A 16-year-old girl was admitted to the ICU with a history of consuming poison (20 ml of deltamethrin containing 12.5mg/ml, total dose = 250mg) following a domestic dispute. She presented with status epilepticus. As per the details gathered from the relatives, the patient was having continuous generalized tonic clonic seizures (GTCs) (status) since one hour prior to admission and was even convulsing during her transfer to the hospital. On arrival the patient was immediately intubated and ventilated and resuscitation started.\nThe convulsions were treated with injection Lorazepam, but there was no response. Further, doses of IV Midazolam/ Valproate/Phenobarbitone were given, but the convulsions continued. A bolus does of Thiopentone was then given, after which she stopped convulsing. She was started on a thiopentone infusion. Despite the thiopentone infusion, she had four episodes of GTCs in the next six hours, which were managed with further boluses of thiopentone (200mg) and increase in rate of the infusion. Inotropes were started and IV fluids were continued which were guided by CVP and arterial BP monitoring. Her rhythm on ECG was normal and lungs were clinically dry. CNS examination was not possible because she was sedated with thiopentone. Her pupils were dilated (6mm) and fixed.\nAn EEG showed 80% suppression of the brain. CT scan showed diffuse cerebral edema with effacement of sulci and chinking of lateral ventricles.\nLab reports showed normal S. cholinesterase levels (4340 IU/L), normal serum electrolytes and urine negative for myoglobin.\nAfter 48 hours of being on thiopentone infusion (24 hours without convulsions), she was weaned off thiopentone infusion. The patient was triggering the ventilator well by the next day (day 4). Supports were hence taken off gradually. The patient's pupils became reactive by day 5.\nIn the following days, the patient was tracheostomized (in view of anticipated prolonged mechanical ventilation) and T-piece trials were initiated soon. By day 11, she was opening eyes to call and was moving all four limbs, but with reduced power. Tracheostomy was decannulated on day 14 [].\nNerve conduction studies were done in view of her poor muscle strength which showed “severe, generalized, predominantly motor axonal polyneuropathy”.\nThe patient was shifted to the ward after 18 days of ICU stay, on supportive care. Wheelchair ambulation was started on day 21 and the patient was discharged on day 26.
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.