warfarin and Purpura

Classic calciphylaxis associated with renal failure is a life-threatening disease. Warfarin-associated calciphylaxis without renal injury has been described, but whether it is a subset of classic calciphylaxis or a different entity remains unknown. We describe 1 case of warfarin-associated calciphylaxis, present data from 2 others from our institution, and review all cases of warfarin-associated calciphylaxis available in the literature. Our review indicates that warfarin-associated calciphylaxis is clinically and pathophysiologically distinct from classic calciphylaxis.. To review warfarin-associated calciphylaxis and determine its relationship to classic calciphylaxis.. We searched MEDLINE and Ovid without language or date restrictions for case reports of calciphylaxis from the inpatient setting using the terms "calciphylaxis and warfarin," "non-uremic calciphylaxis," and "nonuremic calciphylaxis." We defined nonuremic calciphylaxis as a histopathologic diagnosis of calciphylaxis without severe kidney disease (serum creatinine level >3 mg/dL; glomerular filtration rate <15 mL/min; acute kidney injury requiring dialysis; and renal transplantation).. Each patient had been exposed to warfarin before the onset of calciphylaxis.. Patient data were abstracted from published reports. Original patient medical records were requested and reviewed when possible.. We identified 18 patients with nonuremic calciphylaxis, 15 from the literature, and 3 from our institution. Patients were predominantly female (15 of 18 [83%]) with ages ranging from 19 to 86 years. Duration of warfarin therapy prior to calciphylaxis onset averaged 32 months. Lesions were usually located below the knees (in 12 of 18 [67%]). No cases reported elevated calcium-phosphate products (0 of 17 [0%]). Calcifications were most often noted in the tunica media (n = 8 [44%]) or in the vessel lumen and tunica intima (n = 7 [39%]). The most common treatments included substitution of heparin or low-molecular weight heparin for warfarin (n = 13 [72%]), intravenous sodium thiosulfate (n = 9 [50%]), and hyperbaric oxygen (n = 3 [17%]). The survival rate on hospital discharge was remarkably high, with 15 cases (83%) reporting full recovery and 3 cases ending in death.. Warfarin-associated calciphylaxis is distinct from classic calciphylaxis in pathogenesis, course, and, particularly, outcome. This finding should influence clinical management of the disease and informs targeted treatment of the disease.

Topics: Anticoagulants; Calciphylaxis; Female; Humans; Leg Ulcer; Livedo Reticularis; Purpura; Warfarin

Spontaneous retroperitoneal hematoma after warfarin therapy is an extremely rare event. Here, we report a 25-year-old man who was brought in to the emergency service with confusion. On arrival, the patient had hypotension, tachycardia, tachypnea, low-grade fever, and Glasgow Coma Scale score of 12. Abdominal examination revealed distention and mild tenderness in the right upper quadrant of the abdomen. The patient had a history of aortic valve replacement surgery and was on warfarin treatment at an international normalized ratio of 2.4. Our patient progressed to cardiorespiratory arrest. The resuscitation was initiated promptly. Despite all resuscitation measures, including transfusion and administration of high doses of catecholamine, the patient died of hypovolemic shock 3 hours after admission. At autopsy, the external surface of the abdominal great vessels (descending aorta and mesenteric vessels) showed scattered petechial hemorrhages without any visible site of perforation. After comprehensive exploration of the abdomen, no evidence of traumatic event was identified and the cause of internal blood loss was noted as warfarin adverse effect.

Topics: Adult; Anticoagulants; Aorta, Thoracic; Fatal Outcome; Heart Valve Prosthesis; Hematoma; Humans; Male; Mesenteric Arteries; Mesenteric Veins; Purpura; Retroperitoneal Space; Shock; Warfarin

Hypercoagulable states (HS) are inherited or acquired conditions that predispose an individual to venous and/or arterial thrombosis. The dermatologist can play a vital role in diagnosing a patient's HS by recognizing the associated cutaneous manifestations, such as purpura, purpura fulminans, livedo reticularis, livedo vasculopathy (atrophie blanche), anetoderma, chronic venous ulcers, and superficial venous thrombosis. The cutaneous manifestations of HS are generally nonspecific, but identification of an abnormal finding can warrant a further workup for an underlying thrombophilic disorder. This review will focus on the basic science of hemostasis, the evaluation of HS, the skin manifestations associated with hypercoagulability, and the use of antiplatelet and anticoagulant therapy in dermatology.

Topics: Anetoderma; Anticoagulants; Antiphospholipid Syndrome; Calciphylaxis; Hemostasis; Heparin; Humans; Livedo Reticularis; Necrosis; Platelet Aggregation Inhibitors; Purpura; Skin; Skin Diseases; Thrombophilia; Varicose Ulcer; Venous Thrombosis; Warfarin

In general, the current recommendations for treating and prophylaxing thrombotic patients with hereditary defects are similar to those for thrombotic individuals without a defect. Determinations as to the need for long-term anticoagulation require that a clinical assessment be made regarding the relative benefit in preventing thrombotic episodes versus the risk of increased bleeding. With our newly found ability to identify genetic risk factors in a substantial fraction of patients with venous thrombosis and pulmonary embolism, it will be possible to perform rigorously designed studies to determine whether they should be managed with more prolonged or intense anticoagulation after a thrombotic event or more aggressive prophylactic regimens in high risk situations such as a total hip replacement.

Topics: Abnormalities, Drug-Induced; Anticoagulants; Antithrombin III; Antithrombin III Deficiency; Blood Proteins; Coumarins; Disease Susceptibility; Drug Eruptions; Factor V Deficiency; Female; Fibrinolytic Agents; Genetic Predisposition to Disease; Humans; Infant, Newborn; Male; Necrosis; Pregnancy; Pregnancy Complications, Hematologic; Prevalence; Protein C; Protein S Deficiency; Puerperal Disorders; Purpura; Recurrence; Risk; Thrombolytic Therapy; Thrombosis; Warfarin

Skin and soft tissue necrosis is a rare complication of anticoagulation therapy. Two patients who exhibited the spectrum of this disorder are described. The clinical features, etiology, pathophysiology, and treatment of coumarin skin necrosis are outlined, and the English-language literature is reviewed.

Topics: Adult; Aged; Coumarins; Ecchymosis; Female; Hemorrhage; Humans; Male; Middle Aged; Necrosis; Purpura; Thrombophlebitis; Warfarin

Topics: Aged; Animals; Anticoagulants; Aspirin; Bedbugs; Clopidogrel; Humans; Insect Bites and Stings; Male; Platelet Aggregation Inhibitors; Purpura; Warfarin

A myriad of different phenomena exist in the dermatological literature which are based on the concept of locus minores resistentiae. The most commonly described phenomenon is the Koebner phenomenon, which is classically associated with the emergence of psoriatic lesions post trauma. Warfarin-induced skin necrosis (WISN) is a rare but severe side effect that leads to necrosis of the skin, predominantly on areas with increased subcutaneous fat. The presented case reports on WISN within psoriatic plaques.

Topics: Adult; Anticoagulants; Female; Humans; Necrosis; Psoriasis; Purpura; Skin; Warfarin

Topics: Adult; Anticoagulants; Drug Eruptions; Exanthema; Female; Humans; Necrosis; Purpura; Skin; Warfarin

Herein, we report a case of post-transfusion purpura after the reversal of anticoagulation for surgical purposes in a 66-year old ethnic Asian man who was undergoing long-term warfarin therapy for antiphospholipid syndrome. The patient experienced a sudden decrease in platelet count, from 308,000 per μL from the day of admission to 38,000 per μL the following day. Follow-up testing revealed unremarkable red blood cell (RBC) morphology, no evidence of platelet clumping, and negative heparin-induced antibody test results. Platelet antibody testing revealed anti-HPA15a antibodies.

Topics: Aged; Anticoagulants; Antigens, Human Platelet; Asian People; Autoantibodies; Humans; Male; Purpura; Thrombocytopenia; Transfusion Reaction; Warfarin

In this report, we present an interesting case of a patient with Rumpel-Leede phenomenon, a rare occurrence that can result in significant delays in medical treatment. This phenomenon is characterized by the presence of a petechial rash that results from acute dermal capillary rupture. In our patient, it occurred secondary to raised pressure in the dermal vessels caused by repeated inflation of a sphygmomanometer cuff. Contributory factors in Rumpel-Leede phenomenon include prevalent conditions such as diabetes mellitus, hypertension, thrombocytopenia, chronic steroid use, antiplatelets, and anticoagulants.. A 58-year-old Russian woman with diabetes and hypertension presented to our hospital with a non-ST elevation myocardial infarction, and she subsequently developed a petechial rash on her distal upper limbs. A vasculitic screen was performed, with normal results.. Given the timing and distribution of the rash, it was felt that this was an example of Rumpel-Leede phenomenon in a susceptible individual. This is an important diagnosis to be aware of in patients with vascular risk factors presenting for acute medical care who subsequently develop a petechial rash.

Topics: Anticoagulants; Atrial Fibrillation; Blood Pressure Determination; Diabetes Mellitus, Type 2; Female; Humans; Hypertension; Middle Aged; Myocardial Infarction; Purpura; Risk Factors; Warfarin

Topics: Aged, 80 and over; Anticoagulants; Atrial Fibrillation; Facial Dermatoses; Female; Humans; International Normalized Ratio; Purpura; Vomiting; Warfarin

The potentiation of the anticoagulant effects of warfarin by miconazole, when used in oral gel form, is described in three patients. The associated morbidity is examined, emphasising the importance of considering this potentially serious interaction when prescribing antifungal agents to patients on oral anticoagulants.

Topics: Administration, Oral; Aged; Anticoagulants; Antifungal Agents; Blood Coagulation; Candidiasis, Oral; Contusions; Drug Interactions; Female; Gels; Humans; Male; Melena; Miconazole; Middle Aged; Mouth Diseases; Purpura; Stomatitis, Denture; Warfarin

Topics: Adult; Age Factors; Blood Coagulation Tests; Blood Proteins; Carrier Proteins; Complement Inactivator Proteins; Female; Glycoproteins; Homozygote; Humans; Immunoelectrophoresis, Two-Dimensional; Infant, Newborn; Male; Protein C; Protein Deficiency; Purpura; Warfarin

Topics: Humans; Infant, Newborn; Plasma; Protein C Deficiency; Purpura; Warfarin

The vitamin K metabolism of three patients with factitious purpura due to brodifacoum ingestion was studied. These patients, who presented with bleeding disorders due to deficiency of the vitamin K-dependent blood clotting proteins, were refractory to vitamin K1 at standard doses and required fresh frozen plasma to control bleeding until large doses of vitamin K1 were used. Metabolic studies demonstrated a blockade in vitamin K utilization, consistent with the presence of a vitamin K antagonist, but the patients denied use of anticoagulants. Warfarin assays were negative. We show that the factitious purpura in each patient was due to the surreptitious ingestion of brodifacoum, a potent second generation long-acting vitamin K antagonist used as a rodenticide. The coagulopathies responded to long-term therapy with large doses of vitamin K1. The serum elimination half-time for brodifacoum ranged from 16 to 36 days in these patients. The anticoagulant effect is of long duration, requiring chronic vitamin K treatment. With increasing availability of new rodenticides, factitious purpura due to surreptitious ingestion of these potent vitamin K antagonists is emerging as a new problem, previously associated with warfarin, with important implications for diagnosis and treatment.

Topics: 4-Hydroxycoumarins; Administration, Oral; Adult; Blood Coagulation; Blood Coagulation Disorders; Dose-Response Relationship, Drug; Female; Humans; Male; Middle Aged; Purpura; Rodenticides; Vitamin K; Warfarin

An infant with severe homozygous protein C deficiency was brought to medical attention because of purpura fulminans and severe bilateral vitreous hemorrhages in the neonatal period. Infusions of fresh frozen plasma were given for 8 months. On two occasions, attempts to decrease the frequency of fresh frozen plasma infusions to less than twice a day led to episodes of microangiopathic hemolysis, fibrinolysis, and acute renal failure. Infarction of skin and subcutaneous tissues did not recur. Both episodes were controlled after reinstitution of fresh frozen plasma. Complications of therapy with fresh frozen plasma included hyperproteinemia and hypertension. Warfarin therapy was instituted when the baby was 8 months of age, followed by a gradual withdrawal of fresh frozen plasma therapy. The dose of warfarin required to maintain the prothrombin time in a range of 1.8 to 2.2 times normal varied considerably during short periods, a phenomenon that may have been due to several factors: hypercatabolism of the drug with prolonged administration, abnormality of liver function, variation in levels of serum albumin, fluctuations in drug dosage secondary to oral administration, and variations in dietary vitamin K. Protein C determinations by immunologic and functional assays consistently showed detectable but reduced protein C antigen levels with undetectable activity levels, suggesting that a dysproteinemia rather than a deficiency of synthesis is responsible for the child's coagulopathy.

Topics: Blood Coagulation Disorders; Hemolytic-Uremic Syndrome; Homozygote; Humans; Infant, Newborn; Isoantigens; Male; Plasma; Protein C; Protein C Deficiency; Purpura; Vitreous Hemorrhage; Warfarin

We report a case of protein C deficiency which presented with purpura fulminans. The inheritance of protein C deficiency is discussed and the importance of warfarin (Coumadin) treatment in this conditions is emphasized.

Topics: Child; Disseminated Intravascular Coagulation; Female; Femoral Vein; Heparin; Humans; Protein C Deficiency; Purpura; Thrombosis; Warfarin

Coumarin necrosis, a rare complication of coumarin anticoagulation, typically presents with well-defined purpuric patches that progress to bullae formation and necrosis. The vast majority of those affected are women, and most commonly affected sites are the breasts, buttocks, thighs, and abdomen. We present a male patient who manifested a unique reticulated purpura that progressed to bullae formation on the toes of one foot in addition to more classic lesions on the thigh and calf.

Topics: Coumarins; Humans; Male; Middle Aged; Necrosis; Purpura; Skin; Toes; Warfarin

Severe and recurrent purpura fulminans developed in a Chinese boy at one day of age. Results of coagulation studies performed on the patient during attacks were compatible with the diagnosis of disseminated intravascular coagulation. Subsequent investigations have revealed that the patient is homozygous and that his parents are heterozygous for protein C deficiency. Cryoprecipitate and fresh frozen plasma induced a remission, and administration of warfarin has been successful in preventing recurrence of attacks for as long as 8 months without infusion of any plasma components. None of the family members who are heterozygous for protein C deficiency have had thrombotic episodes.

Topics: Combined Modality Therapy; Cryoglobulins; Glycoproteins; Heparin; Homozygote; Humans; Infant, Newborn; Male; Necrosis; Plasma; Protein C; Protein Deficiency; Purpura; Skin; Warfarin

Topics: Aged; Female; Humans; Leg; Male; Middle Aged; Necrosis; Purpura; Skin Diseases; Warfarin

A 67-year-old woman with a history of thrombophlebitis had been taking warfarin sodium for 1 1/2 years when she developed multiple skin lesions resembling warfarin-induced skin necrosis or purpura fulminans. Despite discontinuing the warfarin and administering prednisone, the lesions increased in size. Disseminated intravascular coagulation (DIC) was found and resolved with heparin sodium therapy, and her skin lesions healed. This patient was believed to have an atypical form of purpura fulminans rather than warfarin-induced skin necrosis because of the duration of warfarin therapy and the dramatic resolution with heparin. A monoclonal (IgG) gammopathy was found, which stabilized as the skin lesions resolved, and fulfilled the criteria for a benign (asymptomatic) monoclonal gammopathy.

Topics: Aged; Diagnosis, Differential; Disseminated Intravascular Coagulation; Female; Humans; Hypergammaglobulinemia; Immunoglobulin G; Necrosis; Purpura; Skin Diseases; Warfarin

Topics: Drug Interactions; Drug Synergism; Escherichia coli Infections; Female; Humans; Middle Aged; Nalidixic Acid; Prothrombin Time; Purpura; Thrombophlebitis; Urinary Tract Infections; Warfarin

Topics: Acetaminophen; Anemia, Aplastic; Anticoagulants; Aspirin; Blood Platelets; Bone Marrow; Capillary Fragility; Drug Hypersensitivity; Drug Synergism; Hemorrhagic Disorders; Hemostasis; Heparin; Heparin Antagonists; Humans; Indenes; Platelet Adhesiveness; Purpura; Thrombocytopenia; Vascular Diseases; Warfarin

Topics: Aged; Drug Hypersensitivity; Female; Humans; Necrosis; Purpura; Thrombophlebitis; Warfarin

Topics: Adolescent; Anticoagulants; Child; Complement System Proteins; Female; Glomerulonephritis; Granulomatosis with Polyangiitis; Heparin; Humans; Kidney Diseases; Male; Nephrosis; Nephrotic Syndrome; Proteinuria; Purpura; Warfarin

Topics: Aged; Female; Humans; Prednisolone; Purpura; Warfarin

Topics: Acenocoumarol; Anticoagulants; Coumarins; Dicumarol; Drug Therapy; Ecchymosis; Ethyl Biscoumacetate; Gangrene; Necrosis; Phenindione; Pulmonary Embolism; Purpura; Skin Diseases; Thrombophlebitis; Toxicology; Warfarin