Does umbilical vein catheterization to exchange transfusion lead to portal vein thrombosis?

Guimarães, Hugo; Castelo, L. Álvarez; Guimarães, Joaquim; Cardoso, Augusta; Dorey, Corine Mouton; Mateus, Maria do Nascimento Esteves; Almeida, Ana C.; Dias, Jorge Amil; Ramos, Isabel; Santos, Natacha

doi:10.1007/s004310050853

Cited by 36 publications

(22 citation statements)

References 15 publications

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“…On the other hand, our data are in accord with very recently published adult series of cases with portal vascular occlusion demonstrating that prothrombotic disorders, especially defects within the protein C pathway, contributed to this rare thrombotic manifestation in the patients investigated (Denninger et al, 2000;Egesel et al, 2000). Thus, we suggest that this difference in the aetiology of childhood PVT with respect to genetic prothrombotic risk factors is mainly as a result of the system of patient recruitment, different childhood age populations, and the inclusion or exclusion of catheter-related thrombosis that, in two prospective studies, has been shown not to be commonly associated with a risk of PVT in sick neonates (Schwartz et al, 1997;Guimaraes et al, 1998). Hepatic venous vascular occlusion in neonates and infants is rare and was not found in the previously reported ESPED survey (Nowak-Go Èttl et al, 1997b).…”

Section: Risk Factorsmentioning

confidence: 85%

Abdominal venous thrombosis in neonates and infants: role of prothrombotic risk factors – a multicentre case–control study

Heller

Schobeß²,

Kurnik³

et al. 2000

Br J Haematol

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The factor V (FV) G1691A mutation, the prothrombin (PT) G20210A variant, the methylenetetrahydrofolate reductase (MTHFR) T677T genotype, together with fasting homocysteine (HCY) concentration, lipoprotein (Lp)(a), anti‐thrombin (AT), protein C (PC), protein S (PS) and anti‐cardiolipin antibodies were investigated in 65 consecutively recruited infants (neonate to < 12 months) with renal venous thrombosis (RVT; n = 31), portal vein thrombosis (PVT; n = 24) or hepatic vein thrombosis (HVT n = 10), and 100 age‐ and sex‐matched healthy controls. FV G1691A was found in 14 babies (heterozygous: RVT n = 9, PVT n = 4; homozygous HVT n = 1) and five controls, the MTHFR TT677 genotype together with increased HCY in four infants with thrombosis (RVT n = 2; PVT n = 1; HVT n = 1) compared with one control, and the PT G20210A variant was present in one control only. PC type I deficiency was diagnosed in three patients (RVT n = 2; PVT n = 1) and AT deficiency in two patients (RVT n = 1; PVT n = 1). Three neonates with spontaneous thrombosis showed FV G1691A combined with Lp(a) and the FV G1691A was combined with the PT G20210A genotype in two infants. Additional triggering factors were reported in 27 patients (41·5%). The overall odds ratios (ORs) and 95% confidence intervals (CIs) with respect to the different thrombosis locations were: RVT (OR/CI: 10·9/3·85–31·1; P < 0·0001), PVT (5·47/1·7–17·6; P < 0·0007) and HVT (3·3/0·58–18·7; P = 0·18). The data presented here suggest that genetic prothrombotic risk factors also play an important role in abdominal venous thrombosis during infancy.

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Section: Risk Factorsmentioning

confidence: 85%

Abdominal venous thrombosis in neonates and infants: role of prothrombotic risk factors – a multicentre case–control study

Heller

Schobeß²,

Kurnik³

et al. 2000

Br J Haematol

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“…Today, the PVT etiology is considered multifactorial, with association of prothrombotic and local trigger factors found even in the pediatric age group (6,10,21,23,29,33,34,37,47,52,53) . The causes of PVT may be grouped into three categories: direct injury of the portal vein with subsequent thrombus formation; vascular malformation which includes stenosis or even atresia of the portal vein; and hypercoagulable conditions which favor the thrombus formation (6,15,19,22,39,49,50,52) . Cases that do not fit in these groups are denominated as idiopathic PVT and, due to the great percentage of these cases, recent studies, mainly in adults, have focused on the evaluation of new etiological factors (7,16,17,22,23) .…”

Section: Discussionmentioning

confidence: 99%

Portal vein thrombosis in children and adolescents: 20 years experience of a pediatric hepatology reference center

Ferri

Ferreira

Fagundes

et al. 2012

Arq. Gastroenterol.

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-Context -Portal vein thrombosis refers to a total or partial obstruction of the blood flow in this vein due to a thrombus formation. It is an important cause of portal hypertension in the pediatric age group with high morbidity rates due to its main complication -the upper gastrointestinal bleeding. Objective -To describe a group of patients with portal vein thrombosis without associated hepatic disease of the Pediatric Hepatology Clinic of the Hospital das Clínicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil with emphasis on diagnosis, presentation form and clinical complications, and the treatment of portal hypertension. Methods -This is a descriptive study of a series of children and adolescents cases assisted from January 1990 to December 2010. The portal vein thrombosis diagnosis was established by ultrasound. Results -Of the 55 studied patients, 30 (54.5%) were male. In 29 patients (52.7%), none of the risk factors for portal vein thrombosis was observed. The predominant form of presentation was the upper gastrointestinal bleeding (52.7%). In 20 patients (36.4%), the initial manifestation was splenomegaly. During the whole following period of the study, 39 patients (70.9%) showed at least one episode of upper gastrointestinal bleeding. The mean age of patients in the first episode was 4.6 ± 3.4 years old. The endoscopic procedure carried out in the urgency or electively for search of esophageal varices showed its presence in 84.9% of the evaluated patients. The prophylactic endoscopic treatment was performed with endoscopic band ligation of varices in 31.3% of patients. Only one died due to refractory bleeding. Conclusions -The portal vein thrombosis is one of the most important causes of upper gastrointestinal bleeding in children. In all non febrile children with splenomegaly and/or hematemesis and without hepatomegaly and with normal hepatic function tests, it should be suspect of portal vein thrombosis. Thus, an appropriate diagnostic and treatment approach is desirable in an attempt to reduce morbidity and mortality.

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“…Several investigators believe that umbilical vein catheterization and umbilical sepsis are responsible for portal vein thrombosis (PVT) others disagree. [8][9][10][11][12] The discrepancies between the observations are probably because of the studies that have been retrospective and clinical. In an Indian prospective ultrasonographic study up to 24 months, none of the 11 patients with septicaemia or umbilical sepsis developed portal vein thrombosis.…”

Section: Resultsmentioning

confidence: 99%

A study on demographic and clinical profile of children with extra hepatic portal venous obstruction and with special reference to thrombophilic factors

Jena

Mohanty

Patra

et al. 2017

Int J Community Med Public Health

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Background: Extra-hepatic portal vein obstruction (EHPVO) due to portal vein thrombosis is an important cause of portal hypertension in several region including India. The cause of thrombosis in these patients remains unclear. Objective of the study was to study the demographic features, etiology, clinical, laboratory findings with special reference to thrombophilic factors like protein C, protein S and antithrombin III deficiency in children with EHPVO.Methods: The prospective analysis of 62 patients of EHPVO (<14 years of age) was done in the Department of Hepatology, SCB medical College, Cuttack. After detailed history, clinical examination, Ultrasound abdomen /color Doppler and Upper GI endoscopy, the subjects were analyzed for any deficiency of thrombophilic factors like protein C, protein S and antithrombin III.Results: A total of 62 patients (37 Male, 25 Female) with mean age of 8.3+3.1 years were studied. Growth retardation was present in the form of wasting (alone) 20.9%, stunting (alone) 25.8% and both wasting and stunting was found in 9.8% cases. History of neonatal, umbilical sepsis and umbilical vein catheterization was found in 15.9% and 10.2% of cases respectively. Haemorrhage from oesophageal varices was prevalent symptoms in 85.9% patients. Splenomegaly was found in 91.9% patients and ascites in 9.4% patients. 47 patients studied for protein C, S and antithromibin III. 14 patients were found to have thrombophilia: protein C deficiency in 9, protein S deficiency in 8, Antithrombin III deficiency in 6.Conclusions: The etiology of EHPVO in the majority of patients remain still unclear. It is commonly associated impaired somatic growth. The risk of EHPVO increases in the presence of thrombophilia, resulting from deficiency of naturally occurring anticoagulant proteins like Protein C, Protein S and Antithrombin III.

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Does umbilical vein catheterization to exchange transfusion lead to portal vein thrombosis?

Cited by 36 publications

References 15 publications

Abdominal venous thrombosis in neonates and infants: role of prothrombotic risk factors – a multicentre case–control study

Abdominal venous thrombosis in neonates and infants: role of prothrombotic risk factors – a multicentre case–control study

Portal vein thrombosis in children and adolescents: 20 years experience of a pediatric hepatology reference center

A study on demographic and clinical profile of children with extra hepatic portal venous obstruction and with special reference to thrombophilic factors

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