Aetiology
Petechiae, purpura and ecchymoses result from damage to blood vessels within the skin (causing leakage of blood into surrounding tissues) or thrombocytopaenia (causing spontaneous bleeding without preceding injury).
Causes include:
- Disorders of reduced platelet production, e.g. leukaemia and bone marrow failure.
- Disorders of increased platelet consumption/destruction, e.g. thrombotic thrombocytopaenic purpura, haemolytic uraemic syndrome and idiopathic thrombocytopaenic purpura, SLE.
- Disseminated intravascular coagulation (DIC) can occur secondary to malignancy or severe infection; activation of the coagulation pathways cause widespread clotting (using up coagulation factors and platelets) which then leads to excessive bleeding.
- Drugs affecting platelet function, e.g. NSAIDs, aspirin and clopidogrel.
- Drugs which act on clotting factors, e.g. heparin, warfarin, DOACs.
- Severe clotting disorders such as haemophilia A or B tend not to present with petechiae or purpura (which are more indicative of thrombocytopaenia), but do present with ecchymoses, haematomas and haemarthrosis. This is due to a deficiency of factor VIII (haemophilia A) or IX (haemophilia B), leading to delayed clot formation; any clot that is formed is fragile and frequently dislodged.
- Other disorders causing clotting factor deficiency, e.g. vitamin K deficiency, advanced liver disease, Von Willebrand disease.
Pathological/secondary livedo reticularis can be due to a range of underlying systemic diseases, coagulation disorders which can cause it include:
- Antiphospholipid syndrome – antiphospholipid antibodies produce a prothrombotic state, resulting in blood clots. When small clots form within the skin’s blood vessels, blood flow is disturbed and this produces livedo reticularis.
- Protein C, deficiency, protein S deficiency and antithrombin III deficiency are thought to cause livedo reticularis by a similar prothrombotic mechanism.
- Skin ulcers may also occur due to a similar mechanism of blood vessel obstruction.
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