Heparin-Induced Thrombocytopenia and Thrombosis in Ischemic Stroke

Atkinson, John L.D.; Sundt, Thoralf M.; Kazmier, Francis J.; Bowie, Ejw; Whisnant, Jack P.

doi:10.1016/s0025-6196(12)64857-5

Cited by 30 publications

(9 citation statements)

References 31 publications

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“…A previous study of 137 stroke patients treated with UFH reported that 21 patients (15.3%) developed thrombocytopenia, and 5 of these 21 patients had a recurrent ischemic stroke [10]. In another study, of 18 patients who developed carotid arterial occlusion following endarterectomy, 6 (33%) had an associated heparin-induced coagulation disorder [11]. A recent study of 200 neurological patients treated with UFH for at least 5 days, including 102 patients with cerebrovascular disorders, demonstrated that 41 patients (20.5%) had anti-PF4/heparin Abs and 5 (2.5%) developed HIT, when an enzyme-linked immunosorbent assay (ELISA) was used [12].…”

Section: Introductionmentioning

confidence: 99%

Heparin-Induced Thrombocytopenia: A Serious Complication of Heparin Therapy for Acute Stroke

Kawano¹,

Toyoda²,

Miyata

et al. 2008

Cerebrovasc Dis

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Background: Despite the lack of supporting evidence, unfractionated heparin (UFH) is frequently given to acute ischemic stroke patients. This study was designed to determine the incidence of heparin-induced thrombocytopenia (HIT) during acute stroke and to elucidate the clinical features of stroke patients with HIT. Methods: Of 1,078 consecutive patients with acute ischemic stroke, 392 were given intravenous UFH. Ten of these developed prominent thrombocytopenia without any other underlying etiology; they were suspected of having HIT. These 10 patients were studied retrospectively. The clinical diagnosis of HIT was made according to two published scoring systems. Antiplatelet factor 4/heparin antibodies in the plasma were detected by the enzyme-linked immunosorbent assay (ELISA) and were confirmed by the ¹⁴C-serotonin release assay. Results: Eight patients met the criteria for clinical HIT according to both scoring systems. Of these, serological tests were positive in 2 patients only on ELISA and in 2 patients on both assays. The amount of UFH given was greater in the 4 patients with positive serological findings than in the others (p = 0.043). Three patients developed further thromboembolic events, including 1 patient who developed possible cancer-associated thrombosis. Two patients were dead and the remaining 6 patients were dependent at the time of hospital discharge. The clinical severity and outcome of these patients were relatively unfavorable compared to other acute patients. Conclusions: The prevalence of HIT was 0.5% based on both the clinical scoring systems and serological assays. Monitoring for HIT should be included in the medical management of stroke to avoid further complications.

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Section: Introductionmentioning

confidence: 99%

Heparin-Induced Thrombocytopenia: A Serious Complication of Heparin Therapy for Acute Stroke

Kawano¹,

Toyoda²,

Miyata

et al. 2008

Cerebrovasc Dis

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“…- 35 Atkinson et al 36 have emphasized a relationship between heparin-associated thrombocytopenia and ischemic stroke following carotid endarterectomy. In a typical patient moderate to severe thrombocytopenia develops 5-10 days after heparin has been started.…”

mentioning

confidence: 99%

Antiphospholipid antibodies, prethrombotic states, and stroke.

Coull

Goodnight

1990

Stroke

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“…In one case, the stroke occurred with a normal absolute platelet count. 8 In the other cases, the mean platelet counts were 37,100/mm 3 (range 7,000-84,000/mm 3 ). The average recovery time after the cessation of heparin was 4.0 (range 1-8) days.…”

Section: Hitp and Strokementioning

confidence: 82%

“…Van Der Weyden et al 51 Meytes et al 72 Roberts et al 21 Atkinson et al 8 Cines et al 34 Lindsey et al 134 Kapsch et al 63 Galle et al 108 Stevenson 106 Calhoun and Hesser Excluding case reported by Atkinson et al 8 history of TIA has been reported to have had a stroke due to HITP. 34 In the study of RamirezLassepas et al, 43 although the incidence of HITP was similar in the three groups, all new cerebral ischemic events occurred in the CI group.…”

Section: Phelan55mentioning

confidence: 99%

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Heparin-induced thrombocytopenia.

Becker

Miller

1989

Stroke

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There are two types of heparin-induced thrombocytopenia. Type I is more common, has an early onset, and is mild, transient, and benign. Type I is due to direct heparin-induced platelet aggregation and is rarely associated with thromboembolic sequela. Type II is infrequent, has a late onset, and is more severe. Type II is due to an immune-mediated platelet aggregation caused by IgG and IgM that becomes bound to platelets. In Type II, the antibody titers decline over several months; however, early reexposure can result in a catastrophic secondary immune response. Frequently, Type II is associated with life-or limb-threatening thromboembolic complications (white clots), including stroke. {Stroke 1989;20:1449-1459)

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Heparin-Induced Thrombocytopenia and Thrombosis in Ischemic Stroke

Cited by 30 publications

References 31 publications

Heparin-Induced Thrombocytopenia: A Serious Complication of Heparin Therapy for Acute Stroke

Heparin-Induced Thrombocytopenia: A Serious Complication of Heparin Therapy for Acute Stroke

Antiphospholipid antibodies, prethrombotic states, and stroke.

Heparin-induced thrombocytopenia.

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