Heparin-induced thrombocytopenia with acute aortic and renal thrombosis in a patient treated with low-molecular-weight heparin

Heparin-induced thrombocytopenia is a rare but serious complication of heparin therapy. Most of cases are related to unfractionated heparin, but a few are due to low molecular weight heparin sometimes associated with unfractionated heparin. A patient with pulmonary contusions after chest injury developed a catheter related subclavian vein thrombosis on day 16. He was treated by increasing doses of low molecular weight heparin. Aortic and renal thromboses occurred on day 21. Surgical thrombectomy, performed after starting alternative anticoagulation treatment led to complete arterial recovery. In case of suspicion of heparin-induced thrombocytopenia, with unfractionated or low-molecular-weight heparin, heparin treatment must be discontinued before the results of biological tests become available. Arterial and/or venous thrombosis is a serious complication of heparin-induced thrombocytopenia. The treatment has two aims: first, to restore arterial patency by clot removal by thrombectomy, bypass or thrombolysis, and second, to avoid new thrombosis formation by substitutive anticoagulation treatment: danaparoid may have cross-reaction with heparin, or lepirudin has anaphylactic risks and needs biological follow-up. Heparin-induced thrombocytopenia and thrombosis can be complicated by death or disabilities such as amputations, stroke, renal or bowel infarction. Once HIT has been diagnosed heparin should never be given again, but if cardiopulmonary bypass is required, it might be reintroduced during operation only if serum antibodies have disappeared.

Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.

A patient with pulmonary contusions after chest injury developed catheter-related subclavian vein thrombosis and then, despite escalating low-molecular-weight heparin, aortic and renal thromboses on day 21 suggesting HIT; thrombectomy after alternative anticoagulation restored arterial patency, with lepirudin discussed as a substitutive option.

Explore how this research connects to clinical practice

More peer-reviewed studies in Drug Development.

• Hirudotherapy in Medicine and Dentistry — Jha K et al. (2015)
• Leech therapy: a history — Hyson J (2005)
• Hirudins of the Asian medicinal leech, Hirudinaria manillensis: same same, but different — Lukas P et al. (2019)
• Transcriptomic analysis of the salivary gland of medicinal leech Hirudo nipponia — Lu Z et al. (2018)
• Molecular dynamic and pharmacological studies on protein-engineered hirudin variants of Hirudinaria manillensis and Hirudo medicinalis — Sun Y et al. (2022)
• Cell-free synthesis of the hirudin variant 1 of the blood-sucking leech Hirudo medicinalis — Wüstenhagen D et al. (2020)
• Hirudin variants production by genetic engineered microbial factory — Zhang J, Lan N (2018)
• Hirudin in heparin-induced thrombocytopenia — Lubenow N, Greinacher A (2002)
• Hirudin ameliorates diabetic nephropathy by inhibiting Gsdmd-mediated pyroptosis — Han J et al. (2023)
• Hirudin as alternative anticoagulant--a historical review — Markwardt F (2002)

Browse all ASH-analysed research →