A 43-year-old woman was admitted to the emergency department with acute respiratory failure and hypotension 13 hours after the oral consumption of 300 ml of phoxim pesticide. She had no history of heart disease. The physical examination on admission showed the following: temperature, 36.8 °C; heart rate, 84 beats/min; respiratory rate, 17 beats/min; and blood pressure, 81/42 mm Hg (norepinephrine, 0.2 µg/kg/min). She had clear consciousness, the pupils on both sides were equal and 3.5 mm in diameter, the skin was dry all over the body, there were no wet rales over both lungs on pulmonary auscultation, and there was no murmur on heart auscultation. The arterial blood gas analysis and myocardial enzyme spectrum were normal, while electrocardiography (ECG) showed sinus tachycardia on admission. After admission, the patient was intubated and mechanically ventilated, analgesia and sedation were administered, rapid fluid expansion combined with norepinephrine was administered as an anti-shock treatment, hemoperfusion was performed, and atropine was administered to reverse the inhibitory effects of AOPP on cholinesterase.
Twenty-three hours after admission, the ECG (Fig. 1A) showed extensive lead ST segment elevation. The patient progressively deteriorated over the 36 hours after admission, and the ECG showed ventricular arrhythmia with abnormal Q wave and ST-T segment changes in some leads (Fig. 1B), which indicated severe myocardial injury. Echocardiography revealed an ejection fraction of 30%. The laboratory results showed a notable cTnI level of 11.0 µg/L (reference range, 0.01–0.023); the NT-ProBNP level was 26700 ng/L (reference range, 300–450), the creatine kinase level was 2454 U/L (reference range, 40–200), and the creatine kinase-MB isoenzyme level was 166 U/L (reference range, 0–24). She subsequently developed cardiogenic shock due to severe myocardial injury with complications of ventricular arrhythmia; thus, VA-ECMO was immediately initiated.
Three hours after the initiation of ECMO, the ECG showed a decrease in the ST segment (Fig. 1C). Her hemodynamics improved 6 hours after the initiation of ECMO. On the 3rd day after the initiation of ECMO, the myocardial enzyme indicators decreased significantly, and the left ventricular ejection fraction was 46%. VA-ECMO was withdrawn. On the 11th day after admission, she was transferred out of the intensive care unit, and at the 25-day follow-up, the patient had recovered and was discharged.