A 25-year-old female was brought to the emergency department with a history of nausea, vomiting, dizziness, abdominal pain, and altered sensorium. She was weighing around 55 kgs. She had given history of ingestion of two bottles (refills) of mosquito repellent available in the house, 2 h before she was brought to the hospital. (Each refill containing 45 ml (396 mg) transfluthrin). On examination, patient was conscious, pupils bilaterally semi constricted and sluggishly reactive to light. On auscultation of lungs crepitations were present bilaterally. Respiratory rate was 28/min. Blood pressure was 110/70 mmHg. In emergency ward, gastric lavage was performed and then continuous gastric aspiration was started through Ryles tube. Oral syrup charcoal 10 ml was given, and Ryles tube was closed at proximal end for some time. Then again aspiration through Ryles tube was continued. Atropine 0.6 mg, pantoprazole 40 mg and ondansetron 4 mg were given intravenously. Tonic-clonic convulsions were observed after 1 h of admission in the emergency ward. Injection phenytoin 700 mg bolus, injection diazepam 10 mg, injection hydrocortisone 100 mg, injection frusemide 20 mg, were administered intravenously. Oxygen enrichment was continued. However, patient had continuous uncontrolled convulsions. Then patient was shifted to intensive care unit and midazolam 5 mg and propofol 100 mg (80 mg + 20 mg) were administered intravenously. Endotracheal intubation was successfully performed with 7.5 mm ID endotracheal tube, and cuff was inflated and oxygen enrichment at 4–6 L/min via T-piece was initiated. Midazolam 4 mg/h and propofol 200 mg/h IV infusions were started. SpO2 was maintained at 100%. Blood pressure was 94/62 mmHg. Pulse rate was 74/min. Arterial blood gas (ABG) reports were normal. Neurophysician advised IV mannitol (20%)100 ml twice a day and IV phenobarbitone (SOS) for seizures.\nPatient was seizure free for few hours but again seizures started, and not controlled even with repeat doses of phenytoin, midazolam, propofol, and phenobarbitone. At that time blood pressure was 80/40 mm of Hg, respiratory rate was 35/min, pulse rate was 190/min, and SpO2 was 95%. Serum potassium, calcium, and sodium were 2.98 mmol/L, 2.5 mmol/L and 129 mmol/L, respectively. Injection dopamine was started at 10 μgm/kg/min. Potassium chloride 1.5 g and hypertonic saline were administered. Despite repeated doses of phenytoin, midazolam, propofol and phenobarbitone, seizures were not controlled. Elective ventilation was planned after muscle paralysis to control seizures. Patient was paralyzed by injection vecuronium 4 mg bolus and 4 mg/h IV infusion , and put on controlled mechanical ventilation (CMV) mode for elective ventilation. Vecuronium was continued at 4 mg/h. Blood pressure further decreased gradually and dopamine dose was increased and propofol infusion was stopped. ABG reports did not show any changes. Computed tomography scan of brain and chest X-ray were normal. Input/output charting for fluids was maintained. Central venous pressure remained at 5-8 cm H2O. Patient was kept on a ventilator for 48 h electively and then gradually weaning started. Vecuronium and midazolam infusion were stopped, and mode of ventilation was changed to synchronized intermittent mandatory ventilation (SIMV). Airway pressure support was set to 15 cm H2O with positive end expiratory pressure of 4 cm H2O. Patient's pulse rate was 102 beats/min, blood pressure 132/82 mmHg and SpO2 remained above 96%.\nPatient had total leucocyte count on day 1 of 7200/mm3 and it increased to 22,000/mm3 on the day 2, 32,000/mm3 on the day 3 and 13,000/mm3 on the day 4, all with neutrophilia without other signs of septicaemia, although antibiotics were continued. The counts decreased to 4000/mm3 on day 6. After 48 h on ventilator, dopamine infusion was tapered down in next 6 h and then stopped. About 6 h on SIMV mode, spontaneous respiration was noticed at 16 breaths/min. Muscle relaxation was reversed with inj. neostigmine 2.5 mg and inj.glycopyrrolate 0.4 mg. Patient started breathing spontaneously with adequate tidal excursion and followed verbal commands and then extubated. Oxygen through mask was given at flow of 4–5 L/min. Respiratory rate was 25 breaths/min, blood pressure was 108/72 mmHg and pulse rate, 119/min. Pupils were normally reacting to light. Patient was nebulised with mistabron 3 mg, repeated 8 hourly. Patient was referred to psychiatrist for counselling. On the day 4, patient was shifted to ward and discharged uneventful from hospital on 7th day.
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.