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 35-year-old male was admitted to our emergency department with giddiness as the major complaint following ingestion of an unknown quantity of an unknown poison. Patient was conscious, oriented with stable cardio-respiratory parameters at the time of arrival. After sometime, despite being well oxygenated via face mask, patient started having generalized tonic-clonic seizures. Initial attention to airway, breathing and circulation (ABC) was given, followed by a bolus dose of diazepam. Seizures subsided for a brief period only to recur repeatedly.\nOn repeated enquiry, the patient's relative brought empty bottles of “ALL OUT,” a commercial composition of pyrethroid used as insecticides providing a circumstantial evidence of the nature of the poisoning.\nPatient was given a bolus dose of thiopentone sodium, and soon his trachea was intubated. This was followed by a loading dose of the anti-convulsant phenytoin to control seizures.\nPatient was shifted to the intensive care unit for further management. On examination, he was deeply comatose. There was profuse sweating. His pulse rate was 136 per minute, and the blood pressure was 90/60mmHg. His pupils were dilated bilaterally and sluggishly reacting to light. Examination of the other systems was unremarkable. Hemogram, liver and kidney function tests, X-ray chest, ECG, and arterial blood gases were normal. Patient was put on a ventilator on the SIMV mode.\nAgain the patient started showing tonic–clonic seizures, which were continuous and unresponsive to anti-convulsant therapy. Thereafter, thiopentone sodium and midazolam infusions were administered and titrated clinically as no bedside EEG monitoring was available. Gradually, thiopentone sodium and midazolam infusions were tapered off, and patient was weaned off the ventilator to be extubated after 72 hours. The patient was discharged from the hospital on the 7th day after a psychiatry consultation.