ABSTRACT
TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Propofol-related infusion syndrome (PRIS) is a rare and serious effect of propofol infusion for sedation in critically ill patients. Though there has been an association seen with higher doses of propofol and prolonged infusion times, usually greater than 24 to 48 hours. CASE PRESENTATION: We present a case of an 86-year-old man with history of bradycardia and an implanted permanent pacemaker who was admitted for acute hypoxic respiratory failure caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pneumonia. Throughout hospital stay, this patient had progressively increasing oxygen requirements with appropriate escalation in level of care to the ICU. Due to increasing hypoxia despite non-invasive ventilation, the patient was intubated on day 4 of hospitalization, placed on vasopressors and started on sedation, which included continuous propofol infusion. On day 6 of hospitalization, the patient developed worsening hypotension requiring increased levels of sedation and significant lab abnormalities compared to labs collected the day prior. The patient was noted to have elevated potassium to 5.8 mmol/L, creatinine elevation to 2.41 mg/dL from 1.36 mg/dL, and elevated AST of 184 U/L and ALT of 95 U/L from normal levels. Lactate was 4.5, and creatinine kinase was 1317. Six hours later, repeat liver function tests revealed AST of 2078 U/L and ALT of 966 U/L. In the setting of sudden onset rhabdomyolysis, acute kidney injury, and lactic acidosis, there was concern for PRIS and propofol was discontinued. After extended discussion with the family, aggressive measures including dialysis were declined, and patient died. Of interest, the patient's pacemaker likely prevented the patient from developing bradycardia, classically seen in PRIS. DISCUSSION: Challenges with sedation of intubated patients with SARS-CoV-2 have been clinically observed and deeper sedation levels have been required to promote ventilator synchrony. Propofol continues to be a first-line sedative in critically ill patients, including SARS-CoV-2 patients. These patients require sedation higher infusion rates compared and are therefore at higher risk. Our patient was maintained on 20mcg/kg/min for 27 hours, then subsequently on 45 mcg/kg/min for 34 hours thereafter. Therefore, our patient was at increased risk of PRIS given propofol infusion at high doses was maintained for longer than 24 hours. Moreover, the concurrent use of vasopressors placed him at increased risk. CONCLUSIONS: Although propofol is recommended as a first-line anesthetic agent in critically ill patients with SARS-CoV-2 requiring sedation, the multiorgan failure resulting from PRIS is potentially fatal. Early recognition is crucial for management, which includes discontinuing propofol infusion and hemodialysis if indicated. REFERENCE #1: Hanidziar D, Bittner EA. Sedation of Mechanically Ventilated COVID-19 Patients: Challenges and Special Considerations. Anesth Analg. 2020;131(1):e40-e41. doi:10.1213/ANE.0000000000004887 REFERENCE #2: Payen JF, Chanques G, Futier E, Velly L, Jaber S, Constantin JM. Sedation for critically ill patients with COVID-19: Which specificities? One size does not fit all. Anaesth Crit Care Pain Med. 2020;39(3):341-343. doi:10.1016/j.accpm.2020.04.010 REFERENCE #3: Yamamoto K. Risk of propofol use for sedation in COVID-19 patient. Anaesthesiology Intensive Therapy. 2020;52(4):354-355. doi:10.5114/ait.2020.100477. DISCLOSURES: No relevant relationships by Sravani Gajjala, source=Web Response No relevant relationships by Oki Ishikawa, source=Web Response No relevant relationships by Stacey Jou, source=Web Response No relevant relationships by Zein Kattih, source=Web Response No relevant relationships by Vinayak Shenoy, source=Web Response
ABSTRACT
TOPIC: Cardiovascular Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) myocarditis has recently been described in case reports. A systematic review in early 2021 found fourteen case reports of myocarditis or myopericarditis secondary to this viral infection. We describe an interesting case of proven non-ischemic cardiac dysfunction in the setting of acute infection. Despite steroid treatment, which has been suggested to have favorable outcomes, our patient did not survive. CASE PRESENTATION: We present a case of a 77-year-old man with extensive electrophysiologic and ischemic cardiac disease who presented to the hospital for generalized weakness, malaise, and shortness of breath. The patient's cardiac history was significant for atrial flutter s/p ablation, coronary artery disease s/p coronary artery bypass graft in the distant past, peripheral artery disease s/p right lower extremity revascularization, and carotid stenosis s/p carotid endarterectomy. SARS-CoV-2 PCR test was positive. The patient had increasing hypoxia which required non-invasive ventilation and eventually, tracheal intubation and mechanical ventilation. The hospital course was complicated by the development of persistent chest pain associated with elevated cardiac enzymes. EKG showed diffuse ST-segment depressions. An echocardiogram revealed diffuse left ventricular hypokinesis and a reduced ejection fraction of 20% which was not present previously. In this setting, the patient was ruled in for acute coronary syndrome and underwent cardiac catheterization. Cardiac catheterization demonstrated patent grafts and no significant obstructive disease. A presumptive diagnosis of myocarditis was made. The patient's clinical status deteriorated despite optimal medical treatment, and he developed hemodynamically unstable atrial fibrillation that did not respond to pharmacologic treatment or cardioversion and resulted in cardiogenic shock and, ultimately, his death. DISCUSSION: SARS-CoV-2 myocarditis has been described in select case reports internationally. Many of these cases are described in patients with no previously identified comorbid conditions. This case suggests that in patients with underlying electrophysiologic dysfunction, SARS-CoV-2 myocarditis is associated with poor outcomes. CONCLUSIONS: The mechanism of the effect of SARS-CoV-2 on the heart is unclear and includes myocarditis or myopericarditis. In our patient, cardiac catheterization which was performed during his hospitalization confirmed no ischemic disease and suggested the presence of myocarditis which was ultimately fatal in the setting of refractory cardiogenic shock. Further research is needed into the optimal management of myocarditis associated with SARS-CoV-2. REFERENCE #1: Sawalha K, Abozenah M, Kadado AJ, et al. Systematic Review of COVID-19 Related Myocarditis- Insights on Management and Outcome. Cardiovasc Revasc Med. Feb 2021;23:107-113. REFERENCE #2: Purdy A, Ido F, Sterner S, et al. Myocarditis in COVID-19 presenting with cardiogenic shock: a case series. Eur Heart J Case Rep. Feb 2021;5(2):ytab028. REFERENCE #3: Fried JA, Ramasubbu K, Bhatt R, et al. The Variety of Cardiovascular Presentations of COVID-19. Circulation. 2020;141(23):1930-1936. DISCLOSURES: No relevant relationships by Sravani Gajjala, source=Web Response No relevant relationships by Stacey Jou, source=Web Response No relevant relationships by Zein Kattih, source=Web Response No relevant relationships by Rosaline Ma, source=Web Response No relevant relationships by Akhilesh Mahajan, source=Web Response No relevant relationships by Vinayak Shenoy, source=Web Response