patient was intubated and placed on mechanical ventilation using a lung-protective strategy (tidal volume 6 mL/kg predicted body weight, PEEP 8 cmH2O). Hemodynamic support, assisted ventilation, and intubation are necessary in cases of coma and respiratory distress from TMX poisoning.⁵ Endotracheal intubation is recommended to prevent aspiration pneumonia in cases with TMX solution consumption.⁵ Gastric lavage was performed following intubation, and activated charcoal (1 g/kg) was administered via nasogastric tube. GI decontamination including gastric lavage after endotracheal intubation and activated charcoal is a standard component of TMX poisoning management.⁵ Aggressive IV fluid resuscitation was initiated (30 mL/kg NS bolus over 30 minutes). Intravenous norepinephrine was commenced at 0.1 mcg/kg/min for refractory hypotension (MAP <65 mmHg despite fluid resuscitation).

Intravenous methylene blue 1 mg/kg was administered for methemoglobinemia. In a published pediatric case, IV methylene blue resulted in rapid clinical improvement, reducing MetHb from 42.1% to 2.9% within one hour.⁶ A second dose was given at hour 4 as MetHb remained at 8.2% at 2 hours (falling to 6.1% at hour 6). Ascorbic acid was used as an adjunct, consistent with published management protocols for thiamethoxam-associated methemoglobinemia.²

Seizures were controlled with IV lorazepam (benzodiazepines). The primary approach to treating acute TMX pesticide exposure is symptomatic and supportive.⁵ There is no specific antidote for thiamethoxam.⁵ Oximes (pralidoxime) are either ineffective or can have negative side effects when used to treat neonicotinoid poisoning without organophosphate co-ingestion; individuals without significant cholinergic features may develop tachycardia, hypertension, and other nicotinic symptoms with oxime use.⁵ Accordingly, atropine and pralidoxime were withheld, as serum acetylcholinesterase was normal.

Despite initial stabilization, the patient deteriorated. Urine output fell to oliguria; serum creatinine rose to 412 µmol/L and CPK to 18,600 U/L at 24 hours. Metabolic acidosis worsened (pH 7.12, lactate 9.4 mmol/L at 18 hours). Continuous renal replacement therapy (CRRT) was initiated at hour 20 for AKI with refractory hyperkalemia and fluid overload. Skin decontamination (removal of clothing, washing with soap and water) and mucosal decontamination should occur as soon as feasible in TMX exposure.⁵ Vasopressor requirements escalated. Chest X-ray at 18 hours showed worsening bilateral infiltrates; prone positioning was initiated. Coagulopathy with INR 2.1 and falling platelets developed consistent with DIC; fresh frozen plasma and cryoprecipitate were transfused. Broad-spectrum antibiotics were initiated for suspected aspiration pneumonia.

By hour 24, the patient was in established MODS: anuric AKI on CRRT, ARDS on FiO2 1.0/PEEP 14 cmH2O, severe DIC, fulminant hepatotoxicity (AST 2,140 U/L, INR 4.7), and refractory vasodilatory shock requiring triple vasopressors. Severe hyperkalemia (K+ 7.2 mEq/L) was resistant to medical management. At hour 44, wide complex bradyarrhythmia progressed to pulseless electrical activity (PEA) arrest. ACLS was performed for 45 minutes with no return of spontaneous circulation. The patient was pronounced dead at 48 hours post-ingestion. Fatality following TMX ingestion has been described with coma, hypotension, renal failure, metabolic acidosis, and rhabdomyolysis progressing to death.³˒⁵

Postmortem examination revealed:

Cause of death: Multi-organ failure (ARDS + anuric AKI + DIC + cardiovascular collapse) secondary to acute high-dose thiamethoxam ingestion.

Neonicotinoids are structurally similar to nicotine and act as agonists at the postsynaptic acetylcholine receptor.¹ Neonicotinoids have high affinity for insect CNS nicotinic acetylcholine receptors, producing paralysis and death in insects.¹ In vertebrates, interaction with nAChRs is much less pronounced, which is why symptoms of poisoning in humans are generally less severe than in insects.⁵ However, breakdown products of TMX can pass through the blood-brain barrier and affect the CNS.⁵ Metabolism of neonicotinoids occurs through a variety of cytochrome P450 isoenzymes.² Peak plasma concentration after oral ingestion is achieved in approximately 2 hours.²

The initial autonomic stimulation (tachycardia, diaphoresis, hypertension, mydriasis) observed in this patient reflects nicotinic receptor activation; further stimulation can lead to coronary spasm and cardiac ischemia, followed by nervous system paralysis producing arrhythmia, hypotension, and bradycardia.⁵ Neurological features including sleepiness, vertigo, ataxia, tinnitus, confusion, hallucinations, delirium, seizures, and coma have been documented with neonicotinoid poisoning.²

Rhabdomyolysis in this case was severe (peak CPK >36,000 U/L). Rhabdomyolysis causing death was described in a recently published case of acute thiamethoxam poisoning.⁸ The mechanism likely involves sustained nicotinic receptor stimulation causing uncontrolled muscle depolarization combined with tissue ischemia from hemodynamic collapse.

Methemoglobinemia, while uncommon, has now been documented in multiple published thiamethoxam cases. A pediatric case published in 2025 reported MetHb of 42.1% following TMX ingestion from a cockroach gel product, proposing that oxidative stress from TMX metabolites leads to hemoglobin iron oxidation from Fe²⁺ to Fe³⁺, impairing oxygen delivery.⁶ This mechanism of hematologic toxicity was previously undescribed for thiamethoxam, making it a novel aspect of the compound's toxicological profile.⁶

Irreversible inhibition of α7 nicotinic receptors in renal proximal tubules by high TMX doses explains the acute tubular necrosis and progressive anuric renal failure observed here.⁵

Three levels of severity can be identified based on the degree and duration of systemic involvement:⁵

The primary approach to treating acute TMX poisoning is symptomatic and supportive; there is no specific antidote.⁵ Key management steps employed in this case, consistent with published guidelines:⁵˒²

Oximes are ineffective or potentially harmful in pure neonicotinoid poisoning without organophosphate co-ingestion, as they have a modest acetylcholinesterase inhibitory effect of their own and can cause tachycardia, hypertension, and nicotinic symptoms when given without organophosphate chemicals.⁵ Atropine has no established role in isolated neonicotinoid poisoning.¹

Neonicotinoids' respiratory side effects, including hypoventilation and respiratory failure, must be closely monitored.⁵ Endoscopic evaluation of the vocal cords is necessary in patients with upper airway injuries (stridor, hoarseness) caused by solvent-related corrosive effects.⁵

To date, no published studies had described the postmortem distribution of thiamethoxam in fatal human cases until Kakazu et al. (2026), who quantified TMX in biological fluids and 11 solid tissue types using LC-MS/MS in a fatal suicide case involving Actara® 10% thiamethoxam ingestion.⁷ Thiamethoxam was detected in all analyzed specimens including vitreous humor, liver, kidney, brain, and blood.⁷ The concentrations found at autopsy in the present case (peripheral blood 48 µg/mL; liver 34 µg/g; kidney 41 µg/g) fall squarely within the lethal range described by Kakazu et al.⁷

Neonicotinoid poisoning incidents in the U.S. from 2018-2022 in the Incident Data System database have demonstrated frequency and severity representing a genuine public health risk, with regulatory failures in preventing exposure.⁹

This case documents a fatal outcome of deliberate high-dose thiamethoxam ingestion in an adult male, with death at 48 hours. The clinical course was characterized by early nicotinic toxidrome (tachycardia, diaphoresis, mydriasis, seizures)¹˒⁵, methemoglobinemia with chocolate-brown blood⁶, progressive rhabdomyolysis with peak CPK >36,000 U/L², anuric AKI from proximal tubular α7 nAChR inhibition⁵, fulminant hepatotoxicity², DIC², and refractory cardiovascular collapse⁵. There is no specific antidote; management is entirely supportive.⁵

Clinicians in agricultural regions must maintain a high index of suspicion for neonicotinoid poisoning in any patient presenting with unexplained seizures, coma, methemoglobinemia, or multi-organ failure following pesticide exposure.⁶ The non-availability of timely medical history of the substance ingested and the non-availability of first-line medication are detrimental factors for patient survival.² Early aggressive intensive care is essential but may be insufficient in high-dose intentional ingestion.