Refractory cardiopulmonary failure after glyphosate surfactant intoxication: a case report
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Glyphosate is an herbicide considered to be of low toxicity to humans because its effects are specific to plants. However, fatal reactions to glyphosate have been reported after the ingestion of large amounts. Pulmonary edema, shock, and arrhythmia were the reported causes of mortality.
We present the case of a 57-year-old woman who was admitted to the emergency department unconsciousness after ingestion of glyphosate surfactant in a suicide attempt. Metabolic acidosis, refractory respiratory failure, and shock developed during hospitalization. Despite aggressive supportive care, the patient died in the hospital.
The toxicokinetics of glyphosate surfactant is complicated. Respiratory failure, metabolic acidosis, tachycardia, elevated creatinine, and hyperkalemia are poor prognostic factors if presented. Physicians should consider using hemodialysis early to improve the outcome of patients with glyphosate surfactant intoxication.
KeywordsGlyphosate Metabolic Acidosis Elevated Creatinine Pulseless Electric Activity Refractory Shock
Glasgow Coma Scale
high performance liquid chromatograpy
polymerase chain reaction
parts per million.
Several fatal cases of glyphosate surfactant intoxication were reported in the literature from 1991 to 2008 [1, 2, 3, 4, 5, 6, 7, 8]. The toxicokinetics of glyphosate in humans has not been well established because of its complicated toxicity . Early prognostic factors were analyzed and reported to classify patients with severe intoxication [5, 8]. No antidotal therapy is available; therefore, hemodialysis has been used to treat patients with glyphosate surfactant intoxication, whose symptoms included arrhythmia, shock, hyperkalemia, and metabolic acidosis, despite supportive care [6, 10]. This case is presented to increase awareness of the symptoms experienced by patients with severe glyphosate surfactant intoxication. Early intensive care is necessary, and the necessity of hemodialysis should be determined for these patients [6, 10].
The toxicokinetics of glyphosate alone in humans is not well established, and most of what is known has been derived from animal studies. On ingestion, glyphosate is initially distributed to the small intestine, colon, kidney, and bone; the majority is rapidly excreted without biotransformation in the urine .
There are different formulations of surfactant. The product names and the chemical constituents were as Agri-Dex®- (Polyol fatty acid esters, Polyoxyethyl polyol fatty acid esters and Paraffin base petroleum oil), LI-700®- (Phosphatidylcholine, Propionic acid, and Alkylpolyoxyethylene ether), R-11®- (Octylphenoxypolyethoxyethanol, n-Butanol and Compounded silicone), Latron AG-98®-AG- (Octylphenoxypolyethoxyethanol, isopropanol and Polydimethylsiloxane), and Latron AG-98®-N- (Nonylphenoxypolyethoxyethanol, n-Buthanol and silicone antifoam compound). Other surfactant was used including polyethoxylaed alyl etheramine, trimethylethoxypolyoxypropylammonium chloride, polyethoxysorbitan monolaurate and alkyl polysaccharide.
In one case report, the post-mortem examination of tissue samples analyzed by HPLC/PCR confirmed concentrations of 100 ppm in the brain, 550 ppm in the blood, 60 ppm in the liver, and 3650 ppm in the kidney . The pattern of absorption, metabolism, and elimination was similar in animal studies . In our patient, the transient consciousness maybe related to transient high concentration in brain. Then, the plasma declined rapidly in 2 hours after ingestion, therefore; her consciousness regained.
Respiratory distress, shock, metabolic acidosis, and hyperkalemia are all predictors of poor outcome [5, 8]. Round-up pneumonitis, aspiration pneumonia, and pulmonary edema are all possible causes of respiratory distress. Increased acid production (which affects ATP consumption and production), metabolic derangements (which cause increased acid production and impair the renal elimination of acids) are all possible causes of metabolic acidosis . Shock may be related to primary cardiovascular effects or to secondary effects from acidosis or electrolyte imbalance. The cardiovascular effects of glyphosate surfactant were examined in the aorta and heart of rat. Vasorelaxation and inhibition of heart twitch tension were observed in the study by Chan et al . Bradycardia and ventricular arrhythmia often develop and are fatal in humans [4, 7]. It may also have primary toxicity in the conduction system and secondary toxicity in the circulation system. In our patient, electrolyte imbalance was corrected and acidemia was improved with sodium bicarbonate treatment; however, refractory shock persisted. The cardiovascular effect of glyphosate surfactant can be complicated. Some clinicians treat toxin-induced metabolic acidosis with a buffer, such as sodium bicarbonate, to correct acidemia. However, it has not been definitively shown to improve mortality in patients with metabolic acidosis after the administration of sodium bicarbonate .
Three studies of glyphosate surfactant intoxication in Taiwan have been published. In one of these studies (published in 1991), 7 of 93 patients died after exposure to glyphosate surfactant. The authors concluded that being older than 40 years and having a large ingestion volume are risk factors for mortality . In another of these studies (published in 2000), 11 of 131 patients died within 2.8 days of exposure. The authors identified three risk factors (pulmonary edema, acidosis, and hyperkalemia) associated with a poor prognosis . In the last of these studies (published in 2008), 17 of 58 patients died from glyphosate surfactant intoxication. The authors found 5 factors present at emergency department to be associated with mortality: respiratory failure, metabolic acidosis, tachycardia, elevated creatinine, and hyperkalemia . In our patient, there were respiratory failure, metabolic acidosis, elevated creatinine, pulmonary edema and hyperkalemia initially related to poor prognosis.
Indication of emergent dialysis
Indication of emergent dialysis
Large volume ingestion (> 200 ml)
Urine output < 0.5 ml/kg/h
Serum creatinine > 1.5 or GFR decreased by 25%
Volume overload- unresponsive to diuretics
Respiratory compromise- including pulmonary edema and hypoxia
Cardiovascular dysfunction- shock or EKG abnormalities
Electrolyte changes- hyperkalemia and acidemia
The toxicokinetic of glyphosate surfactant is complicated and the further detailed study is necessary to reveal definite mechanism of human toxicity. There are poor prognostic factors after analyze patients' presentation after intoxication. Physicians should consider using hemodialysis early to improve the outcome of patients with severe glyphosate surfactant intoxication.
Written informed consent was obtained from the patient for publication of this case report.
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