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      The Utility of Preoperative Level of Erythrocytosis in the Prediction of Postoperative Blood Loss and 30-day Mortality in Patients with Tetralogy of Fallot

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          Abstract

          Background:

          Postoperative major bleeding is a relatively common complication of patients undergoing corrective surgery of tetralogy of Fallot (TOF). Life-threatening blood losses can lead to aggressive transfusions or reoperation. Little is known about the risk factors associated with a bleeding tendency in TOF patients. This study aimed to establish predictive models for postoperative blood loss and mortality in TOF patients.

          Methods:

          We conducted a retrospective observational study involving patients with TOF who were posted for corrective cardiac surgery in a single hospital between 2010 and 2015. Hospital records including sociodemographic, pre- and intra-operative characteristics were extracted. Postoperative blood loss (within 24 and 48 h) and 30-day mortality were the primary and secondary outcomes, respectively. Multivariate linear and logistic regression models were used to identify determinants of outcomes.

          Results:

          A total of 60 patients were included in this study. The median age was 1 year (interquartile range = 0.62–5) and the male to female ratio of 1.7:1. Mean postoperative blood loss within 24 h was 283 ± 212 mL. In multivariate linear regression, preoperative hematocrit (β = 6.63, P = 0.042) and duration of intraoperative oxygenator with CPB (β = 5.16, P = 0.025) were significantly correlated with postoperative blood loss within 24 h. After adjusting for sociodemographic, intra- and post-operative characteristics, preoperative hematocrit (odds ratio [OR] = 1.10, 95% confidence interval [CI] = 1.01–1.21), and postoperative red blood cell transfusions (OR = 3.88, 95% CI = 1.16–12.9) showed statistically significant association with 30-day mortality. The area under the receiver operating characteristic curve of the multivariable model was 0.863.

          Conclusions:

          Preoperative levels of erythrocytosis appear to predict postoperative blood loss and short-term mortality in TOF patients undergoing corrective surgery.

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          Most cited references10

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          Long-term survival in patients with repair of tetralogy of Fallot: 36-year follow-up of 490 survivors of the first year after surgical repair.

          We sought to analyze risk factors for long-term survival (up to 36 years) after surgical repair of tetralogy of Fallot (TOF). Survival after repair is excellent, but data >20 years are rare. From 1958 to 1977, 658 patients underwent correction of TOF at our institution and were analyzed for survival. Of this patient group (age 12.2 +/- 8.6 years [mean +/- SD], range 2 to 67), 39.7% had a previous palliation. Operative (n = 139) and 1-year (n = 29) deaths were excluded for long-term calculations, resulting in a study group of 490 patients. Actuarial 10-, 20-, 30- and 36-year survival rates were 97%, 94%, 89% and 85%, respectively. Mortality increased 25 years postoperatively from 0.24%/year to 0.94%/year (p = 0.003). The most common cause of death was sudden death (n = 13), followed by congestive heart failure (n = 6). Multivariate correlates of impaired long-term survival were date of operation (before 1970, p = 0.0104), preoperative polycythemia (p = 0.0487) and use of a right ventricular (RV) outflow patch (p = 0.0079). Postoperative systolic RV/left ventricular pressure ratio and age showed no influence. Patients without preoperative polycythemia and an RV outflow patch (n = 164) had a 36-year actuarial survival rate of 96% and normal life expectancy. Cyanosis, operative experience of the surgeon and an RV outflow tract patch influence long-term outcome after repair of TOF in older children. Early repair by experienced surgeons to avoid polycythemia and excessive RV hypertrophy is supported by this study. However, mortality risk increases 25 years postoperatively, and thus heart monitoring should be intensified.
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            Cyanotic congenital heart disease (CCHD): focus on hypoxemia, secondary erythrocytosis, and coagulation alterations.

            Children with cyanotic congenital heart disease (CCHD) have complex alterations in their whole blood composition and coagulation profile due to long-standing hypoxemia. Secondary erythrocytosis is an associated physiological response intended to increase circulating red blood cells and oxygen carrying capacity. However, this response is frequently offset by an increase in whole blood viscosity that paradoxically reduces blood flow and tissue perfusion. In addition, the accompanying reduction in plasma volume leads to significant deficiencies in multiple coagulation proteins including platelets, fibrinogen and other clotting factors. On the one hand, these patients may suffer from severe hyperviscosity and subclinical 'sludging' in the peripheral vasculature with an increased risk of thrombosis. On the other hand, they are at an increased risk for postoperative hemorrhage due to a complex derangement in their hemostatic profile. Anesthesiologists caring for children with CCHD and secondary erythrocytosis need to understand the pathophysiology of these alterations and be aware of available strategies that lessen the risk of bleeding and/or thrombosis. The aim of this review is to provide an updated analysis of the systemic effects of long-standing hypoxemia in children with primary congenital heart disease with a specific focus on secondary erythrocytosis and hemostasis.
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              Fibrinogen function is impaired in whole blood from patients with cyanotic congenital heart disease.

              Patients with cyanotic congenital heart disease (CCHD) have haemostatic abnormities associated with bleeding and thrombo-embolic events. The haemostatic abnormalities are not fully understood, but recent studies indicate that elevated haematocrit and fibrinogen function may be of importance. The aim of this study was to characterise the haemostatic profile and examine the potential role of haematocrit on clot formation and strength in CCHD patients. Furthermore to examine whether CCHD patients with history of haemoptysis have diminished fibrinogen function compared to those without haemoptysis.
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                Author and article information

                Journal
                Ann Card Anaesth
                Ann Card Anaesth
                ACA
                Annals of Cardiac Anaesthesia
                Medknow Publications & Media Pvt Ltd (India )
                0971-9784
                0974-5181
                Apr-Jun 2017
                : 20
                : 2
                : 188-192
                Affiliations
                [1 ] Department of Anesthesiology, Hospital Universitario del Valle, Cali, Colombia
                [2 ] Faculty of Health, School of Medicine, Universidad del Valle, Hospital Universitario del Valle, Cali, Colombia
                [3 ] Department of Anesthesiology, Centro Medico Imbanaco, Cali, Colombia
                Author notes
                Address for correspondence: Dr. Andres Zorrilla-Vaca, School of Medicine, Universidad del Valle, Cra 4B No. 36-00, Cali, Colombia. E-mail: andres.zorrilla@ 123456correounivalle.edu.co
                Article
                ACA-20-188
                10.4103/aca.ACA_25_17
                5408524
                28393779
                58b8626c-be73-4300-9258-abc248652a55
                Copyright: © 2017 Annals of Cardiac Anaesthesia

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

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                Categories
                Original Article

                anesthesia,blood loss,mortality,patient safety,predictors,tetralogy of fallot

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