A 22-year-old man is brought to the emergency department after developing acute weakness, nausea, and vomiting. The patient is a farmer and was working in the fields when the symptoms began. Blood pressure is 100/62 mm Hg, pulse is 60/min, and respirations are 16/min. On physical examination, he is diaphoretic, and his clothes are soiled with vomit and feces. The pupils are 1 mm bilaterally. Lung auscultation reveals diffuse wheezing. Neurologic examination shows diffuse weakness, hyporeflexia, and muscle fasciculations. The patient is treated with the appropriate initial medication, which improves his wheezing, but he remains weak. Administration of which of the following medications is the most appropriate next step in management?

Question

A 22-year-old man is brought to the emergency department after developing acute weakness, nausea, and vomiting.  The patient is a farmer and was working in the fields when the symptoms began.  Blood pressure is 100/62 mm Hg, pulse is 60/min, and respirations are 16/min.  On physical examination, he is diaphoretic, and his clothes are soiled with vomit and feces.  The pupils are 1 mm bilaterally.  Lung auscultation reveals diffuse wheezing.  Neurologic examination shows diffuse weakness, hyporeflexia, and muscle fasciculations.  The patient is treated with the appropriate initial medication, which improves his wheezing, but he remains weak.  Administration of which of the following medications is the most appropriate next step in management?

Quizplus · Accepted Answer

11ec25c8_d16b_9bfc_bc81_4b361dd75226_MD0003_00 This patient who developed diaphoresis, nausea and vomiting, fecal incontinence, and diffuse weakness with muscle fasciculation after working in an agricultural field has signs of cholinergic toxicity, likely due to organophosphate pesticide exposure. Organophosphates inhibit acetylcholinesterase, leading to overstimulation of the muscarinic (mnemonic: DUMBELS-see table) and nicotinic (ie, muscle fasciculations, weakness, paralysis) cholinergic receptors. Management of organophosphate toxicity includes patient stabilization (ie, airway, breathing, circulation), decontamination (ie, removal of soiled clothes and irrigation of skin to prevent continued exposure), and reversal of cholinergic hyperstimulation. Atropine, a competitive inhibitor of acetylcholine at the muscarinic receptor, should be given immediately and leads to resolution of muscarinic symptoms (eg, bronchospasm). However, atropine does not have activity at the nicotinic receptors and cannot treat neuromuscular dysfunction. Therefore, pralidoxime, a cholinesterase-reactivating agent that has both nicotinic and muscarinic activity, should be given to treat neurotoxicity. Pralidoxime should be given only after atropine, because pralidoxime can cause transient acetylcholinesterase inhibition, which can momentarily worsen symptoms. (Choice A) Antitoxin therapy is used for the treatment of botulism, which usually occurs after the ingestion of contaminated food. Although botulism can manifest with gastrointestinal symptoms, it typically causes cranial nerve abnormalities followed by descending muscle weakness. Wheezing and diaphoresis are unexpected. (Choice B) Naloxone is used to treat opioid overdose, which can cause pinpoint pupils but would not be expected to cause nausea/vomiting, diarrhea, wheezing, or diaphoresis. (Choice C) Physostigmine is an acetylcholinesterase inhibitor that is sometimes used for the treatment of anticholinergic toxicity (ie, flushing, mydriasis, anhidrosis, fever, urinary retention). It would worsen this patient's symptoms. (Choice D) Plasma exchange may be used for Guillain-Barré syndrome, which can cause weakness but is not associated with signs of cholinergic excess. In addition, the weakness in this condition is typically ascending (ie, progresses from feet to involve the chest and upper extremities) and less abrupt in onset. Educational objective: Organophosphates inhibit acetylcholinesterase, leading to symptoms of muscarinic (mnemonic: DUMBELS) and nicotinic (neuromuscular dysfunction) cholinergic hyperstimulation. Management includes atropine, a competitive inhibitor of acetylcholine at the muscarinic receptor (reverses muscarinic symptoms), followed by pralidoxime, a cholinesterase-reactivating agent that has both nicotinic and muscarinic activity (reverses neurotoxicity).

A 22-Year-Old Man Is Brought to the Emergency Department After