Delayed-onset heparin-induced thrombocytopenia presenting with multiple arteriovenous thromboses: case report

Omran, Abbas Salehi; Karimi, Abbasali; Ahmadi, Hossein; Yazdanifard, Parin

doi:10.1186/1752-1947-1-131

Cited by 6 publications

(4 citation statements)

References 6 publications

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“…Another case report provided insufficient documentation to determine whether aHIT was present [23]. Some cases were excluded as no testing for HIT antibodies was performed, and the diagnosis of HIT was deemed uncertain [24].…”

Section: Five Ahit Disordersmentioning

confidence: 99%

Autoimmune Heparin-Induced Thrombocytopenia

Warkentin

2023

JCM

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Autoimmune thrombocytopenia (aHIT) is a severe subtype of heparin-induced thrombocytopenia (HIT) with atypical clinical features caused by highly pathological IgG antibodies (“aHIT antibodies”) that activate platelets even in the absence of heparin. The clinical features of aHIT include: the onset or worsening of thrombocytopenia despite stopping heparin (“delayed-onset HIT”), thrombocytopenia persistence despite stopping heparin (“persisting” or “refractory HIT”), or triggered by small amounts of heparin (heparin “flush” HIT), most cases of fondaparinux-induced HIT, and patients with unusually severe HIT (e.g., multi-site or microvascular thrombosis, overt disseminated intravascular coagulation [DIC]). Special treatment approaches are required. For example, unlike classic HIT, heparin cessation does not result in de-escalation of antibody-induced hemostasis activation, and thus high-dose intravenous immunoglobulin (IVIG) may be indicated to interrupt aHIT-induced platelet activation; therapeutic plasma exchange may be required if high-dose IVIG is ineffective. Also, aHIT patients are at risk for treatment failure with (activated partial thromboplastin time [APTT]-adjusted) direct thrombin inhibitor (DTI) therapy (argatroban, bivalirudin), either because of APTT confounding (where aHIT-associated DIC and resulting APTT prolongation lead to systematic underdosing/interruption of DTI therapy) or because DTI inhibits thrombin-induced protein C activation. Most HIT laboratories do not test for aHIT antibodies, contributing to aHIT under-recognition.

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Section: Five Ahit Disordersmentioning

confidence: 99%

Autoimmune Heparin-Induced Thrombocytopenia

Warkentin

2023

JCM

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Section: Heparin-induced Thrombocytopenia With Thrombosismentioning

confidence: 99%

“…22 However, involvement of multiple vascular beds may occur in cases of severe HIT with DIC and limb ischemia due to microvascular thrombi may occur with a mortality rate as high as 20%. 23 Early recognition and timely intervention is the key to improving prognosis. HIT is of 2 types: Type I is associated with a mild transient decrease in platelet count with the lowest usually not below 1,00,000/mm 3 and usually occurs within 2 days of heparin initiation.…”

Section: Heparin-induced Thrombocytopenia W I T H Thrombosismentioning

confidence: 99%

Clotting Catastrophies in the Intensive Care Unit

Sinha

Todi

2019

Indian Journal of Critical Care Medicine

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Clotting catastrophies are rarely encountered challenges in the Intensive Care Unit (ICU) and their presentation and progress maybe devastating and fulminant. Dramatic onset and involvement of multiple vascular beds should alert the clinician to look for these disorders. Outcomes may be improved with rapid diagnosis and prompt institution of specific therapies and interdisciplinary liaison holds the key to success.How to cite this articleSinha S, Todi SK. Clotting Catastrophies in the Intensive Care Unit. Indian J Crit Care Med 2019;23(Suppl 3):S197–S201.

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“…27 Multiple thrombotic events are not uncommon, 27 and patients with catastrophic outcomes involving multiple vascular beds have been reported. 28,29 Although HIT most often presents with macrovascular thrombosis, severe HIT complicated by DIC can be associated with limb ischemia and microvascular thrombosis, even in the absence of deep vein thrombosis (DVT) or treatment with warfarin. 30,31 In addition, patients with acute HIT who are treated with warfarin can develop warfarin-induced skin necrosis 32 and/or venous limb gangrene, 33 due to microvascular occlusions secondary to acquired deficiency of protein C.…”

mentioning

confidence: 99%

How I treat catastrophic thrombotic syndromes

Ortel

Erkan

Kitchens

2015

Blood

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Catastrophic thrombotic syndromes are characterized by rapid onset of multiple thromboembolic occlusions affecting diverse vascular beds. Patients may have multiple events on presentation, or develop them rapidly over days to weeks. Several disorders can present with this extreme clinical phenotype, including catastrophic antiphospholipid syndrome (APS), atypical presentations of thrombotic thrombocytopenic purpura (TTP) or heparin-induced thrombocytopenia (HIT), and Trousseau syndrome, but some patients present with multiple thrombotic events in the absence of associated prothrombotic disorders. Diagnostic workup must rapidly determine which, if any, of these syndromes are present because therapeutic management is driven by the underlying disorder. With the exception of atypical presentations of TTP, which are treated with plasma exchange, anticoagulation is the most important therapeutic intervention in these patients. Effective anticoagulation may require laboratory confirmation with anti–factor Xa levels in patients treated with heparin, especially if the baseline (pretreatment) activated partial thromboplastin time is prolonged. Patients with catastrophic APS also benefit from immunosuppressive therapy and/or plasma exchange, whereas patients with HIT need an alternative anticoagulant to replace heparin. Progressive thrombotic events despite therapeutic anticoagulation may necessitate an alternative therapeutic strategy. If the thrombotic process can be controlled, these patients can recover, but indefinite anticoagulant therapy may be appropriate to prevent recurrent events.

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Delayed-onset heparin-induced thrombocytopenia presenting with multiple arteriovenous thromboses: case report

Abstract: Background: Delayed-onset heparin-induced thrombocytopenia with thrombosis, albeit rare, is a severe side effect of heparin exposure. It can occur within one month after coronary artery bypass grafting (CABG) with manifestation of different thrombotic events.

Cited by 6 publications

References 6 publications

Autoimmune Heparin-Induced Thrombocytopenia

Autoimmune Heparin-Induced Thrombocytopenia

Clotting Catastrophies in the Intensive Care Unit

How I treat catastrophic thrombotic syndromes

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