Acute respiratory dysfunction after surgery for acute type A aortic dissection

Abstract

Objective: Acute respiratory dysfunction (ARD) can occur after acute type A aortic dissection, but relatively little is known about ARD in such patients. This study aims to analyse the clinical impact of ARD after surgery for acute type A aortic dissection and to assess possible treatment options. Methods: We reviewed our institutional database to identify patients who underwent surgery for acute type A dissection between October 1994 and January 2008 (n = 276). Postoperative ARD was defined as oxygenation impairment (PaO 2 /FiO 2 <150) that occurred within 72 h of surgery and was not related to other documented causes of acute respiratory failure. Results: A total of 37 patients (13%) (27 male, mean age 60.7 AE 11 years) experienced ARD after surgery for acute type A dissection. Intensive care unit stay was significantly longer for patients with ARD than those without (18 AE 11 days vs 7.5 AE 6 days, respectively, p < 0.0001). However, hospital mortality was not significantly different between groups (16% for ARD patients vs 19% for patients without ARD, p = 0.6). Logistic regression analysis identified preoperative multiple malperfusion as the only risk factor for ARD (OR 3.2, 95% confidence interval (C.I.): 2.2-4.9). Peak C-reactive protein levels were significantly higher in ARD patients (17.7 AE 6.7 vs 9.6 AE 5.4 mg dl À1 , p = 0.04). Prone positioning ventilation was performed in 15 patients (40%) with severely impaired oxygenation and resulted in an immediate increase in mean oxygenation index from 71.6 AE 8.8 to 138 AE 92.6 ( p < 0.001). There was a tendency towards a shorter total time of mechanical ventilation (355 AE 188 h vs 433 AE 318 h, p = 0.2) and shorter ICU stay (405 AE 198 h vs 505 AE 265 h, p = 0.2) in the prone positioning subgroup. Conclusions: ARD is a relatively common complication of surgery for acute type A dissection and is associated with increased morbidity and resource utilisation. Patients with preoperative malperfusion are at increased risk for development of ARD. Prone positioning is a viable treatment option that significantly improves pulmonary oxygenation. #

Effects of inhaled nitric oxide for postoperative hypoxemia in acute type A aortic dissection: a retrospective observational study

“…The enrollment criteria were as follows: (I) patients who received repairment surgery for AADA; (II) patients with a persistent postoperative hypoxemia, which was defined as the blood gas exam showed that ratio of arterial partial pressure of oxygen (PaO 2 ) to fraction of inspired oxygen (FiO 2 ) was equal to or less than 200 mmHg (PaO 2 /FiO 2 ≤ 200) occurring within 24 h after ICU admission, lasting more than 2 h, and in the absence of other causes of pulmonary insufficiency such as cardiogenic pulmonary edema, pneumonia, pleural effusion, segmental atelectasis, pneumothorax, and pulmonary artery embolism [12]. The exclusion criteria were as follows: (I) patients who died within 24 h after surgery; (II) patients who developed severe postoperative complications such as: coma, cardiogenic shock, and gastrointestinal ischemia.…”

Novel risk factors for the healthcare associated infections (HAIs) in patients with Stanford type A aortic dissection (TAAD)

“…We found that the patients with TAAD undergoing arch replacement were prone to a higher HAIs incidence rate (60%, 60 episodes/100 patients), the top three HAIs types were HAP (43%), VAP (27%) and BSIs (17%). The inflammation after TAAD, long duration of DHCA, and inadequate cooling of the lungs during surgery (20), intraoperative transfusion of banked blood (21) would increase the risk of pneumonia. Multivariate logistic regression analysis indicated that longer DHCA was an independent risk factor for postoperative HAIs.…”

Effects of pulmonary static inflation with 50% xenon on oxygen impairment during cardiopulmonary bypass for stanford type A acute aortic dissection

“…Higher serum proinflammatory cytokine levels indicate higher morbidity in preoperative ALI in AAD, [4,37] whereas the primary biological function of serum IL-10 is to attenuate inflammatory responses and prevent impairment of endothelial dysfunction. [38] TXB 2 is the stable metabolite of TXA 2 , [39,40] a pro-inflammatory mediator.…”