Characteristics and outcomes of Stanford type A aortic dissection patients with severe post-operation hyperbilirubinemia: a retrospective cohort study

Abstract

<jats:title>Abstract</jats:title> <jats:p><jats:bold>Background</jats:bold>: Hyperbilirubinemia is one of the common complications after cardiac surgery and is associated with increased mortality. However, to the best of our knowledge, the reports on clinical significance of postoperative severe hyperbilirubinemia in Stanford type A aortic dissection (AAD) patients were limited. <jats:bold>Methods</jats:bold>: Patients who underwent surgical treatment for AAD in our center between January 2015 and December 2018 were retrospectively screened. In-hospital mortality, long-term mortality, acute kidney injury (AKI), and the requirement of continuous renal replacement therapy (CRRT) were assessed as endpoints. Univariate and multivariate regression models were employed to identify the risk factors of these endpoints. <jats:bold>Results</jats:bold>: After screening, 271 patients were included in our present study. Of the included patients, 222 (81.9%) experienced postoperative AKI, and 50 (18.5%) received CRRT. The in-hospital mortality was 30.3%. The 1-year, 2-year, and 3-year cumulative mortality were 32.9%, 33.9%, and 35.3%, respectively. Multivariate Logistic regression analysis indicated that age (<jats:italic>P</jats:italic> &lt; 0.033), AKI stage 3 (<jats:italic>P</jats:italic> &lt; 0.001), the amount of blood transfusion after surgery (<jats:italic>P</jats:italic> = 0.019), mean arterial pressure (MAP) in the first postoperative day (<jats:italic>P</jats:italic> = 0.012), the use of extracorporeal membrane oxygenation (ECMO) (<jats:italic>P</jats:italic> = 0.02), and the peak total bilirubin (TB) concentration (<jats:italic>P</jats:italic> = 0.023) were independent risk factors of in-hospital mortality. The optimal cut-off value of peak TB on predicting in-hospital mortality was 121.2 μmol/L. Patients with post-operation TB ≥ 121 μmol/L was associated with worse long-term survival as well. <jats:bold>Conclusions</jats:bold>: Severe post-operation hyperbilirubinemia is a common clinical situation in patients had AAD repair. In AAD patients with severe post-operation hyperbilirubinemia, older age, lower MAP, increased blood transfusion, stage 3 AKI, the use of ECMO, and the increased peak TB lead to increase in-hospital mortality.</jats:p>

Risk factors of mortality in AAAD patients who had severe postoperative hyperbilirubinemia and received CRRT

“…And, 2.3% of the AAAD surgery patients had severe hyperbilirubinemia and CRRT after surgery. Our recent study showed that the in‐hospital mortality increased from 14% in all AAAD surgery patients to 30.3% in those with severe postoperative hyperbilirubinemia 11 . Additionally, previous studies showed that early mortality rates of AAAD surgery patients receiving CRRT were ranged from 25% to 40% 8,9,11 .…”

“…The standard surgical strategy employed in our center has been described previously 11 . Briefly, the AAAD surgery mainly included the following aspects: (1) cardiopulmonary bypass (CPB) was rapidly established, (2) the primary entry site was resected by open distal anastomosis under deep hypothermic circulatory arrest (DHCA) and selective anterograde cerebral perfusion, (3) aortic valve was preserved whenever possible, and (4) aortic arch replacement in patients with an entry site located in or extending into the aortic arch.…”

“…Our previous study showed that the incidence of both CRRT and severe hyperbilirubinemia (bilirubin concentration ≥85.5 µmol/L) were about 19% and indicated that increased peak bilirubin concentration and the use of CRRT were associated with significantly increased mortality risk in AAAD surgery patients with severe hyperbilirubinemia 11 . However, the prognosis of the AAAD surgery patients with severe hyperbilirubinemia and severe AKI requiring CRRT was not evaluated very well.…”

“…Hyperbilirubinemia is a common severe complication after AAAD surgery as well, with an incidence of 13–17% 10,11 . Severe hyperbilirubinemia could induce oxidative stress, cell apoptosis, respiratory failure, thrombocytopenia, and even neurological dysfunction, which promotes multiple organ dysfunction syndromes and increases in‐hospital mortality 12,13 .…”

“…Severe hyperbilirubinemia could induce oxidative stress, cell apoptosis, respiratory failure, thrombocytopenia, and even neurological dysfunction, which promotes multiple organ dysfunction syndromes and increases in‐hospital mortality 12,13 . Hyperbilirubinemia and AKI often occur simultaneously in patients with postoperative heart failure after AAAD surgery, 11 and severe hyperbilirubinemia could aggravate renal ischemia‐reperfusion injury and increased the incidence of severe AKI as well 14 …”