Marrow Notes 8 Edition

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This patient with bradycardia, miosis, diaphoresis, excessive secretions (eg, bronchonhea, tearing), and weakness with fasciculations has signs of cholinergic toxicity. Most cases of cholinergic toxicity are due to organophosphate pesticides. However, the occurrence in multiple patients in a city setting suggests intentional organophosphate exposure, possibly due to a chemical weapon (eg, sarin, soman). Organophosphates inhibit acetylcholinesterase in the muscarinic and nicotinic cholinergic synapses, leading to decreased acetylcholine degradation and overstimulation of the corresponding receptors. In addition to widespread increased visceral smooth muscle tone and glandular secretions due to muscarinic hyperactivity (mnemonic: DUMBELLS), nicotinic hyperactivity causes muscle weakness and paralysis that can lead to rapid respiratory depression and death. Initial management of organophosphate toxicity includes atropine, a competitive inhibitor of acetylcholine at the muscarinic receptor, which relieves muscarinic hyperstimulation. However, atropine does not have activity at the nicotinic receptors and cannot treat neuromuscular dysfunction. Therefore, pralidoxime, a cholinesterase- reactivating agent that works at both nicotinic and muscarinic sites, should be administered to any patient with neuromuscular dysfunction (eg, weakness, fasciculations). It should be given only after atropine because pralidoxime can cause transient acetylcholinesterase inhibition, which can momentarily worsen symptoms (Choice A) Diphenhydramine is an inverse agonist of the histamine H1 receptor, which allows it to function as an antihistamine. Because the H1 receptor is similar to the muscannic receptor, diphenhydramine has some antimuscarinic effects (eg, urinary retention). However, it is less potent than atropine, and it would not reverse nicotinic dysfunction (weakness). (Choice B) Hemodialysis is sometimes used to treat toxic alcohol poisoning, which usually presents with altered mental status, as well as vision changes (methanol) or flank pain and hematuria (ethylene glycol) It is not Indicated in cholinergic toxicity Choice C) Hyperbaric oxygen is used to treat severe carbon monoxide poisoning, which presents with nausea, dizziness, and altered mental status. Patients typically have cherry-red cheeks and lips. (Choice D) Physostigmine is an acetylcholinesterase inhibitor that is sometimes used to treat anticholinergic toxicity (le, flushing, mydriasis, anhidrosis, fever, urinary retention). It would worsen this patient's symptoms. Educational objective: Organophosphates inhibit acetylcholinesterase, leading to symptoms of muscarinic (mnemonic: DUMBELLS) 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 treats both nicotinic and muscarinic symptoms

40-year-old woman is brought to the emergency department due to difficulty breathing and muscle weakness. She was one of several people who developed symptoms in a movie theater. Temperature is 36.7 C (98.1 F), blood pressure is 112/62 mm Hg, pulse is 51/min, and respirations are 24/min. On physical examination, the patient is diaphoretic. The pupils are pinpoint and unreactive, and significant tearing is noted. Diffuse rhonchi and wheezing are present in the lungs bilaterally. Muscle strength is diminished throughout, and fasciculations are noted in the extremities. First-line therapy is administered, but the patient remains weak. #NEETPG #INTREGRATED #NEXT #Clinical #PYQ

This patient's clinical presentation is sufficient to initiate prompt urinary catheterization for suspected urinary retention. Bedside ultrasound or bladder scan (if available) can also help in diagnosis but should not delay urinary catheterization. Urinary catheterization can document a postvoid residual bladder volume (>50 mL is considered diagnostic for urinary retention) and provides symptomatic relief by draining urine from the distended bladder. This patient should also discontinue amitriptyline therapy. (Choice A) An abdominal CT scan would reveal a distended bladder in this patient and may also show hydronephrosis and hydroureter However, CT scans are more expensive and time-consuming than urinary catheterization and will not provide symptomatic relief. Choice B) Upright abdominal x-ray is not as reliable for evaluating urinary retention as it may not show a distended bladder (unless obstructed by a bladder stone). Abdominal x-rays are more useful for diagnosing ileus or small-bowel obstruction. Amitriptyline may cause ileus, but these patients typically develop nausea, vomiting, hypoactive bowel sounds, distended abdomen, diffuse mild abdominal pain, and abdominal imaging showing dilated bowel loops without air/fluid levels. This patient's normal bowel sounds, infraumbilical fullness, and lack of wet diapers for 2 days make urinary retention more likely than ileus. (Choice C) Intravenous fluids, analgesics, and observation are the treatment for nephrolithiasis (kidney stones). Patients with kidney stones typically present with intense flank pain and hematuria instead of suprapubic fullness. Intravenous fluids could potentially worsen this patient's obstructive urinary symptoms. Take Home Point Drugs with anticholinergic properties can cause acute urinary retention by preventing detrusor muscle contraction and urinary sphincter relaxation. The treatment involves urinary catheterization and discontinuing the medication.