Authors: Gudisa Bereda (Department of Pharmacy, Rift Valley University, Addis Ababa, Ethiopia)
Categories: Case Report, acetylcholinesterase inhibition, atropine, cholinergic toxicity, organophosphate poisoning, pralidoxime, supportive care
Source: Clinical Case Reports
Doi: 10.1002/ccr3.71183
Organophosphate (OP) pesticides are widely used in agriculture and can cause acute cholinergic toxicity by inhibiting the enzyme acetylcholinesterase, leading to an accumulation of acetylcholine. A 45‐year‐old male plumber was admitted to the emergency department 4 h after ingesting an unknown quantity of a 50% emulsifiable concentration of diazinon. He presented with sialorrhea, excessive tearing, emesis, and constricted pupils. Laboratory tests revealed a significant reduction in serum cholinesterase activity. A chest X‐ray showed no signs of pulmonary edema or lung abnormalities. The patient was found to be moderately dehydrated and was managed with intravenous normal saline (20 mL/kg) during the first 4 h of treatment. He received 1770 mg of pralidoxime over the first 12 h, along with 9.44 mg of atropine in the first 8 h, followed by 84.96 mg of atropine over the next 3 days. The patient's condition significantly improved after 48 h of intensive treatment, with symptom resolution and normalization of cholinesterase levels. His neurological function progressively returned to normal, and he was discharged on day seven without any lasting complications, having made a full recovery. This case highlights the critical importance of prompt diagnosis and immediate treatment of organophosphate poisoning to prevent life‐threatening outcomes. Continuous monitoring and appropriate supportive care are essential for ensuring a successful recovery.
Keywords: acetylcholinesterase inhibition, atropine, cholinergic toxicity, organophosphate poisoning, pralidoxime, supportive care
A preprint version of this manuscript was previously published by Bereda G. (2025) on MDPI Preprints.org with the DOI: https://doi.org/10.20944/preprints202503.2275.v1. Organophosphate poisoning (OPP) is a major global health issue, particularly in agricultural settings [1]. Organophosphates inhibit acetylcholinesterase, leading to the accumulation of acetylcholine and overstimulation of the cholinergic system [2, 3]. This results in muscarinic symptoms (e.g., salivation and diarrhea), nicotinic symptoms (e.g., muscle weakness), and central nervous system (CNS) manifestations (e.g., seizures). The severity of symptoms depends on the dose of exposure and individual susceptibility [4]. Diagnosis is based on clinical features and confirmed by low serum cholinesterase levels [1]. Treatment involves decontamination, administration of atropine and pralidoxime, respiratory support, and continuous monitoring [4]. This case report presents the clinical presentation, diagnostic findings, and treatment approach for a patient with acute cholinergic toxicity due to organophosphate poisoning.
A 45‐year‐old male plumber was admitted to the emergency department 4 h after ingesting an unknown amount of 50% emulsifiable diazinon concentration. He presented with excessive sweating, salivation, and tearing. The patient had attempted suicide following a quarrel with his father over land inheritance. Upon arrival at the hospital, the patient underwent immediate decontamination, including the removal of contaminated clothing and thorough skin washing. His airway, breathing, and circulation were stabilized, with respiratory support and secretion management to prevent further deterioration. Intravenous atropine (0.02 mg/kg/h) was administered promptly in the emergency department. Four hours later, due to worsening symptoms, he was transferred to the intensive care unit (ICU) for continued monitoring and treatment.
The patient had no known history of chronic illnesses, prior poisonings, or underlying medical conditions. He denied any drug allergies or previous hospitalizations related to toxic exposures. He lived in an urban area with a crowded and poorly ventilated home. His family history was unremarkable, with no reported genetic disorders or prior pesticide‐related incidents. He was a non‐smoker, did not consume alcohol, and had no history of substance abuse. Upon ICU admission, the patient was in severe distress. His vital signs indicated hypotension (95/67 mmHg), tachycardia (109 beats/min), and tachypnea (25 breaths/min), with a normal body temperature of 37.1°C, and oxygen saturation was 89% on room air. Neurological examination revealed fluctuating consciousness, muscle tremors, increased muscle tone, and spasms in the upper limbs. His pupils were constricted (miosis). Respiratory examination showed wheezing, increased work of breathing, and decreased breath sounds, indicating respiratory compromise. Cardiovascular examination revealed tachycardia but no murmurs. Gastrointestinal examination noted hyperactive bowel sounds and excessive secretions. Skin examination confirmed profuse sweating. His Glasgow Coma Scale (GCS) score was 10/15 (E3M4V3), reflecting moderate loss of consciousness.
Laboratory results showed elevated liver enzymes, with an aspartate aminotransferase (AST) level of 71 U/L and an alanine aminotransferase (ALT) level of 94 U/L, while alkaline phosphatase remained normal. Mild leukocytosis was present (white blood cell 16.9 × 10^3^/mm^3^), but kidney function was normal. Arterial blood gas analysis indicated respiratory acidosis with a pH of 7.06, low bicarbonate (20.1 mmol/L), elevated partial pressure of carbon dioxide (9.8 kPa), and a partial pressure of oxygen of 14.1 kPa. Serum electrolytes revealed hypokalemia (2.54 mmol/L), and serum cholinesterase activity was markedly reduced (2370 U/L). Biochemical tests showed elevated blood glucose (15 mmol/L), creatine kinase (10.76 μkat/L), and lactate levels (3.4 mmol/L). Urinalysis was positive for diazinon metabolites. A chest X‐ray showed no signs of pulmonary edema or lung abnormalities. A brain CT scan ruled out intracranial causes for the altered mental status. Electroencephalography (EEG) displayed abnormal slow delta waves, primarily in the frontal and frontotemporal regions.
The patient was also found to be moderately dehydrated, which was managed with intravenous normal saline (20 mL/kg) over the first 4 h. He was managed with oxygen therapy (4 L/min) until his SpO2 exceeded 95%. A continuous infusion of pralidoxime was initiated at 30 mg/kg for the first 12 h, followed by a maintenance infusion of 10 mg/kg for another 12 h. Although pralidoxime is effective peripherally, its limited ability to cross the blood–brain barrier reduces its effectiveness on central nervous system manifestations of organophosphate poisoning. Serial measurement of urinary diazinon metabolites can guide the appropriate duration of pralidoxime therapy, avoiding both premature discontinuation and prolonged, unnecessary treatment.
Atropine infusion was started at 0.02 mg/kg/h for the first 4 h and continued at the same rate for an additional 4 h. Over the next 3 days, atropine was administered at a reduced dose for 8 h/day before being tapered off. The patient received a total of 1770 mg of pralidoxime over the first 12 h, along with 9.44 mg of atropine in the first 8 h and 84.96 mg over the next 3 days. Atropine was gradually reduced as symptoms such as bradycardia, hypersecretion, and bronchospasm improved. The patient achieved atropinisation as evidenced by drying of secretions, resolution of bronchospasm, and normalization of heart rate.
Over the next 48 h, the patient showed steady improvement, with a reduction in cholinergic symptoms and stabilization of vital signs. By the fourth day in the ICU, he was able to breathe independently, and his level of consciousness improved. He was discharged on day seven with guidelines for ongoing monitoring of potential delayed neurotoxic effects. A monthly follow‐up was scheduled to assess recovery and screen for long‐term complications such as delayed neuropathy or cognitive impairments.
Organophosphate compounds are widely used as pesticides and insecticides [5, 6]. Acute cholinergic syndrome following organophosphate poisoning is characterized by symptoms resulting from overstimulation of cholinergic receptors due to the accumulation of acetylcholine [7]. This syndrome can be classified based on the predominant receptor types affected. Muscarinic symptoms result from stimulation of muscarinic receptors and include excessive salivation (sialorrhea), increased tear production (lacrimation), urinary incontinence, increased gastrointestinal motility leading to diarrhea, nausea, vomiting, and abdominal cramps. Other muscarinic features include miosis, bradycardia, and bronchoconstriction, which may cause breathing difficulties due to airway narrowing [8].
Nicotinic symptoms stem from activation of nicotinic receptors at the neuromuscular junction [9], presenting as muscle fasciculations, progressive muscle weakness—especially involving respiratory muscles—hypertension due to sympathetic stimulation, and tachycardia, which may be compensatory. Central nervous system manifestations may also occur, including altered mental status (confusion), convulsions, and coma due to CNS overstimulation [10].
The clinical findings in this case report correspond with existing literature, particularly muscarinic symptoms (salivation, lacrimation, urination, diarrhea, gastrointestinal distress, bradycardia, and bronchoconstriction) and nicotinic features (muscle weakness, hypertension, and tachycardia) [4]. However, CNS manifestations such as anxiety, confusion, or seizures, which are reported in prior studies, were not observed in this case.
Signs and symptoms typically include respiratory distress due to bronchoconstriction and respiratory muscle paralysis, hypersalivation and sweating due to secretory hyperactivity, miosis from parasympathetic overdrive, and cyanosis caused by respiratory failure or hypoxia. The underlying pathophysiology involves irreversible inhibition of acetylcholinesterase (AChE), resulting in acetylcholine (ACh) accumulation at synaptic junctions [11]. This leads to continuous stimulation of muscarinic and nicotinic receptors, disrupting neuromuscular function and causing paralysis and respiratory compromise. The resulting cholinergic crisis reflects overstimulation of both autonomic and central nervous systems [12] (Figure 1).
FIGURE 1 Pathophysiology of acute cholinergic syndrome induced by organophosphate poisoning.
The diagnosis of organophosphate poisoning is primarily clinical, supported by a history of pesticide or insecticide exposure, characteristic cholinergic signs and symptoms, and laboratory tests measuring plasma or red blood cell acetylcholinesterase (AChE) activity, which is typically decreased [13]. Toxicological screening may also confirm organophosphate presence. The diagnostic approach in the new case report aligns with existing literature, emphasizing both clinical assessment and laboratory confirmation [14].
Management includes critical decontamination (removal of contaminated clothing and skin washing), supportive care (airway protection and oxygen), and antidote administration. Atropine is used to counter muscarinic effects, while pralidoxime (2‐PAM) reactivates AChE when given early [15]. Continuous monitoring of respiratory, cardiac, and neurologic status is essential. Management in this case report—decontamination, supportive care, atropine, and pralidoxime—is consistent with established guidelines.
Prognosis depends on exposure severity, treatment timeliness, and complications. Severe exposures worsen outcomes, while early recognition and prompt treatment improve prognosis [8]. In this case, the patient recovered promptly without cardiac or neurological complications, reflecting favorable outcomes with timely intervention. Treatment includes atropine, pralidoxime, and supportive care. Outcomes vary, with risks of respiratory failure or neurological sequelae. This case report presents similar symptoms but may highlight refined diagnostics, updated treatment protocols, and favorable recovery timelines (Table 1).
This case underscores the role of acetylcholinesterase inhibition in organophosphate toxicity and highlights the importance of early atropine and pralidoxime treatment. However, as a single case, it may not be generalizable.
Organophosphate poisoning is a medical emergency needing rapid diagnosis, antidote treatment, and respiratory support. Early intervention improves survival, but ongoing monitoring is vital to detect delayed complications. Continuous follow‐up is essential to manage delayed neuromuscular effects and ensure full recovery.
Gudisa Bereda: conceptualization, investigation, methodology, project administration, resources, supervision, validation, visualization, writing – original draft, writing – review and editing.
Written informed consent was obtained from a patient for anonymized patient information to be published in this article.
The author declares no conflicts of interest.
The author has nothing to report.
Bereda G., “Organophosphate Poisoning: Insights From a Case Report of Acute Cholinergic Syndrome,” Clinical Case Reports 13, no. 10 (2025): e71183, 10.1002/ccr3.71183.
Further detail about the report can be made available upon request.
Further detail about the report can be made available upon request.