Administration of prophylactic glucocorticoids has been suggested as a strategy to reduce postoperative AKI and other adverse events after cardiac surgery requiring cardiopulmonary bypass. In this post hoc analysis of a large placebo-controlled randomized trial of dexamethasone in 4465 adult patients undergoing cardiac surgery, we examined severe AKI, defined as use of RRT, as a primary outcome. Secondary outcomes were doubling of serum creatinine level or AKI-RRT, as well as AKI-RRT or in-hospital mortality (RRT/death). The primary outcome occurred in ten patients (0.4%) in the dexamethasone group and in 23 patients (1.0%) in the placebo group (relative risk, 0.44; 95% confidence interval, 0.19 to 0.96). In stratified analyses, the strongest signal for potential benefit of dexamethasone was in patients with an eGFR,15 ml/min per 1.73 m 2 . In conclusion, compared with placebo, intraoperative dexamethasone appeared to reduce the incidence of severe AKI after cardiac surgery in those with advanced CKD. 26: 294726: -295126: , 201526: . doi: 10.1681 Acute kidney injury is one of the most ominous complications after cardiac surgery with cardiopulmonary bypass (CPB). Approximately 1% of patients undergoing cardiac surgery require RRT for severe postoperative AKI, and experience strikingly high in-hospital mortality rates exceeding 40%. 1-3 Less severe AKI is far more common and identifies patients still at increased risk of shortand long-term mortality, prolonged length of hospital stay, and higher hospital costs. 4,5 The pathogenesis of AKI after cardiac surgery is complex and includes patient-related factors such as age and comorbidities (e.g., CKD and diabetes mellitus) as well as surgical factors such as type of procedure and duration of CPB. [6][7][8] Cardiac surgery results in a postoperative systemic inflammatory response syndrome due to a variety of factors including surgical trauma, exposure of blood to the artificial surface of the bypass circuit, tissue hypoperfusion, hemolysis, hemodilution, blood transfusion, and hypothermia. 9-12 Inflammation is believed to play a key role in the pathophysiology of AKI after cardiac surgery with CPB. A number of proinflammatory pathways are activated during CPB and can lead to leukocyte extravasation, lipid peroxidation, renal medullary congestion, and tubular cell injury. 1,9 Multiple strategies have been proposed to attenuate the inflammatory response after cardiac surgery with CPB, including the use of glucocorticoids. To date, the effect of glucocorticoids on AKI after cardiac surgery has been evaluated as a primary outcome in 14 randomized controlled trials, the largest of which included 216 patients. 3 A meta-analysis of these studies (which included a total of 888 patients) concluded that glucocorticoids have no protective effect on AKI after cardiac surgery. 3 However, these studies were underpowered, particularly to detect severe AKI. J Am Soc NephrolWe therefore conducted a post hoc analysis of severe AKI in the Dexamethasone for Cardiac Surgery (DE...
Prevention of endothelial barrier dysfunction using imatinib preserved microcirculatory perfusion and oxygenation during and after cardiopulmonary bypass. Moreover, imatinib-induced protection of endothelial barrier integrity reduced fluid-resuscitation requirements and attenuated renal and pulmonary injury markers.
While experimental data state that protamine exerts intrinsic anticoagulation effects, protamine is still frequently overdosed for heparin neutralisation during cardiac surgery with cardiopulmonary bypass (CPB). Since comparative studies are lacking, we assessed the influence of two protamine-to-heparin dosing ratios on perioperative haemostasis and bleeding, and hypothesised that protamine overdosing impairs the coagulation status following cardiac surgery. In this open-label, multicentre, single-blinded, randomised controlled trial, patients undergoing on-pump coronary artery bypass graft surgery were assigned to a low (0.8; n=49) or high (1.3; n=47) protamine-to-heparin dosing group. The primary outcome was 24-hour blood loss. Patient haemostasis was monitored using rotational thromboelastometry and a thrombin generation assay. The low protamine-to-heparin dosing ratio group received less protamine (329 ± 95 vs 539 ± 117 mg; p<0.001), while post-protamine activated clotting times were similar among groups. The high dosing group revealed increased intrinsic clotting times (236 ± 74 vs 196 ± 64 s; p=0.006) and the maximum post-protamine thrombin generation was less suppressed in the low dosing group (38 ± 40 % vs 6 ± 9 %; p=0.001). Postoperative blood loss was increased in the high dosing ratio group (615 ml; 95 % CI 500-830 ml vs 470 ml; 95 % CI 420-530 ml; p=0.021) when compared to the low dosing group, respectively. More patients in the high dosing group received fresh frozen plasma (11 % vs 0 %; p=0.02) and platelet concentrate (21 % vs 6 %; p=0.04) compared to the low dosing group. Our study confirms in vitro data that abundant protamine dosing is associated with increased postoperative blood loss and higher transfusion rates in cardiac surgery.
Right ventricular function is associated independently with 2-year all-cause mortality in a heterogenic cardiac surgery population.
Although hemodilution is attributed as the main cause of microcirculatory impairment during cardiopulmonary bypass (CPB), this relationship has never been investigated. We investigated the distinct effects of hemodilution with or without CPB on microvascular perfusion and subsequent renal tissue injury in a rat model. Male Wistar rats (375-425 g) were anesthetized, prepared for cremaster muscle intravital microscopy, and subjected to CPB (n = 9), hemodilution alone (n = 9), or a sham procedure (n = 6). Microcirculatory recordings were performed at multiple time points and analyzed for perfusion characteristics. Kidney and lung tissue were investigated for mRNA expression for genes regulating inflammation and endothelial adhesion molecule expression. Renal injury was assessed with immunohistochemistry. Hematocrit levels dropped to 0.24 ± 0.03 l/l and 0.22 ± 0.02 l/l after onset of hemodilution with or without CPB. Microcirculatory perfusion remained unaltered in sham rats. Hemodilution alone induced a 13% decrease in perfused capillaries, after which recovery was observed. Onset of CPB reduced the perfused capillaries by 40% (9.2 ± 0.9 to 5.5 ± 1.5 perfused capillaries per microscope field; P < 0.001), and this reduction persisted throughout the experiment. Endothelial and inflammatory activation and renal histological injury were increased after CPB compared with hemodilution or sham procedure. Hemodilution leads to minor and transient disturbances in microcirculatory perfusion, which cannot fully explain impaired microcirculation following cardiopulmonary bypass. CPB led to increased renal injury and endothelial adhesion molecule expression in the kidney and lung compared with hemodilution. Our findings suggest that microcirculatory impairment during CPB may play a role in the development of kidney injury.
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