Thrombosis after umbilical venous catheterisation: prospective study with serial ultrasound

Abstract

BackgroundUmbilical venous catheters (UVCs) are associated with thrombus formation. Most studies on thrombosis in infants with UVCs focus on only one part of the route, and none assessed a control group of infants without UVCs.ObjectiveTo determine the incidence and location of thrombi in infants after umbilical catheterisation and compare this with a control group of infants without umbilical catheters.DesignProspective observational study with serial ultrasonography of the UVC route from the umbilico-portal confluence to the heart. Ultrasonography was performed until day 14 after catheterisation in cases and day 14 after birth in controls.ResultsThrombi in the UVC route were detected in 75% (30/40) of infants with UVCs in the study group, whereas no thrombi were detected in the control group of infants without UVCs (0/20) (p<0.001). Six thrombi (20%) were located in the right atrium. Most of these were also partly present in the ductus venosus. Six thrombi (20%) were located in the ductus venosus only, and in 12 infants (40%), the thrombus was at least partly located in the umbilico-portal confluence. Thrombi persisted after UVC removal in 25/30 cases. Two infants with thrombotic events were treated with low-molecular-weight heparin and resolution was found. In the other 23 infants managed expectantly, 2 died due to necrotising enterocolitis, 1 was lost to follow-up and in 20 spontaneous regression was seen.ConclusionsThrombotic events occur frequently in infants after umbilical catheterisation. Most thrombi were asymptomatic and regressed spontaneously with expectant management. Routine screening for thrombi in UVCs is therefore not advised.

Portal vein thrombosis and food protein-induced allergic proctocolitis in a premature newborn with hypereosinophilia: a case report

“…In our infant, PVT occurred with no history of central venous catheterization as a single lesion, nonocclusive and not propagating, within the left portal vein, which was fortuitously identified in the ultrasonography and completely resolved with expectant management. Accordingly, our case is in line with previous reports addressing that for the treatment of neonatal thrombosis, a 'watch and wait' approach may be applicable to most cases, especially cases with asymptomatic thrombi [16,21]. Eosinophils have been believed to be possible direct target cells in cellular immune responses induced by CMP [23].…”

“…However, serious complications including liver lobe atrophy, portal hypertension and gastrointestinal hemorrhage can develop later in childhood largely in persistent, extensive and occlusive PVT [20,22]. A recent prospective case-control study on thrombosis in the UVC route with serial ultrasound screening did not demonstrate any thrombus forming process in 20 matched control neonates at 27-41 weeks' gestation without UVC until median day 13 (1-17) after birth [16]. In our infant, PVT occurred with no history of central venous catheterization as a single lesion, nonocclusive and not propagating, within the left portal vein, which was fortuitously identified in the ultrasonography and completely resolved with expectant management.…”

“…These molecules may lead to tissue and endothelial cell damage through cytotoxic effects, can inhibit the anticoagulant and fibrinolytic pathways, and can enhance activation of platelets and the tissue factor (extrinsic) coagulation pathway as shown in the various following mechanisms: 1) MBP and ECP neutralize negatively charged heparansulphate and exogenous heparin that bind to antithrombin by themselves or stimulating platelet factor 4 release, leading to failure to hinder factor X activation and thrombin generation [24,25]; 2) MBP, ECP and EPO block anionic thrombomodulin that mediates thrombin dependent-activation of protein C with inhibitory effects on factor V and factor VIII [26,27]; 3) MBP, ECP and EPO inhibit factor XII that can activate fibrinolysis [28]; 4) Eosinophils produce platelet-activating factor [29] and activate platelets along with MBP and EPO as strong platelet agonists [30]; 5) Eosinophils release tissue factor that activates factor X via factor VII activation and can stimulate tissue factor expression of endothelial cells via EPO [31]; 6) Eosinophils express CD40 ligand and contribute to initiation and progression of thrombosis [32]. In our infant, the development of PVT in the situation without UVC may be a result of the common intersection of multiple factors including hypereosinophilia, the immature hemostatic system of preterm newborn susceptible to thromboembolism [15], and hemodynamic changes by the adjacent ductus venosus involution after birth [16]. The initial eosinophilia before oral feeding may be from congenital conditions including immune responses to foreign antigens such as CMP, leading to sensitization in utero.…”

“…A prospective study of 123 premature neonates born at < 33 weeks' gestation or with < 1500 g birthweight revealed the high PVT incidence of 43% [21]. In the majority of cases, neonatal PVT affects the left portal vein encompassing umbilico-portal confluence, is clinically silent, is associated with UVC, particularly inadequate peripheral placement of catheter tips under the diaphragm, and shows favorable shortterm outcomes with spontaneous resolution of the most thrombi without anticoagulant or fibrinolytic therapy [16,20,21]. However, serious complications including liver lobe atrophy, portal hypertension and gastrointestinal hemorrhage can develop later in childhood largely in persistent, extensive and occlusive PVT [20,22].…”

“…Neonates, particularly preterm infants, have factors elevating thrombotic risk including the immature and developing coagulation and fibrinolytic systems with little reserve capacity, small vessel diameters, and numerous affected disorders that can disrupt hemostatic balance [15,16]. Most (up to 94%) of neonatal thrombosis cases have been reported to be associated with indwelling central venous catheters, including umbilical catheters [16].…”