A 13-year-old girl was admitted in our accident emergency with history of Bilbo 505 ingestion. The patient had ingested approximately 20 mL of Bilbo (chlopyrifos 50% and cypermethrin 5%) which was found to be a combination of OP and pyrethriod compound, with alkyl benzene sulfuric acid as emulsifier []. On arrival, the patient had difficulty in breathing which was accompanied by multiple episodes of vomiting. On examination, she was drowsy and had pinpoint pupils with an up-rolling of eye balls. There was no associated neck rigidity. Her heart rate was 92/min; peripheral oxygen saturation was 50%–70%, and auscultation of chest revealed bilateral crepitations, with excessive oral secretions. A chest radiograph revealed bilateral pulmonary infiltrates []. In view of her deteriorating clinical condition, the patient was intubated and mechanically ventilated. Gastric lavage was done to facilitate gastrointestinal decontamination. The patient received four doses of intravenous atropine, each of 6 mg. This was followed by administering atropine infusion at 6 mg/h till signs of atropinization were evident. Pralidoxime 2 g was administered intravenously in 100 mL of normal saline over 20 min, followed by repeat doses of 1 g pralidoxime four times a day. After an improvement in clinical course, tracheal extubation was done after 72 h of atropinization and pralidoxime administration. Her atropine dose was gradually tapered over the next 2 days and stopped thereafter.\nHowever, on day 7, she developed cough, breathlessness, and diarrhea for which she received oxygen supplementation, darolac sachet (containing lactobacillus sporegens), dextromethorphan hydrobromide, and chlorpheniramine maleate syrup. However, after 48 h (day 10), there was an increase in excessive frothy secretions from mouth, severe breathlessness, and diarrhea. It was accompanied by tachycardia and bilateral crepitations in both lung fields. She was immediately intubated, and considering the cholinergic symptoms of poisoning, atropine was restarted at an infusion of 3 mg/h. She responded rapidly to the antidote and was extubated uneventfully after 24 h. The dose of atropine was weaned-off by day 15. However, on day 18, the patient again had cholinergic symptoms characterized by miosis, excessive salivation, lacrimation, diarrhea, blurring of vision, and up-rolling of eyeballs. Atropine was restarted at low dose of 1.6 mg/h and the patient was asymptomatic. Simultaneously we sent her plasma and red blood cell cholinesterase and it was is in normal range. The patient was observed for prolonged poisoning effects and was kept under observation in a high dependency unit. She had few episodes of urinary incontinence, blurring of vision, and cough on day 25 of poisoning, which subsided without any further need of atropine administration. She had no new symptoms of lacrimation, bronchorrhea, and miosis. The patient was observed for few more days to look for delayed intermediate symptoms or rebound cholinergic symptoms. She was discharged after a month of poisoning and was being followed telephonically. Since the last telephonic contact, the patient was not known to have any symptoms and was living a healthy life.
A 24-year-old female was admitted to our intensive care unit (ICU) with repeated episodes of seizures following deliberate ingestion of an unknown quantity of the anti-lice medication BUTOX (Deltmethrin 1.2%). On arrival in the emergency department, the patient was given a bolus dose of Lorazepam, and soon intubated, and then a loading dose of phenytoin was commenced. Gastric lavage was not performed as patient had repeated convulsions. On examination, she was deeply comatose, and was getting generalized tonic clonic seizures. Her pulse rate was 130/min regular, and her blood pressure was 136/76 mmHg. Her pupils were equal (2 mm in size) bilaterally briskly reacting to light. Other systemic examinations were unremarkable. An arterial blood gas showed mild metabolic acidosis. Hemogram, renal and liver function tests, electrocardiogram, and chest X-ray were normal. After repeat doses of Lorazepam and phenytoin, the patient was put on mechanical ventilatory support. A therapeutic coma was induced using a combination of Midazolam and Thiopentone sodium, as the patient continued to have convulsions. In the next 36 hours, Thiopentone and Midazolam were gradually tapered off after electroencephalography documentation of complete suppression of burst activity. She was gradually weaned off the ventilator after 72 hours. She was discharged from the hospital on Day 5 after psychiatry consultation.