22/08/2026
Herbicide Poisoning
Su***de is becoming rampant and is a major public health problem. The mechanism is different during the season. In the rainy season the most common are agricultural chemicals like pesticides, herbicide and insecticides.
We need an urgent national Poison Information Center that is able to provide information about the country's wide poisoning data, give information on poisonous material information and identification, provide analytical lab services, and conduct toxicovigilance activities. These days a number of patients are coming to health facilities after intentional ingestion of chemicals. Some of the chemicals are not well known; no antidotes are available, and there is no capability of identifying their chemical composition.
One of our patients took this herbicide. Before today, I had never heard of it. The well-known herbicides in our setup were 2,4-D and Glycel (Ayimerte, ጅምላ፟ ጨራሽ) with the active ingredient, glyphosate.
1. 2,4-D: 2,4-dichlorophenoxyacetic acid (2,4-D)
🧭 It mainly causes uncoupling of oxidative phosphorylation and inhibits the voltage-gated chloride channel (CLC-1) in skeletal muscles. Dysfunction of CLC-1 induces myotonia, interfering with the utilization of acetylcoenzyme A (acetyl-CoA) or acting as a false messenger at cholinergic receptors.
🧭Direct injury to the gastrointestinal tract causes vomiting and diarrhea, which induces hypovolemia and electrolyte abnor-malities.
Other clinical features include neuromuscular findings (myalgia, rhabdomyolysis, weakness, myopathy, myotonia, and fascic-ulations), central nervous system effects (agitation, sedation, confusion, and miosis), tachycardia, hypotension, acute kidney injury, and hypocalcemia.
Tachypnea with respiratory alkalosis occurs in patients with phenoxy herbicide poisoning, which is consistent with increased mitochondrial respiration from mild uncoupling.
🧭More severe poisoning is characterized by metabolic acidosis, hyperventilation, hyperthermia, elevated creatine kinase, generalized muscle rigidity, progressive hypotension, pulseless electrical activity, or asystole.
🧭The mortality from acute phenoxy herbicide poisoning is high. When death occurs, it is usually delayed by 24 to 48 hours postingestion and results from cardiorespiratory arrest.
Management
🧭All patients with significant poisonings, particularly those with symptomatic oral ingestions, should be treated cautiously, including continuous monitoring for 24 to 48 hours, preferably in an intensive care unit.
🧭for primary and general hospitals: if the amount is large on history... immediate referral to a center with dialysis and an ICU center.
🧭There are no specific antidotes for phenoxy herbicides, but sodium bicarbonate or other alkalinizing agents favorably alter the kinetics of phenoxy herbicides.
🧭Maintaining an adequate urine output (> 1 mL/kg/h) optimizes the renal excretion of phenoxy herbicides as well as decreases renal toxicity from rhabdomyolysis.
🧭Urgent hemodialysis is recommended in patients with severe poisoning.
🧭Intubation and mechanical ventilation may be needed for decreased GCS and severe metabolic acidosis.
2.GLYPHOSATE (የጻረ አረም አይነት _ ጅምላ ጨራሽ)
🧭Glyphosate inhibits 5-enolpyruvylshikimate-3-phosphate synthase
🧭The formulation is irritating, and high concentrations are corrosive, causing direct injury to the gastrointestinal tract. Patients with severe poisoning manifest multisystem effects, suggesting that the formulation is either nonspecific in its action or that it interferes with a physiologic process common to a number of systems.
🧭 It is not known whether the manifestations of glyphosate poisoning represent a primary (toxic) or secondary (downstream) effect. Disruptions of oxidative phosphorylation globally impair normal cellular function as a result of limited energy supply. Hypotension and dysrhythmias impair tissue perfusion, and liver and kidney injuries induce metabolic disequilibria and acidemia, which impair normal physiologic processes. Pulmonary toxicity induces hypoxia, which fur-ther compromises normal cellular functioning.
🧭Clinical Manifestations
🪡Abdominal pain with nausea, vomiting, and/or diarrhea are the most common manifestations of acute poisoning. Gastrointestinal burns and necrosis occur with high doses of concentrated formulations and are associated with hemorrhage. Severe poisoning manifests as multiorgan failure, including hypotension; cardiac dysrhythmias; kidney and liver dysfunction; hyperkalemia; pancreatitis; pulmonary edema or pneumonitis; altered levels of consciousness, including encephalopathy; seizures; and metabolic acidosis. Proposed risk factors for death include a large exposure, delayed presentation to hospital, elevated glyphosate concentration, and increasing age.
Management
All patients except for those with trivial exposures should be observed for a minimum of 6 hours. If gastrointestinal symptoms are noted, then the patient should be observed for a minimum of 24 hours given that clinical toxicity may progress.
🪡Antidotes. No specific antidotes are proposed or tested for the treatment of acute poisoning with glyphosate-containing herbicides, which relates in part to the unknown mechanism of toxicity.
Do not do Gastric lavage
🪡From primary and general hospitals: early referral to a center with ICU and dialysis service.
Resuscitation and Supportive Care.
🪡All patients should receive prompt resuscitation, close observation, and routine supportive care; other treatments are largely empirical. The airway is usually maintained, but respiratory distress and failure occur, which require supplemental oxygen and possibly mechanical ventilation.
🪡The optimal management of hypotension is complicated because its etiology is potentially related to hypovolemia, negative inotropy, and/or reduced vascular resistance. If the response to prompt administration of 20 to 30 mL/kg intravenous fluid to the patient is insufficient or there is increasing pulmonary congestion, then vasopressors are recommended.
🪡Biochemical and acid–base abnormalities, such as hyperkalemia, should be corrected. Hemodialysis or hemofiltration should be administered to patients developing acute kidney injury per usual guidelines if active treatment is to be pursued. Survival is reported with severe glyphosate poisoning (respiratory failure, persistent ventricular tachycardia and shock refractory to inotropes, and acidemia) using extracorporeal membrane oxygenation therapy.
🪡 Dialysis is recommended for severe poisoning.
3. Tribenuron-methyl… Herbicide
🪡Methyl 2-[4-methoxy-6-methyl-1,3,5-triazin-2-yl (methyl) carbamoyl sulfamoyl] benzoate
🪡The Toxic Group is herbicides—sulphonylureas. Also contains oily substances or hydrocarbon solvents as a vehicles
750 mg per gram wettable powder
CLINICAL FEATURES
🪡Human poisoning is only likely from ingestion.
Irritation of the gastrointestinal tract may cause nausea, vomiting and diarrhoea.
🪡The molecular structure is similar to that of the sulfonylurea antidiabetic agents, so it is conceivable that they may cause hypoglycemia. This may present with sweating, dizziness and tachycardia progressing to confusion, agitation, coma and seizures.
🪡Many pesticides are formulated in oily substances or hydrocarbon solvents. These vehicles not only have potential systemic toxicity but are also volatile and easily inhaled. Therefore, patients may present with symptoms and signs of aspiration, such as cough, tachypnea, and crepitations.
🪡Skin and eye irritation may occur, particularly after contact with granular or powder formulations.
Management
🪡Asymptomatic patients who have accidentally ingested diluted formulations can be monitored at home in the care of a reliable observer if there is transport available to access medical help should the patient become symptomatic.
Assessment and admission are required for:
🤜All symptomatic patients
🤜Ingestion of a toxic dose
🤜Ingestion of an unknown amount of a concentrated preparation
🤜Eye/skin/inhalational exposures with more than mild transient symptoms
🤜 All deliberate ingestions should be observed for at least 6 hours for onset or worsening of symptoms.
Feared complication
🪡Hypoglycemia
🤜Chemical pneumonitis from hydrocarbon poisoning of the solvent.
Dr. Kassaye Demeke Altaye (MD, Associate Professor of ECCM, Clinical Epidemiologist)
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