The clinical usefulness of electrophysiological studies is well documented in organophosphate (OP) poisoning [1–3]. We report a case of acute fenitrothion poisoning with unusual polyneuropathy, which suggests that electrophysiological study… Click to show full abstract
The clinical usefulness of electrophysiological studies is well documented in organophosphate (OP) poisoning [1–3]. We report a case of acute fenitrothion poisoning with unusual polyneuropathy, which suggests that electrophysiological study may also be useful in other critical illnesses following OP poisoning. A 60-year-old female visited our emergency department 3 h after ingesting 100ml of 40% fenitrothion co-ingested with ethanol. Based on initial vital signs, physical examination, and laboratory test results, she was suspected as having mild cholinergic toxicity. She was admitted to the ICU for close clinical observation and received atropine (2.0–4.0 mlg/ day) and pralidoxime (12 g/day). On hospital day three, she exhibited delayed respiratory failure and acute lung injury, which required the endotracheal intubation and mechanical ventilation. After collecting blood cultures, third generation cephalosporin and metronidazole were administered. By hospital day 16, although her aspiration pneumonia and clinical conditions considerably improved, she could not be weaned off the mechanical ventilator. She exhibited decreased deep tendon reflex, sensory change and motor weakness of the extremities. Electrophysiological studies on hospital day 21 revealed unusual polyneuropathy without a characteristic decrement response on repetitive nerve stimulation (RNS) and decreased amplitude of sensory (digital nerve 9.0–9.7 microvoltage) and motor action potential (median nerve 3.4–4.6 millivoltage, ulnar nerve 3.8–4.2 millivoltage, common peroneal nerve 2.3–2.9 millivoltage), which completely recovered by HD 36 with antidote therapy and conservative care. She was discharged on hospital day 42.
               
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