Warfarin-Induced Skin Necrosis

Elrod, James P.; Karzenski, Stacey

doi:10.1055/s-2007-1002682

Cited by 60 publications

(29 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Genetic abnormalities in the anticoagulant factors, protein C and protein S, are linked with an increased risk of deep-vein thrombosis of the lower limbs. 10,11 Warfarin-induced necrosis of the skin in such individuals, however, is associated with extensive thrombosis of the postcapillary venules and small veins within subcutaneous adipose tissue, 12 demonstrating that alterations in the dynamic balance of anticoagulant factors can have a profound role in local hemostatic activity. Disorders in prothrombotic components are also associated with vascular bed-specific pathology.…”

Section: Clinical Vascular Bed-specific Hemostatic Pathologymentioning

confidence: 99%

Regulation of Vascular Bed–Specific Prothrombotic Potential

Edelberg

Christie

Rosenberg

2001

Circulation Research

View full text Add to dashboard Cite

Abstract-Hemostasis is the result of interdependent and complex systemic and local endothelial pathways that govern vascular integrity and rheology. A striking feature of hypercoagulable conditions is the focal nature of the resultant thrombotic pathology. Such disorders in hemostasis may be associated with distinct vascular beds, thus implying that the relative combined contribution of individual regulatory pathways may be specific and/or unique to a particular locale in the vasculature. Systemic factors and platelets mediate the formation of fibrin deposition; however, it is the diverse interrelationships in the interaction of these systemic elements with the local endothelial components that dictate vascular bed-specific hemostatic regulation. Indeed, the local activation of coagulation cascades, rather than increases in systemic thrombotic potential, is what leads to fibrin formation in different vascular beds. Hence, the propensity for congenital or acquired disorders to result in local thrombotic pathology is based on the relative contribution of the various hemostatic regulatory pathways in individual vascular beds. The present review highlights the role of local endothelial regulation in the interaction between local and systemic elements that contribute to vascular bed-specific prothrombotic potential. (Circ Res. 2001;89:117-124.)

show abstract

Section: Clinical Vascular Bed-specific Hemostatic Pathologymentioning

confidence: 99%

Regulation of Vascular Bed–Specific Prothrombotic Potential

Edelberg

Christie

Rosenberg

2001

Circulation Research

View full text Add to dashboard Cite

show abstract

“…Warfarin potassium had been reported to suppress not only production of vitamin Kdependent coagulant factors, but also that of protein C, which reduces the activity of factors V and VIII. More over, suppression of protein C was faster than that of the vitamin K-dependent coagulant factors, which might re sult in transient hypercoagulable state [22], In our study, antithrombin III seemed to be effective in preventing recurrent embolism. Hemorrhagic complica tions were seldom noted in this group, although there were many patients at high risk of hemorrhage, with advanced age, large infarct, and/or hypertension.…”

Section: Discussionmentioning

confidence: 42%

Antithrombin III and Low-Dose Heparin in Acute Cardioembolic Stroke

Yasaka¹,

Yamaguchi²,

Moriyasu³

et al. 1995

Cerebrovasc Dis

View full text Add to dashboard Cite

We retrospectively studied the incidence of recurrent embolization and hemorrhagic complications during a 2-week period after the onset of cardioembolic stroke according to the form of anticoagulation given immediately after the event. Twenty-six patients had full-dose heparin (F/H group), 37 had low-dose heparin (L/H group), 81 were treated with warfarin potassium (W group), and 20 were treated with antithrombin III (AT group), while 227 patients (non-A/C group) received no anticoagulation. The incidence of early recurrence was significantly lower in all anticoagulated groups (3.8% in the F/H group, 5.4% in the L/H group, 3.7% in the W group and 0% in the AT group), than that in the non-A/C group (20.3%). There were no significant differences in the incidence of hemorrhagic complications among the groups. Not only full-dose anticoagulation but also antithrombin III or low-dose heparin therapy may prevent the recurrence of embolization in acute cardioembolic stroke.

show abstract

“…The lesions are well-defined, painful, initially erythematous or hemorrhagic, and include the formation of hemorrhagic blisters, skin necrosis and pressure ulcers. 5,6 The use of lower doses of warfarin is believed to reduce the risk of the patient developing a state of hypercoagulability caused by the fall in protein C levels in the first 36 hours of anticoagulant therapy. 7 Therapeutic regimens are suggested to maintain protein C levels stable during the critical period following initiation of warfarin use, with a low initial dose (1-2 mg/day) and daily increases of 1-2 mg/day until reaching the desired international normalized ratio (INR) in around 10 days.…”

Section: Discussionmentioning

confidence: 99%

Trombocitopenia induzida por heparina e necrose cutânea por varfarina: relato de caso

Kaiber

Malucelli

Baroni

et al. 2010

An. Bras. Dermatol.

View full text Add to dashboard Cite

This paper describes a case of heparin-induced thrombocytopenia complicated by warfarininduced skin necrosis in a 74-year old female patient hospitalized with diagnoses of a hip fracture, deep vein thrombosis and pulmonary thromboembolism. Warfarin-induced skin necrosis is a rare complication of anticoagulant therapy, with high morbidity and mortality that may be associated with heparin-induced thrombocytopenia. Keywords: Heparin; Necrosis; Thrombocytopenia; Warfarin Resumo: É relatado um caso de trombocitopenia induzida por heparina complicada, com necrose cutânea induzida por varfarina em paciente de 74 anos, sexo feminino, internada com diagnóstico de fratura do colo do fêmur, trombose venosa profunda e tromboembolismo pulmonar. A necrose cutânea induzida por varfarina é uma complicação rara da terapia anticoagulante, com alta morbidade e mortalidade, que pode estar associada à trombocitopenia induzida por heparina.

show abstract

Warfarin-Induced Skin Necrosis

Cited by 60 publications

References 55 publications

Regulation of Vascular Bed–Specific Prothrombotic Potential

Regulation of Vascular Bed–Specific Prothrombotic Potential

Antithrombin III and Low-Dose Heparin in Acute Cardioembolic Stroke

Trombocitopenia induzida por heparina e necrose cutânea por varfarina: relato de caso

Contact Info

Product

Resources

About