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Reply to the correspondence letter by G. Demirel et al.

Evaluation and treatment of intracardiac thrombus in 10 neonates

We appreciate the interest of Dr. Demirel and associates in our article describing a thrombus obstructing the right ventricle outflow tract in a neonate with 677TT methylenetetrahydrofolate reductase genotype [6]. In this case, surgical thrombectomy was used as a method of choice for the treatment of a life-threatening thrombosis.

Other strategies for management of intracardiac thrombi include supportive care only, anticoagulant therapy with either unfractionated heparin or low molecular weight heparins, and thrombolytic therapy [2, 7]. Although recombinant tissue plasminogen activator (r-tPA) has become the agent of choice for thrombolysis, the optimal dosing and duration of treatment are still unknown [7]. Demirel G. and associates [3] report the use of r-tPA in eight neonates with intracardiac thrombosis. r-tPA was used at a dose of 200 μg/kg/h for 6 h infusion in a day for 6 days, and concurrently, enoxaparin was administered subcutaneously at a dose of 1.5 mg/kg twice daily. None of their patients experienced therapy-related hemorrhagic complications.

In our Pediatric Cardiac Intensive Care Unit, we use r-tPA infusions at 0.5 mg/kg/h for 6 h and concurrent therapy with unfractionated heparin at a dose of 20 U/kg/h. As some reports show that continuous infusion for a long duration may be associated with an increased risk of major bleeding [1, 4], we do not extend therapy beyond 6 h. Using this protocol, complete or partial resolution of intracardiac thrombi was achieved in patients after cardiac surgery. However, in a few cases, major intrathoracic bleeding required treatment with blood products and chest reopening.

Although central line and congenital heart disease appear to be the most important associated risk factors for thrombosis in neonates and children [5], laboratory testing for thrombophilia is also performed. The testing may be particularly important for those patients who are at high risk of the thrombosis recurrence (patients with abnormal flow states, polycythemia, presence of synthetic materials, need for further cardiac surgery, or catheterization).

References

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    Al-Jazairi AS, Al-Gain RA, Bulbul ZR, Cherfan AJ (2010) Clinical experience with alteplase in the management of intracardiac and major cardiac vessels thrombosis in pediatrics: a case series. Ann Saudi Med 30:227–232

  2. 2.

    Bendaly EA, Batra AS, Ebenroth ES, Hurwitz RA (2008) Outcome of cardiac thrombi in infants. Pediatr Cardiol 29:95–101

  3. 3.

    Demirel G, Oguz SS, Celik IH et al (2010) Evaluation and treatment of neonatal thrombus formation in 17 patients. Clin Appl Thromb Hemost (in press)

  4. 4.

    Gupta AA, Leaker M, Andrew M et al (2001) Safety and outcomes of thrombolysis with tissue plasminogen activator for treatment of intravascular thrombosis in children. J Pediatr 139:682–688

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    Humberto AM, Roberto AP, Luis MB, Alejandro GO (2001) Complications of central venous catheters. Curr Opin Clin Nut Metab Care 4:207–210

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    Kovacikova L, Skrak P, Zahorec M (2011) Thrombus obstructing the right ventricle outflow tract in a neonate with methylenetetrahydrofolate reductase 677TT genotype. Eur J Pediatr (in press)

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    Monagle P, Chalmers E, Chan A et al (2008) Antithrombotic therapy in neonates and children: American College of Chest Physicians evidence-based clinical practice guidelines (8th edition). Chest 133(6 Suppl):887S–968S

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Correspondence to Lubica Kovacikova.

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Kovacikova, L. Reply to the correspondence letter by G. Demirel et al.. Eur J Pediatr 170, 1225 (2011). https://doi.org/10.1007/s00431-011-1472-z

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Keywords

  • Congenital Heart Disease
  • Enoxaparin
  • Unfractionated Heparin
  • Thrombophilia
  • Polycythemia