acenocoumarol and Leg-Ulcer

Vitamin K antagonists are widely used in thromboembolic diseases. Hemorrhagic complications related to drug overdose represent their main side effect. We report a rare side effect, a severe and unexpected type of skin vasculitis - necrotic leg ulcer - induced by vitamin K antagonist.. A 63-year-old female with a history of diabetes developed hyperalgesic necrotic ulcerations on the lower limbs one month after starting an acenocoumarol-based treatment for ischemic heart disease. Histological examination revealed lymphocytic vasculitis with fibrinoid necrosis. Etiological explorations searching for vasculitis were negative. In the absence of a precise etiology, drug-induced ulcer was suspected. Low molecular weight heparin was prescribed to replace acenocoumarol. The lesions slowly resolved with topical treatment.. The chronological criteria and the negativity of etiological explorations allowed the diagnosis of vitamin K antagonist-induced necrotic skin ulcer. Clinicians should be aware of this rare complication induced by oral anticoagulants because of its practical therapeutic implications. This is the first case of necrotic leg ulcer induced by acenocoumarol corresponding histologically to necrotising lymphocytic vasculitis.

Topics: Acenocoumarol; Anticoagulants; Diabetes Mellitus, Type 2; Drug Substitution; Female; Heparin, Low-Molecular-Weight; Humans; Hyperalgesia; Leg Ulcer; Middle Aged; Necrosis; Vasculitis; Vitamin K

Topics: Acenocoumarol; Aged, 80 and over; Anticoagulants; Asthma; Atrial Fibrillation; Calciphylaxis; Calcium; Diabetes Complications; Female; Humans; Hypertension; Leg Ulcer; Livedo Reticularis; Polypharmacy; Thrombophilia

Vitamin K antagonists (VKAs) are widely used in thromboembolic diseases. We report five cases of necrotic leg ulcers having a particularly severe course and in which withdrawal of VKA treatment alone enabled healing.. Five patients presented with necrotic leg ulcers clinically evocative of necrotic angiodermatitis or vasculitis. Histological features were variable, including inconstantly inflammatory lesions (leukocytoclastic vasculitis) and microthrombosis. None of the patients had laboratory signs of autoimmune disease. Healing occurred in all patients only after withdrawal of VKA therapy (fluindione or acenocoumarol). Associated vascular diseases included superficial venous, distal arterial insufficiency and postphlebitic disease. In three cases, thrombotic factors were observed: hyperhomocysteinaemia or heterozygous Factor V Leiden mutation.. Although the causative role of VKAs is based solely on chronological criteria, this potential side effect deserves publication because of its practical therapeutic consequences. The physiopathological mechanisms accounting for the role of VKAs, including immunoallergic phenomena and, above all, microcirculatory thrombotic processes, are hypothetical and not universally accepted.

Topics: Acenocoumarol; Activated Protein C Resistance; Aged; Aged, 80 and over; Anticoagulants; Diabetic Angiopathies; Factor V; Female; Humans; Hyperhomocysteinemia; Leg Ulcer; Male; Necrosis; Phenindione; Polyarteritis Nodosa; Postoperative Complications; Purpura; Thrombophilia; Varicose Ulcer; Vasculitis, Leukocytoclastic, Cutaneous; Vitamin K

A 63-year-old woman was referred to the dermatology outpatient department with extremely painful ulcers on the right lower leg. Medical history listed hypertension, diabetes mellitus and chronic obstructive pulmonary disease. Intensive analgesia was insufficient. Blood analysis, microbial cultures and venous ultrasound did not reveal a cause. At histopathologic examination of an ulcer, arteriolosclerosis was revealed. The patient was treated for Martorell arteriolosclerotic ulcer with nifedipine, acenocoumarol and split-thickness skin grafts followed by vacuum-assisted closure therapy. Two weeks postoperative, analgesia was discontinued and all ulcers were healed. Nifedipine and acenocoumarol were continued in the outpatient setting to prevent relapses. Patients with long-standing hypertension are particularly prone to cutaneous arteriolosclerosis. Thrombosis of the cutaneous arterioles results in painful ischemic ulcers. This disease probably frequently goes unrecognised.

Topics: Acenocoumarol; Arteriolosclerosis; Combined Modality Therapy; Diagnosis, Differential; Female; Humans; Leg Ulcer; Middle Aged; Nifedipine; Skin Transplantation; Treatment Outcome

Two patients with developing venous gangrene of the lower extremity and contraindications to systemic thrombolytic therapy are presented. Low-dose intraarterial burst therapy with urokinase provided rapid amelioration of symptoms and avoided amputation without any serious bleeding complications in both patients.

Topics: Acenocoumarol; Adult; Anticoagulants; Contraindications; Female; Gangrene; Heparin; Humans; Infusions, Intra-Arterial; International Normalized Ratio; Leg; Leg Ulcer; Plasminogen Activators; Shock, Septic; Thrombolytic Therapy; Thrombophlebitis; Ultrasonography; Urokinase-Type Plasminogen Activator; Venous Thrombosis

Topics: Acenocoumarol; Adult; Humans; Leg Ulcer; Male; Necrosis; Protein C Deficiency; Skin

Topics: Acenocoumarol; Aphasia; Blood Coagulation Tests; Female; Heparin; Humans; Intracranial Embolism; Intracranial Embolism and Thrombosis; Leg; Leg Ulcer; Pregnancy; Pregnancy Complications; Pregnancy Complications, Cardiovascular; Thrombophlebitis; Thrombosis