UNCOMMON AMONGST COMMON: ANGIOTENSIN II-INDUCED PERIPHERAL ISCHEMIA IN REFRACTORY SEPTIC SHOCK

Abstract

SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Angiotensin (AT) II, a naturally occurring hormone, modulates blood pressure through direct vasoconstriction of the circulatory system and through stimulation of various catecholamines and vasopressin. Derived from the hydrolysis of AT I via the AT-converting enzyme (ACE) in the pulmonary & renal endothelium, AT II has been studied for cases of vasodilatory shock since the 1930’. Most recently, the ATHOS-3 trial demonstrated AT II’s utility as a rescue vasopressor agent, highlighting its catecholamine-sparing effects. CASE PRESENTATION: 34-year-old African American male presented with 3-day history of dyspnea, productive cough and an episode of hemoptysis. Upon presentation, he was febrile, tachycardic, hypotensive and hypoxic prompting endotracheal intubation and vasopressor support. Laboratory studies were significant for leukocytosis with bandemia, lactic acidosis, acute kidney injury, transaminitis & positive for influenza A. Despite aggressive critical care management with maximum ventilator requirements, broad-spectrum antibiotics, renal replacement therapy & proning, his overall condition continued to worsen. AT II was initiated on Day 2 of ICU admission for refractory hypotension secondary to septic shock. Approximately 48-72 hours after the initiation of AT II, he developed skin discoloration and blistering in all extremities secondary to both arterial and venous thromboemboli despite prophylaxis. The lesions ultimately progressed leading to gangrenous necrosis extending proximally to the torso. Unfortunately, on day 7 of ICU admission, patient suffered a cardiac arrest and expired despite ACLS efforts. DISCUSSION: In our patient, we exhibited similar results to those described in the ATHOS-3 trials. Administration of the AT II resulted in an overall improvement in the patient’s mean arterial pressure, systemic vascular resistance and reduced norepinephrine requirements. We also observed a concomitant improvement in serum lactate, indicating improvement in overall organ perfusion. There are no absolute contraindications to AT II administration, but ATHOS-3 did report an increased incidence of both venous and arterial thromboembolic events in patients who received AT II. Although AT II has been FDA approved for the management of refractory septic shock, more studies are necessary to define those populations most at risk of the adverse effects. CONCLUSIONS: AT II is an important vasopressor agent used in refractory shock; however, more studies are needed to understand the adverse effects in populations most at risk. Reference #1: National Center for Biotechnology Information. PubChem Database. Angiotensin II, CID=172198, https://pubchem.ncbi.nlm.nih.gov/compound/Angiotensin-II (accessed on Mar. 26, 2020) DISCLOSURES: No relevant relationships by Krupa Gandhi, source=Web Response No relevant relationships by Mohit Mody, source=Web Response