Independent risk factors for hypoxemia after surgery for acute aortic dissection

Wei, Sheng; Yang, Haiqin; Chi, Yong; Niu, Zhaozhuo; Sun, Lu

doi:10.15537/smj.2015.8.11583

Cited by 27 publications

(40 citation statements)

References 26 publications

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“…None of the intraoperative variables were associated with hypoxemia in univariate analysis, but the CPB time was associated with hypoxemia in multivariable regression model. BMI was identified as an independent predictor of postoperative hypoxemia in the study, consistent with the study by Sheng and colleagues [ 14 ]. Actually, the association of obesity and hypoxemia is not limited to aortic surgery [ 18 ].…”

Section: Discussionsupporting

confidence: 91%

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Nomogram for the prediction of postoperative hypoxemia in patients with acute aortic dissection

Jiang

Jin

et al. 2018

BMC Anesthesiol

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BackgroundPostoperative hypoxemia is quite common in patients with acute aortic dissection (AAD) and is associated with poor clinical outcomes. However, there is no method to predict this potentially life-threatening complication. The study aimed to develop a regression model in patients with AAD to predict postoperative hypoxemia, and to validate it in an independent dataset.MethodsAll patients diagnosed with AAD from December 2012 to December 2017 were retrospectively screened for potential eligibility. Preoperative and intraoperative variables were included for analysis. Logistic regression model was fit by using purposeful selection procedure. The original dataset was split into training and validating datasets by 4:1 ratio. Discrimination and calibration of the model was assessed in the validating dataset. A nomogram was drawn for clinical utility.ResultsA total of 211 patients, involving 168 in non-hypoxemia and 43 in hypoxemia group, were included during the study period (incidence: 20.4%). Duration of mechanical ventilation (MV) was significantly longer in the hypoxemia than non-hypoxemia group (41(10.5140) vs. 12(3.75,70.25) hours; p = 0.002). There was no difference in the hospital mortality rate between the two groups. The purposeful selection procedure identified 8 variables including hematocrit (odds ratio [OR]: 0.89, 95% confidence interval [CI]: 0.80 to 0.98, p = 0.011), PaO2/FiO2 ratio (OR: 0.99, 95% CI: 0.99 to 1.00, p = 0.011), white blood cell count (OR: 1.21, 95% CI: 1.06 to 1.40, p = 0.008), body mass index (OR: 1.32, 95% CI: 1.15 to 1.54; p = 0.000), Stanford type (OR: 0.22, 95% CI: 0.06 to 0.66; p = 0.011), pH (OR: 0.0002, 95% CI: 2*10− 8 to 0.74; p = 0.048), cardiopulmonary bypass time (OR: 0.99, 95% CI: 0.98 to 1.00; p = 0.031) and age (OR: 1.03, 95% CI: 0.99 to 1.08; p = 0.128) to be included in the model. In an independent dataset, the area under curve (AUC) of the prediction model was 0.869 (95% CI: 0.802 to 0.936). The calibration was good by visual inspection.ConclusionsThe study developed a model for the prediction of postoperative hypoxemia in patients undergoing operation for AAD. The model showed good discrimination and calibration in an independent dataset that was not used for model training.

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Section: Discussionsupporting

confidence: 91%

“…The incidence of hypoxemia was lower than those reported in the literature (20% vs. 30%) [ 4 , 14 ]. Different definitions of postoperative hypoxemia may explain its different incidences.…”

Section: Discussioncontrasting

confidence: 55%

Nomogram for the prediction of postoperative hypoxemia in patients with acute aortic dissection

Jiang

Jin

et al. 2018

BMC Anesthesiol

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“…Postoperative hypoxemia in TAAD patients was defined as a PaO 2 /FiO 2 ratio of 200 mmHg or lower (5,6). Postoperative refractory hypoxemia was defined as a persistent PaO 2 /FiO 2 ratio ≤100 mmHg despite conventional therapy within 6 hours of admission to the CSICU.…”

Section: Methodsmentioning

confidence: 99%

“…Hypoxemia is a frequent postoperative surgical complication in TAAD and is associated with increased mechanical ventilation duration, intensive care unit (ICU) stay, mortality and hospital costs (3). Although studies have raised questions about the association between TAAD and the risk factors for postoperative hypoxemia (4)(5)(6), the mechanism of hypoxemia in TAAD remains unclear but may…”

Section: Introductionmentioning

confidence: 99%

Initial clinical impact of inhaled nitric oxide therapy for refractory hypoxemia following type A acute aortic dissection surgery

Hao

Lai

et al. 2019

J. Thorac. Dis.

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Background: To evaluate the effect of inhaled nitric oxide (iNO) therapy on oxygenation and clinical outcomes in patients with refractory hypoxemia after surgical reconstruction for acute type A aortic dissection (TAAD). Methods: A before-and-after interventional study was conducted in patients with refractory hypoxemia after surgical reconstruction for TAAD. Postoperative refractory hypoxemia was defined as a persistent PaO 2 /FiO 2 ratio ≤100 mmHg despite conventional therapy. From January to November 2016, conventional treatment was carried out for refractory hypoxemia. From December 2016 to October 2017, on the basis of conventional therapy, we explored the use of iNO to treat refractory hypoxemia. Results: Fifty-three TAAD patients with refractory hypoxemia were enrolled in this study. Twenty-seven patients received conventional treatment (conventional group), while the remaining 26 patients received iNO therapy. The PaO 2 /FiO 2 ratio was significantly higher in the iNO group after treatment than in the conventional group when analyzed over the entire 72 hours. The duration of invasive mechanical ventilation was significantly reduced in the iNO group (69.19 vs. 104.56 hours; P=0.003). Other outcomes, such as mortality (3.85% vs. 7.41%, P=1.000), intensive care unit (ICU) duration (9.88 vs. 12.36 days, P=0.059) and hospital stay (16.88 vs. 20.76 days, P=0.060), were not significantly different between the two groups. Conclusions: iNO therapy might play an ameliorative role in patients with refractory hypoxemia after surgical reconstruction for TAAD. This therapy may lead to sustained improvement in oxygenation and reduce the duration of invasive mechanical ventilation.

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“…Our previous study showed that a large number of AD patients may combine with acute lung injury (ALI), which severely affected the prognosis. Unfortunately, the exact mechanism of AAD complicated with ALI is still not well defined [2, 3]. Our previous study indicated that pulmonary microvascular endothelial barrier injury may present in patients with AAD, together with massive migration of macrophages and secretion of MMP-9, which finally induced ALI after interrupting the air-blood barrier [4].…”

Section: Introductionmentioning

confidence: 99%

Dephosphorylation of Y685-VE-Cadherin Involved in Pulmonary Microvascular Endothelial Barrier Injury Induced by Angiotensin II

Wang

Dai

et al. 2016

Mediators of Inflammation

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Angiotensin II (AngII) caused pulmonary microvascular endothelial barrier injury, which induced acute aortic dissection (AAD) combined with acute lung injury (ALI). However, the exact mechanism is unclear. We investigated the role of dephosphorylation of Y685-VE-cadherin in the AngII induced pulmonary microvascular endothelial barrier injury. Mice or pulmonary microvascular endothelial cells (PMVECs) were divided into control group, AngII group, AngII+PP2 (Src kinase inhibitor) group, and PP2 group. PP2 was used to inhibit the phosphorylation of Y685-VE-cadherin. Pathological changes, infiltration of macrophages and neutrophils, and pulmonary microvascular permeability were used to determine the pulmonary microvascular endothelial barrier function. Flow cytometry was used to determine the apoptosis of PMVECs, and immunofluorescence was used to determine the skeletal arrangement. Transendothelial resistance was used to detect the permeability of endothelial barrier. Phosphorylation of Y685-VE-cadherin was significantly reduced after AngII stimulation (P < 0.05), together with skeletal rearrangement, and elevation of endothelial permeability which finally induced endothelial barrier injury. After PP2 interference, the phosphorylation of Y685-VE-cadherin was further reduced and the endothelial permeability was further elevated. These data indicated that AngII could induce pulmonary injury by triggering endothelial barrier injury, and such process may be related to the dephosphorylation of Y685-VE-cadherin and the endothelial skeletal rearrangement.

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Independent risk factors for hypoxemia after surgery for acute aortic dissection

Cited by 27 publications

References 26 publications

Nomogram for the prediction of postoperative hypoxemia in patients with acute aortic dissection

Nomogram for the prediction of postoperative hypoxemia in patients with acute aortic dissection

Initial clinical impact of inhaled nitric oxide therapy for refractory hypoxemia following type A acute aortic dissection surgery

Dephosphorylation of Y685-VE-Cadherin Involved in Pulmonary Microvascular Endothelial Barrier Injury Induced by Angiotensin II

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