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 .
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.