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.
The patient was a 16-month-old boy who was admitted to our hospital’s emergency department with a 15-min history of nausea, shortness of breath, and dyspnea. He subsequently developed cyanosis and impairment of consciousness. Foreign body inhalation had initially been diagnosed and the Heimlich maneuver served as the urgent treatment, but no foreign body was coughed up. On physical examination, he was unconscious, bilateral pupil diameter was 3 mm and sluggishly reactive to light. He exhibited rapid and shallow breathing with nasal flaring. The three concave signs were positive. Lung auscultation revealed clear breath sounds present bilaterally. His pulse rate was 161 per minute, and the blood pressure was 75/35 mmHg. Generalized tonic-clonic convulsions were observed after 5 min of admission in the emergency ward. 10% chloral hydrate 5 ml (5 mg/kg) was firstly administered via enema. After intravenous access was available, 2 mg midazolam was administered intravenously twice with intervals of 5 min, as well as intramuscular injection of phenobarbital 0.1 g. Despite of these interventions, the patient kept having uncontrolled convulsions for about 35 min, then 20 mg propofol by intravenous infusion was given to finally control his seizures. The patient’s trachea was intubated during the treatment, and then he was transferred to the intensive care unit for mechanical ventilation. During the hospitalization, meperfluthrin poisoning was considered when his parents provided a critical information that they found an empty liquid mosquito repellent bottle (Jiaojie®) in the location where the patient’s symptoms onset. According to the instruction, nearly 30 ml of meperfluthrin containing 8 mg / ml, total dose of 240 mg, was ingested.\nAfter hospitalization, he presented with fever and had a total leucocyte count of 23,600/mm3 and C-reactive protein (CRP) of 116.4 mg/L on day 1. The chest radiograph (as arrowed in Fig. a) only revealed a little bilateral pulmonary exudate. Serum electrolytes, lactate dehydrogenase (LDH), creatine phosphokinase (CRK), alanine aminotransferase, aspartate aminotransferase and creatinine level were normal. Cholinesterase was 6188 U/L. Initial arterial blood gas (ABG) analysis showed pH 7.218, pO2 76 mmHg, pCO2 48.1 mmHg, HCO3 19.6 mmol/L, base excess − 8 mmol/L, plasma lactate 4.28 mmol/L. Cerebrospinal fluid (CSF) analysis and cranial computed tomography (CT) showed no abnormalities. On the second day of hospitalization, X-ray chest radiograph (as arrowed in Fig. b) showed multiple patchy and cord-like high-density shadows in the lungs bilaterally. Meanwhile, auscultation of the lungs revealed coarse crackles and wheezes. On day 3, Chest CT (Fig. ) revealed consolidation and atelectasis in the lower lobe of right lung and upper lobe of left lung, and multiple striated exudation could be seen in both lungs. On day 5, his X-ray chest radiograph (as arrowed in Fig. c) displayed consolidation and atelectasis in the right lower lobe and left upper lobe. His brain magnetic resonance imaging (MRI) (as arrowed in Fig. ) showed abnormal signal beside the anterior horn of the right lateral ventricle, and electroencephalogram (EEG) showed the diffused 2.0–4.0 Hz slow wave activity. Fiberoptic bronchoscopy revealed edema and congestion of mucous membrane without erosion or ulcers. The sputum culture gave a positive result for Hemophilus influenzae.\nAccording to the clinical symptoms, laboratory results and imaging findings, the patient was diagnosed with meperfluthrin poisoning, status epilepticus and severe pneumonia. Methylprednisolone (1 mg/kg every 12 h) by intravenous drip infusion and aerosolized beclomethasone dipropionate were prescribed to reduce pulmonary inflammation. Cefoperazone-sulbactam (60 mg/kg every 8 h) was administrated to control lung infection. Mannitol and monosialoteterahexosyl ganglioside were used to reduce intracranial pressure and protect injured nerve cells. He was successfully weaned off from the ventilator on day 15. Routine blood tests and CRP revealed no abnormalities after retesting. After a recheck on day 20, the chest X-ray radiograph (Fig. d) showed a significant improvement of the bilateral pulmonary exudate. After obvious symptoms relief, he was transferred to the rehabilitation department and the hyperbaric oxygen therapy was utilized for further neural repair. After a psychiatric consultation, he was discharged from the hospital on day 30. No symptoms had occurred after 12 months of follow up. The chronology of events was showed in Table .