Elmhurst Hospital Center / Icahn School of Medicine at Mount Sinai Queens, NY
Jazmín Mexía. Cabrales, MD1, Bibhuti Adhikari, MD1, Juan Urraca, MD2, Jean Singh, MD2 1Elmhurst Hospital Center / Icahn School of Medicine at Mount Sinai, Queens, NY; 2Elmhurst Hospital Center / Icahn School of Medicine at Mount Sinai, New York City, NY 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 [1,2]. 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 revealedWBC 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 CT 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 IV if symptoms worsen. The patient was provided supportive management with IV 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 (3). 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 [4]. 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 [3].
Disclosures: Jazmín Cabrales indicated no relevant financial relationships. Bibhuti Adhikari indicated no relevant financial relationships. Juan Urraca indicated no relevant financial relationships. Jean Singh indicated no relevant financial relationships.
Jazmín Mexía. Cabrales, MD1, Bibhuti Adhikari, MD1, Juan Urraca, MD2, Jean Singh, MD2. P4441 - Toxic Origins: Acute Pancreatitis Caused by Organophosphate Ingestion, ACG 2025 Annual Scientific Meeting Abstracts. Phoenix, AZ: American College of Gastroenterology.
