Coumarin necrosisY44.2

Author:Prof. Dr. med. Peter Altmeyer

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Last updated on: 29.10.2020

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Synonym(s)

coumarin induced necrosis; coumarin necrosis; Coumarin necrosis; Coumarin Necrosis

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DefinitionThis section has been translated automatically.

Rare haemorrhagic necrosis with anticoagulative treatment with coumarins.

Occurrence/EpidemiologyThis section has been translated automatically.

Incidence: 0.1%, especially for hereditary protein C deficiency.

EtiopathogenesisThis section has been translated automatically.

In the initiation phase of phenprocoumon therapy, the protein C values and FVII drop faster than the other factors of the prothrombin complex due to shorter half-lives, resulting in a temporary state of hypercoagulopathy. In the case of pre-existing PC deficiency, thromboembolic complications or coumarin necrosis can thus occur, particularly in the initiation phase of this therapy.

ManifestationThis section has been translated automatically.

Occurs mainly in women. Known risk factors are: protein C deficiency, obesity, inadequate overlapping administration of heparins, estrogen deficiency.

LocalizationThis section has been translated automatically.

Mammae, legs, buttocks.

Clinical featuresThis section has been translated automatically.

2-10 days after the start of therapy, circumscribed, often following a livedo pattern, deep red to blue-red, jagged spots; rapid confluence. Large, succulent, red-blue to blue-black painful lesions result. Formation of large hemorrhagic blisters. Within the next few days, extensive, deep-reaching, painful ulcers limited to the lesion develop.

LaboratoryThis section has been translated automatically.

Protein C degradation.

HistologyThis section has been translated automatically.

Fatty tissue necroses; in early stages: detection of hyaline thrombi in the venules of the corium and subcutaneous fat tissue; fibrinoid necroses of the vascular walls, erythrocyte extravasations.

Differential diagnosisThis section has been translated automatically.

Complication(s)This section has been translated automatically.

Septic wound infections with the risk of multiorgan failure.

External therapyThis section has been translated automatically.

Symptomatic stage-appropriate local therapy with necrosectomy, granulation-promoting wound dressings (e.g. Varihesive E) and sterile draping, see below Wound treatment. Healing after several weeks with the formation of deep scars.

Internal therapyThis section has been translated automatically.

Changeover of the coumarin preparations to heparin. Counteraction by vitamin K (e.g. konakion solution) 1-5 trp. for mild, 5-10 trp. for severe depending on coagulation status and underlying disease. The effect of changing the therapy is controversial. Presumably, the course of the disease cannot be influenced by it. If the coumarin therapy is maintained, no further necroses need to occur in the course of the disease.

Progression/forecastThis section has been translated automatically.

The course of the disease cannot be influenced by discontinuing the therapy. Healing after several weeks. Formation of deep scars.

LiteratureThis section has been translated automatically.

  1. Goerge Tet al.(2014) Extensive Counarinnekrose-a vasculopathy under oral anticoagulation. JDDG 12: 263-264
  2. Greinacher A et al (2003) Heparin-induced thrombocytopenia. Dtsch Ärztebl 100: 2220-2229
  3. Harenberg J et al (2001) Cutaneous reactions to anticoagulants. Recognition and management. At J Clin Dermatol 2: 69-75
  4. Jorg I et al (2002) Anticoagulant-related skin reactions. Expert Opinion Drug Saf 1: 287-294
  5. Loop M et al (2004) Late onset of clinical symptoms and recurrent ecchymotic skin lesions in a 12-year-old girl with a severe double heterozygous protein C deficiency. J Pediatr Hematol Oncol 26: 2-4
  6. Luderschmidt, Schramm C (1990) Coumarin necrosis. Phlebology 43: 622-623

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Last updated on: 29.10.2020