Lipid emulsion/quetiapine
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Various toxicities following overdose: 2 case reports A 35-year-old woman and a 64-year-old woman developed various toxicities following intentional overdose of antipsychotic quetiapine. Additionally, the 35-year-old woman developed non-cardiogenic pulmonary oedema and fat infiltration of lungs while receiving lipid emulsion for toxicities secondary to quetiapine overdose [not all times to reactions onsets stated]. Case 1: A 35-year-old woman presented following intentional acute overdose with ingestion of quetiapine 36g. She was somnolent and had slurred speech. She could be aroused to loud voice and light sternal rub, but fell asleep quickly. Her initial vital signs were as follows: HR 132 bpm, RR 18 breaths/minute, BP 123/79mm Hg, temperature 37°C and oxygen saturation 95%. Initial examination showed tachycardia, encephalopathy and dry mucous membranes. She received physostigmine, and her mental status improved. After 1 hour, she was encephalopathic again. She received physostigmine again, but significant improvement was not observed. Therefore, she was intubated because of obtundation and hypoxia. Prior to intubation, analysis of her arterial blood gases revealed the following: pH 7.38, partial pressure of CO2 38.7mm Hg, bicarbonate 22.9 mmol and partial pressure of O2 68mm Hg with a base deficit of 2 mmol. Her concomitant medications included lamotrigine. Quetiapine serum concentration was 7079.3 ng/mL. Her BP dropped to 78/35mm Hg, with HR being 141 bpm. She was found to have developed cardiovascular collapse. At 10 hours following quetiapine ingestion, ECG showed QTc 558ms (prolongation of QTc). Eleven hours following quetiapine ingestion, she developed status epilepticus with eight seizures over 20 minutes. She was treated with lorazepam and midazolam. She received norepinephrine for hypotension. Her HR was 140–150 beats/minute. She then started receiving 20% lipid emulsion therapy with a bolus of 1.5 mL/kg over 5 minutes, followed by a drip at 0.25 mL/kg/min. Following administration of lipid emulsion 2000mL, norepinephrine was discontinued. Her BP was 106/60mm Hg. On the following day, she was extubated with flumazenil. However, she developed respiratory distress as well as hypoxia in the night. Therefore, she was intubated again. A CT angiogram demonstrated new diffuse interstitial changes and airspace opacities with ground glass appearance as well as bilateral small pleural effusions. Differential diagnoses included pulmonary oedema, multifocal pneumonia or lipid emulsion induced fat infiltration of her lungs. She was found to have developed respiratory distress and hypoxia because of non-cardiogenic pulmonary oedema and fat infiltration of lungs secondary to lipid emulsion. Her triglycerides were 67 mg/dL and lipase was normal. Her WBC increased, and her maximum temperature was 38.1°C. She received unspecified antibiotics. A repeat electrocardiogram showed improvement of QTc to 440ms. After 2 days, she was extubated. One week following quetiapine ingestion, no oxygen support was required, and her
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