EHA Library - The official digital education library of European Hematology Association (EHA)

PEDIATRIC VENOUS THROMBOEMBOLISM: A SINGLE CENTRE EXPERIENCE
Author(s): ,
Nihal Nihal Ozdemir
Affiliations:
Pediatric Hematology Oncology,ISTANBUL UNIVERSITY, CERRAHPASA MEDICAL FACULTY,Istanbul,Turkey
,
Gürcan Dikme
Affiliations:
Pediatric Hematology Oncology,ISTANBUL UNIVERSITY, CERRAHPASA MEDICAL FACULTY,Istanbul,Turkey
,
Hande Kızılocak
Affiliations:
Pediatric Hematology Oncology,ISTANBUL UNIVERSITY, CERRAHPASA MEDICAL FACULTY,Istanbul,Turkey
,
Basak Koç
Affiliations:
Pediatric Hematology Oncology,ISTANBUL UNIVERSITY, CERRAHPASA MEDICAL FACULTY,Istanbul,Turkey
Tiraje Celkan
Affiliations:
Pediatric Hematology Oncology,ISTANBUL UNIVERSITY, CERRAHPASA MEDICAL FACULTY,Istanbul,Turkey
(Abstract release date: 05/19/16) EHA Library. Ozdemir G. 06/09/16; 133111; E1562
Dr. Gul Ozdemir
Dr. Gul Ozdemir
Contributions
Abstract
Abstract: E1562

Type: Eposter Presentation

Background
Pediatric venous thromboembolism (VTE) and associated complications are rare but increasing. We reviewed our experience of pediatric VTE in 20 years.

Aims
To identify predictors of pediatric VTE, efficacy of treatment and prevalence of complications.

Methods
A retrospective chart review of patients aged 1 to 18 years with VTE was done.Data were collected on demographics, risk factors, thrombophilia work-up, treatment, and relapse. Neonatal and catheter related thrombosis cases were excluded.

Results
Sixty-five pediatric patients (M/F: 1.5) were recruited. Median age at diagnosis was 8.7 years (range: 1 month -17 years). Thrombotic locations were cerebral veins (n=34), lower extremities (n=12), upper extremities (n=7), DVT & pulmonary embolism (n=1), splenic and/or portal veins (n=7), renal vein (n=2), mesenteric veins (n=1), and purpura fulminans (n=1). In 35 patients (53%), a probable acquired risk factor was identified; the most common risks were leukemia, mastoiditis, vasculitis, congenital heart defect and infections. Thrombophilia work-up showed FV Leiden mutation (n=12), low protein C (n=12), high FVIII levels (n=10), low anti-thrombin-3 (n=4), high homocytein level (n=3), prothrombin 20210a mutation (n=3) in 33 patients (50%). Fifty-four patients received anti-coagulant therapy; the majority (n=49) received low molecular weight heparin (LMWH) and acetylsalicylic acid (n=4). Three received warfarin, one was on dabigatran study and one received rivoraxabin. Low molecular weight was given as single dose at a dose of 100 u/kg to all patients. Five had recurrent thrombosis under treatment, one was on dabigatran and the rest were on LMWH. One patient with vasculitis had post-thrombotic syndrome.

Conclusion
 The etiology of pediatric venous thromboembolic disease (VTE) is multifactorial, and in most children, 1 or more clinical and inherited risk factors are present. In our experience low dose LMWH may be used with success in pediatric VTE.

Session topic: E-poster

Keyword(s): Anticoagulation, Low molecular weight heparin, Pediatric, Thrombophilia
Abstract: E1562

Type: Eposter Presentation

Background
Pediatric venous thromboembolism (VTE) and associated complications are rare but increasing. We reviewed our experience of pediatric VTE in 20 years.

Aims
To identify predictors of pediatric VTE, efficacy of treatment and prevalence of complications.

Methods
A retrospective chart review of patients aged 1 to 18 years with VTE was done.Data were collected on demographics, risk factors, thrombophilia work-up, treatment, and relapse. Neonatal and catheter related thrombosis cases were excluded.

Results
Sixty-five pediatric patients (M/F: 1.5) were recruited. Median age at diagnosis was 8.7 years (range: 1 month -17 years). Thrombotic locations were cerebral veins (n=34), lower extremities (n=12), upper extremities (n=7), DVT & pulmonary embolism (n=1), splenic and/or portal veins (n=7), renal vein (n=2), mesenteric veins (n=1), and purpura fulminans (n=1). In 35 patients (53%), a probable acquired risk factor was identified; the most common risks were leukemia, mastoiditis, vasculitis, congenital heart defect and infections. Thrombophilia work-up showed FV Leiden mutation (n=12), low protein C (n=12), high FVIII levels (n=10), low anti-thrombin-3 (n=4), high homocytein level (n=3), prothrombin 20210a mutation (n=3) in 33 patients (50%). Fifty-four patients received anti-coagulant therapy; the majority (n=49) received low molecular weight heparin (LMWH) and acetylsalicylic acid (n=4). Three received warfarin, one was on dabigatran study and one received rivoraxabin. Low molecular weight was given as single dose at a dose of 100 u/kg to all patients. Five had recurrent thrombosis under treatment, one was on dabigatran and the rest were on LMWH. One patient with vasculitis had post-thrombotic syndrome.

Conclusion
 The etiology of pediatric venous thromboembolic disease (VTE) is multifactorial, and in most children, 1 or more clinical and inherited risk factors are present. In our experience low dose LMWH may be used with success in pediatric VTE.

Session topic: E-poster

Keyword(s): Anticoagulation, Low molecular weight heparin, Pediatric, Thrombophilia

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