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[Severe thrombocytopenia induced by heparin in an infant with acute myocarditis]
Insights
A child developed severe heparin-induced thrombocytopenia (HIT) during myocarditis treatment. Both standard and low molecular weight heparin triggered HIT, complicating patient management.
Area of Science:
- Pediatric Cardiology
- Hematology
- Pharmacology
Background:
- Acute myocarditis presents a significant clinical challenge, often requiring anticoagulant therapy.
- Heparin-induced thrombocytopenia (HIT) is a serious immune-mediated complication of heparin use.
- Managing anticoagulation in pediatric patients with HIT requires careful consideration of alternative agents.
Observation:
- A pediatric patient with acute myocarditis developed severe thrombocytopenia (80.10(9)/l) on day 5 of standard heparin therapy.
- Despite initial negative aggregation tests, thrombocytopenia persisted, and intra-cardiac thrombi necessitated a switch to low molecular weight heparin (Fraxiparin).
- A third thrombus led to Fraxiparin discontinuation, with subsequent positive aggregation tests confirming HIT to both heparin types.
Findings:
- The patient exhibited positive platelet aggregation tests for both standard heparin and low molecular weight heparin (Fraxiparin).
- This confirmed a diagnosis of heparin-induced thrombocytopenia (HIT) induced by both anticoagulant classes.
- The case highlights the potential for cross-reactivity in HIT.
Implications:
- This case underscores the importance of vigilant monitoring for HIT in pediatric patients receiving heparin products.
- It emphasizes the need for advanced diagnostic testing, including aggregation assays, to confirm HIT.
- The findings necessitate a critical review of diagnostic and therapeutic strategies for HIT in complex pediatric cases, particularly those involving myocarditis.
Abstract:
A severe heparin-induced thrombocytopenia is reported in a child suffering from acute myocarditis. Thrombocytopenia (80.10(9)/l) occurred on day 5 (D5) of heparin therapy which was thus discontinued during 8 hours but reintroduced on the view of a negative platelet aggregation test using standard heparin. On D10, while thrombocytopenia persisted the presence of two intra-cardiac thrombi led to replace standard heparin by low molecular weight heparin (Fraxiparin), associated with vitamin K antagonist (phenindione). On D12, a 3rd intra-cardiac thrombus required immediate discontinuation of Fraxiparin therapy. Platelet aggregation tests performed on D14 were positive in the presence of standard heparin and of low molecular weight heparin, thus demonstrating the existence of thrombocytopenia induced by standard heparin and secondly by low molecular weight heparin. This observation led the authors to discuss the diagnosis and the therapeutic management of heparin-induced thrombocytopenia.