Heparin-induced thrombocytopenia and thrombosis syndrome after cardiac surgery

DuBose, Joseph J.; Sutherland, Michael; Moulton, Michael; Krishnan, Bhaktan; Cohn, Jerry; Pratt, J. M.

doi:10.1016/j.cursur.2003.09.001

Cited by 3 publications

(13 citation statements)

References 8 publications

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“…Ancak, heparine bağlı trombositopeniler daha çok 7-10. günlerde ortaya çıkmaktadır. [9,10,18] Hastalarımızda ise bu dönemde trombosit sayılarının yükselme eğiliminde olduğu görülmüştür.…”

Section: Hastalar Ve Yöntemlerunclassified

The incidence of thrombocytopenia after cardiopulmonary bypass in children with Down syndrome

Karagöl¹

2011

Turk Kardiyol Dern Ars

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Section: Hastalar Ve Yöntemlerunclassified

The incidence of thrombocytopenia after cardiopulmonary bypass in children with Down syndrome

Karagöl¹

2011

Turk Kardiyol Dern Ars

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“…These data, and extensive experience with bivalirudin in PCI, support its use as an anticoagulant in patients with HIT who require coronary intervention. Bivalirudin is an attractive alternative because of its relatively short half‐life, smaller dose‐requirement, easy monitoring via aPTT measurement, and metabolism primarily via proteolytic degradation, which potentially provides a greater margin of safety in patients with renal or hepatic dysfunction when compared with other direct thrombin inhibitors (11, 37).…”

Section: Update Of the Therapeutics Of Hitmentioning

confidence: 99%

“…It characteristically occurs within the first 4 days of therapy and usually resolves without treatment or complication (11). HIT type II, caused by immunoglobulin formation against circulating heparin-PF4 complexes, is mediated in most cases by IgG, with a smaller portion associated with IgA or IgM (11). In most cases, platelet count drops beginning on approximately the fifth day of administration of UFH or LMWH (11).…”

Section: Classific Atio N Description An D Terms Associated Wi Th Hitmentioning

confidence: 99%

“…HIT type II, caused by immunoglobulin formation against circulating heparin-PF4 complexes, is mediated in most cases by IgG, with a smaller portion associated with IgA or IgM (11). In most cases, platelet count drops beginning on approximately the fifth day of administration of UFH or LMWH (11). In the case of previous sensitization, however, the course of progression may be more abrupt.…”

Section: Classific Atio N Description An D Terms Associated Wi Th Hitmentioning

confidence: 99%

“…Furthermore, an alternative anticoagulant should be started after discontinuation of heparin. This is because of the fact that the patient is at high risk of developing thrombosis after heparin is stopped (4,6,(9)(10)(11)31). If a patient is on UFH, substituting to LMWH is to be avoided as there will be cross-reactivity between UFH and LMWH, although the incidence of patients developing HIT after LMWH therapy is lower than after UFH (4,11).…”

Section: H It : a DI A Gno S T Ic A Nd Th E Rap Eu T Ic D Il E Mm A Imentioning

confidence: 99%

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Heparin-induced thrombocytopenia and recent advances in its therapy

et al. 2007

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Objectives: To highlight therapeutic controversies, and present a critical review of the most recent evidence on the management of heparininduced thrombocytopenia (HIT). Data sources: A MEDLINE search from October 1996 until October 2006 was carried out. Pertinent literature was identified and other references identified from the bibliographic citations of the articles identified on MEDLINE. Study selection: Articles related to the treatment of HIT including meta-analyses, systematic reviews, critical reviews, randomized and non-randomized trials, as well as case-reports, were reviewed. Results and conclusion: The diagnostic and therapeutic dilemmas associated with HIT can be overwhelming and call for an evidence-based approach in the management of this frequently fatal event. HIT is associated with significant morbidity and mortality. The evidence suggests when heparin is stopped, alternative anticoagulant therapy with one of the newer agents such as lepirudin and argatroban is of benefit in avoiding deaths and morbidity.

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A fatal complication after repair of post-infarction ventricular septal rupture: heparin-induced thrombocytopenia with thrombosis: case report

Nazlı¹,

Çolak²,

Demircelik³

et al. 2015

CVJA

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Heparin-induced thrombocytopenia (HIT) is a rare but potentially devastating and life-threatening complication from using heparin. HIT not only causes thrombocytopenia, but it also carries an increased risk for fatal thrombotic complications. In this report, we describe the case of a patient in whom fatal HIT developed after successful surgical repair of a posterior post-infarction ventricular septal rupture with cardiopulmonary bypass.

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Heparin-induced thrombocytopenia and thrombosis syndrome after cardiac surgery

Cited by 3 publications

References 8 publications

The incidence of thrombocytopenia after cardiopulmonary bypass in children with Down syndrome

The incidence of thrombocytopenia after cardiopulmonary bypass in children with Down syndrome

Heparin-induced thrombocytopenia and recent advances in its therapy

A fatal complication after repair of post-infarction ventricular septal rupture: heparin-induced thrombocytopenia with thrombosis: case report

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