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1.
Liver Transpl ; 28(10): 1628-1639, 2022 10.
Article in English | MEDLINE | ID: mdl-35352459

ABSTRACT

There is a paucity of evidence about the coagulation profile regarding the complexity of children undergoing liver transplantation (LT). This study aimed to investigate intraoperative hemostatic changes during pediatric LT according to the etiology for LT and examine the ability of rotational thromboelastometry (ROTEM® , TEM International GmbH, Munich, Germany) as a point-of-care monitoring method. We evaluated 106 patients aged 3 months to 17 years undergoing LT for acute liver failure (ALF) and chronic liver disease, which consists of patients with cholestatic disease, metabolic/genetic disease, and cancer. A total of 731 ROTEM® measurements, including 301 ellagic acid to initiate clotting via the intrinsic pathway, 172 tissue factor to initiate the extrinsic clotting cascade (EXTEM), and 258 cytochalasin D to inhibit platelet activity reflecting fibrinogen (FIBTEM), were analyzed at predetermined time points (the preanhepatic, anhepatic, and postreperfusion phases). We simultaneously conducted conventional coagulation tests. In children with ALF, preanhepatic measurements of conventional coagulation tests and ROTEM® showed a more hypocoagulable state than other diseases. During LT, the coagulation profile was deranged, with a prolonged clotting time and reduced clot firmness, changes that were more profound in the cholestatic disease group. Maximum clot firmness (MCF) on EXTEM and FIBTEM were well correlated with the platelet count and fibrinogen concentration (r = 0.830, p < 0.001 and r = 0.739, p < 0.001, respectively). On the EXTEM, MCF with 30 mm predicted a platelet count <30,000/mm3 (area under the curve, 0.985), and 6 mm predicted a fibrinogen concentration <100 mg/dl on the FIBTEM (area under the curve, 0.876). However, the activated partial thromboplastin time and prothrombin time were significant but only weakly correlated with the clotting time on the ROTEM® . In children undergoing LT, coagulation profiles depend on the etiology for LT. During LT, ROTEM® parameters could help detect thrombocytopenia and hypofibrinogenemia and guide transfusion therapy as a point-of-care monitoring method.


Subject(s)
Hemostatics , Liver Transplantation , Blood Coagulation Tests/methods , Child , Cytochalasin D , Ellagic Acid , Fibrinogen , Humans , Liver Transplantation/adverse effects , Thrombelastography/methods , Thromboplastin
2.
Pediatr Cardiol ; 40(8): 1618-1626, 2019 Dec.
Article in English | MEDLINE | ID: mdl-31482237

ABSTRACT

Ventricular performance and its loading condition change drastically after surgical correction of congenital heart defect. Pressure-volume loops analysis can provide quantitative information about ventriculo-arterial coupling (VAC) indicating the interaction between ventricular contractility and loading condition. Therefore, we investigated changes in VAC after corrective surgery for ventricular septal defect (VSD)/tetralogy of Fallot (TOF), and implication of ventriculo-arterial decoupling as a prognostic factor of post-operative outcomes. In children with VSD/TOF, pre- and post-operative arterial elastance (Ea), end-systolic ventricular elastance (Ees) and VAC (Ea/Ees) were non-invasively estimated using echocardiographic parameters. Post-operative outcomes included maximum vasoactive-inotropic score, the duration of mechanical ventilation and hospital stay. Preoperatively, patients with VSD had significantly lower Ea and Ees than patients with TOF; however, VAC were preserved in both. In patients with VSD, post-operative Ea increased disproportionately to change in Ees, resulting in increased VAC. Post-operative higher VAC in patients with VSD was independently associated with maximum vasoactive-inotropic score (odds ratio [OR] 63.9; 95% Confidence Interval [CI] 4.0-553.0; P = 0.003), prolonged mechanical ventilation (OR 6.3; 95% CI 1.1-37.8; P = 0.044) and longer hospitalization (OR 17.6; 95% CI 1.6-187.0; P = 0.018). In patients with TOF, Ea and Ees reduced post-operatively; however, VAC remained unchanged and was not associated with post-operative outcomes. Despite of different loading condition, preoperative VAC maintained in both of VSD and TOF. However, particularly in VSD patients, abrupt increase in post-operative loading state induces contractility-load decoupling, which leads to worse post-operative outcomes.


Subject(s)
Heart Septal Defects, Ventricular/physiopathology , Heart Ventricles/physiopathology , Tetralogy of Fallot/physiopathology , Case-Control Studies , Child , Echocardiography , Female , Heart Septal Defects, Ventricular/surgery , Humans , Male , Postoperative Period , Retrospective Studies , Tetralogy of Fallot/surgery , Treatment Outcome , Ventricular Function, Left
3.
Pediatr Transplant ; : e13237, 2018 Jun 15.
Article in English | MEDLINE | ID: mdl-29908011

ABSTRACT

Structural alterations in the cirrhotic heart may contribute to electromechanical abnormalities, represented by QT prolongation. The aim of this study was to investigate the changes in QTc according to the operative stage during pediatric LT and to identify which baseline echocardiographic parameters were associated with intraoperative QTc prolongation. Data were evaluated from 39 children undergoing LT for chronic liver disease (median age 9 months). In 19 patients (48.7%), baseline QTc was prolonged ≥440 ms (462 ± 19 ms). Through the period of post-reperfusion, QTI, QTc, and JTI progressively increased, although values partially recovered toward the end of surgery. High LVMI (≥82.51 g/m2 ) was associated with baseline QTc ≥ 440 ms (OR = 1.034, P = .032). In the 5 minutes post-reperfusion stage, marked QTc prolongation (defined as QTc ≥ 500 ms; n = 24, 61.5%) was significantly associated with high EDVI (OR = 1.060, P = .027) and SVI (OR = 1.075, P = .026). In children with chronic liver disease, increased ventricular volumes and mass may increase the risk of QTc prolongation during LT, suggesting that repolarization abnormalities might be contributed by structural changes characteristic of cirrhotic cardiomyopathy.

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