Multiple drugs

Abstract

Various toxicities following drug administration via incorrect route; lack of efficacy: case report A 44-year-old woman developed cardiac arrest, ventricular fibrillation, cardiovascular collapse, pulseless cardiac electrical activity, sinus bradycardia, cardiopulmonary collapse, haemodynamic instability, global coronary hypoperfusion and myocardial injury secondary to bupivacaine toxicity following its inadvertent administration through an incorrect route. Additionally, she exhibited lack of efficacy during treatment with medium chain triglycerides/soya oil emulsion for local anaesthetic systemic toxicity. The woman was hospitalised on 03 August 2018, with symptoms of severe neck pain radiating to both arms, accompanied by weakness. Subsequent analyses confirmed hyperesthesia, multiple intervertebral hernias, cervical spinal stenosis and retrolisthesis. She was fitted for a brachial plexus block at the cervical paravertebral approach. A cervical paravertebral block at the C6 level was attempted. However, she inadvertently received a neuraxial injection of 0.5% bupivacaine [bupivacaine hydrochloride solution] in incremental doses over several minutes, to a total of 10mL (as suggested by the rapid loss of consciousness and cardiovascular collapse that ensued). After two minutes, she developed paraesthesia in the arms. She became confused. She developed apnoea and became unresponsive. Pulseless cardiac electrical activity and sinus bradycardia developed. The woman underwent cardiopulmonary resuscitation (CPR) using chest compressions and bag-mask ventilation. She received endotracheal intubation. Spontaneous circulation was restored after 4 minutes. She was then shifted to the ICU. A presumptive diagnosis of bupivacaine toxicity [local anaesthetic systemic toxicity; LAST] was made, and she was administered IV bolus 20% medium chain triglycerides/ soya oil emulsion [Lipofundin] 100mL, followed by a continuous infusion of 400mL over 30 minutes. However, in spite of this, she developed ventricular fibrillation 23 minutes after the first cardiopulmonary collapse, requiring resumption of CPR. She also required chest compressions. She required repeated defibrillation attempts for sustained ventricular fibrillation. She also required adrenaline every 4–5 minutes, and amiodarone after three defibrillation attempts. Return of spontaneous circulation was achieved after 47 minutes of CPR. Her sinus rhythm was restored. She opened her eyes and made purposeful movements during cardiac arrest. Following return of spontaneous circulation, ECG revealed ST depression in leads I, II, aVL and V2–V6. Nor-adrenaline was continuously administered to maintain haemodynamic stability. She was sedated with fentanyl and midazolam. A transthoracic ECG revealed absence of abnormal motions in the heart wall, an ejection fraction of 40% and minor dilatation of all chambers, with regurgitation through the mitral and tricuspid valves. Subsequently, blood tests were performed and results were found to be abnormal, including elevated troponin levels, suggestive of global coronary hypoperfusion and myocardial injury. The following morning, she achieved haemodynamic stability. She was fully conscious. She was subsequently extubated. She developed nonoliguric acute kidney injury [aetiology not stated] and required continuous furosemide infusion. Six days later, she was shifted to the ward. She complained dizziness, decreased hearing and pain in the chest wall due to prolonged chest compressions. After an additional 2 weeks of observation, she was discharged from the hospital.