S3576 Toxic Origins: Acute Pancreatitis Caused by Organophosphate Ingestion

Introduction: Organophosphate (OP) poisoning is a common toxicologic emergency, typically presenting with cholinergic symptoms such as bradycardia, miosis, and bronchorrhea. Acute pancreatitis is a rare but recognized complication, likely due to cholinergic overstimulation causing increased pancreatic secretions and sphincter of Oddi contraction. Awareness of this association is essential for timely diagnosis and management. Case Description/Methods: A 30-year-old man was brought in by EMS after an ingestion of 100 ml of insecticide (a 2,2 dichlorovinyl dimethyl phosphate). Patient reported severe abdominal pain and several episodes of non bilious vomiting. On exam, he was somnolent but arousable and had drooling, miosis, and hyperlacrimation, as well as epigastric and suprapubic tenderness. Labs revealed WBC 19.9/mcl (4.8-10.8/mcl) lipase of 1,295 U/L (10-140 U/L), triglycerides of 200 mg/dl (<150 mg/dl), and ethanol <10 mg/dl. US and computed tomography abdomen were performed with no evidence of gallstones, bile duct dilation or edematous enlargement of the pancreas. Poison control center recommended monitoring the patient for 24 hours and starting atropine 3-5 mg intravenous if symptoms worsen. The patient was provided supportive management with intravenous fluids, opioids and antiemetics. After 24 hours, he was able to tolerate a solid diet and was discharged after consultation with the poison control center and psychiatry. Discussion: Organophosphate (OP) poisoning commonly causes bradycardia, bronchospasm, bronchorrhea, miosis, hypersalivation, lacrimation, urination, diarrhea, vomiting and diaphoresis, but can rarely lead to acute pancreatitis. The acetylcholinesterase enzyme is inhibited by the organophosphate leading to sphincter of Oddi contraction increasing the internal pressure in the pancreas. Exocrine secretions from the pancreas are also found to be increased during organophosphate poisoning. Our patient ingested 2,2-dichlorovinyl dimethyl phosphate and lacked other plausible causes of pancreatitis, such as ethanol or medication use, gallstones, and hypertriglyceridemia. Normally, the treatment of OP poisoning is atropine, which blocks the activity of acetylcholine by decreasing the internal pressure in the pancreas. Although our patient had a prompt recovery with supportive care, recognition of acute pancreatitis due to organophosphate poisoning can be critical for appropriate management in more severe cases.

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Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001141764.94000.f3
Primary Topic
Pesticide Exposure and Toxicity
Type
article
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article

S3576 Toxic Origins: Acute Pancreatitis Caused by Organophosphate Ingestion

Jaime Cabrales, Bibhuti Adhikari, Jean C. Singh, Juan Urraca
The American Journal of Gastroenterology
Pesticide Exposure and Toxicity
article

S3576 Toxic Origins: Acute Pancreatitis Caused by Organophosphate Ingestion

Jaime Cabrales, Bibhuti Adhikari, Jean C. Singh, Juan Urraca
article en

Abstract

Introduction: Organophosphate (OP) poisoning is a common toxicologic emergency, typically presenting with cholinergic symptoms such as bradycardia, miosis, and bronchorrhea. Acute pancreatitis is a rare but recognized complication, likely due to cholinergic overstimulation causing increased pancreatic secretions and sphincter of Oddi contraction. Awareness of this association is essential for timely diagnosis and management. Case Description/Methods: A 30-year-old man was brought in by EMS after an ingestion of 100 ml of insecticide (a 2,2 dichlorovinyl dimethyl phosphate). Patient reported severe abdominal pain and several episodes of non bilious vomiting. On exam, he was somnolent but arousable and had drooling, miosis, and hyperlacrimation, as well as epigastric and suprapubic tenderness. Labs revealed WBC 19.9/mcl (4.8-10.8/mcl) lipase of 1,295 U/L (10-140 U/L), triglycerides of 200 mg/dl (<150 mg/dl), and ethanol <10 mg/dl. US and computed tomography abdomen were performed with no evidence of gallstones, bile duct dilation or edematous enlargement of the pancreas. Poison control center recommended monitoring the patient for 24 hours and starting atropine 3-5 mg intravenous if symptoms worsen. The patient was provided supportive management with intravenous fluids, opioids and antiemetics. After 24 hours, he was able to tolerate a solid diet and was discharged after consultation with the poison control center and psychiatry. Discussion: Organophosphate (OP) poisoning commonly causes bradycardia, bronchospasm, bronchorrhea, miosis, hypersalivation, lacrimation, urination, diarrhea, vomiting and diaphoresis, but can rarely lead to acute pancreatitis. The acetylcholinesterase enzyme is inhibited by the organophosphate leading to sphincter of Oddi contraction increasing the internal pressure in the pancreas. Exocrine secretions from the pancreas are also found to be increased during organophosphate poisoning. Our patient ingested 2,2-dichlorovinyl dimethyl phosphate and lacked other plausible causes of pancreatitis, such as ethanol or medication use, gallstones, and hypertriglyceridemia. Normally, the treatment of OP poisoning is atropine, which blocks the activity of acetylcholine by decreasing the internal pressure in the pancreas. Although our patient had a prompt recovery with supportive care, recognition of acute pancreatitis due to organophosphate poisoning can be critical for appropriate management in more severe cases.

The American Journal of GastroenterologyVol. 120(10S2)
Openalex Percentile: Top 77%
Pesticide Exposure and Toxicity
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