Epinephrine

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An event is serious (based on the ICH definition) when the patient outcome is:

• * death

• * life-threatening

• * hospitalisation

• * disability

• * congenital anomaly

• * other medically important event

A 12-year-old boy did not regain pulses despite administration of epinephrine [route and dosage not stated].

The boy, who had a medical history of haemoglobin sickle cell (HbSC) disease alpha-thalassemia trait, with mild sickle-related complications, presented to hospital in springs of 2020 with acute respiratory failure in the setting of a positive PCR for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). He was evaluated in the emergency department and discharged home, as he did not meet the hospitalisation criteria. On the following day, due to fever, weakness and pallor, he was referred to the emergency department. He was febrile, tachycardic and tachypnoeic with an oxygen saturation of 97%. Physical examinations was significant for laboured breathing. His nasopharyngeal swabs were positive for SARS-CoV-2. He started receiving off-label ceftriaxone and doxycycline as azithromycin was not available. He also required noninvasive bilevel positive airway pressure prior transferring to the pediatric intensive care unit (PICU). On arrival to the PICU, he was intubated by unspecified anaesthetics. ECG revealed normal QTc interval. He started receiving off-label enteral hydroxychloroquine 600mg every 12 hours. He also received enoxaparin sodium. His baseline haemoglobin was 107 g/dL. In order to reduce HbS%, exchange transfusion was suggested. On day 2 of hospitalisation, he was exchanged with ten units of sickle-negative, C, E, and K antigen crosshatched compatible packed red blood. He became hypotensive following transfusion and required fluid resuscitation. He received norepinephrine and epinephrine. He also received off-label vancomycin and piperacillin/tazobactam [piperacillin-tazobactam] until the negative blood cultures at 48 hours. His treatment with epinephrine and norepinephrine was discontinued. His creatinine was found to be elevated suggesting acute renal failure. His nasopharyngeal swabs were positive for SARS-CoV-2. His condition met the criteria for mild paediatric acute respiratory distress syndrome, along with COVID-19. His bilateral infiltrates were consistent with acute pulmonary disease. On day 4 of hospitalisation, his secretions were found to be thick and copious, in addition to worsened bilateral infiltrates. His routine workup showed lowered level of haemoglobin, with stable WBCs count and improved platelets count, D-dimer was 18.2μg/mL, consistent with the coagulopathy of COVID-19, but it was down-trending. From the day of hospitalisation, his fibrinogen level was increasing consistently, and it suggested worsening of inflammation. Liver function revealed lowered albumin and elevated AST. Basic metabolic panel indicated improving acute kidney injury. Eventually, he became hypoxaemic in the setting of an acute drop in tidal volumes delivered by the ventilator. In spite of manual ventilation and 100% oxygen administration, his oxygen saturation remained at 70%. In line suctioning and increased ventilator setting did not improve hypoxaemia. He became bradycardic. As his heart rate was 60 beats/minute, chest compression was started. He remained on ventilator during CPR protocol. In spite of chest compressions, bilateral needle thoracostomy and multiple epinephrine administrations did not regain the pulse (lack of efficacy), and he died with hypoxaemia. Autopsy was not performed.