[5] Livedoid vasculopathy has been linked to various conditions that can induce hypercoagulability, including neoplasms, autoimmune connective-tissue diseases, and inherited and acquired thrombophilias.

[8] The oxygen partial pressure in the skin decreases as a result of the blood flow obstruction, triggering a cutaneous response that presents as pruritus with itchy papules and erythematous-violaceous, purpuric plaques.

Atrophic scars, persistent hyperpigmentation, mononeuritis multiplex from vasa nervorum thrombosis, and cutaneous hemosiderosis in the lower limbs from erythrocytes oozing from the high-pressure regimen veins due to hemosiderin deposits in the skin are among the chronic complications associated with livedoid vasculopathy.

[7] Few things are known about the origins of dermal vessel thrombosis in livedoid vasculopathy, what sets off its initial episodes and relapses, and why it primarily affects the lower limbs.

[4] Livedoid vasculopathy has been linked to rheumatoid arthritis, systemic lupus erythematosus, scleroderma, polyarteritis nodosa, mixed and undifferentiated connective tissue diseases, and Sjogren's syndrome.

[9] Livedoid vasculopathy is caused by a number of inherited and acquired coagulation abnormalities, such as polymorphisms in factor V, plasminogen activator inhibitor-1 (PAI-1), prothrombin, and methylenetetrahydrofolate reductase (MTHFR).

[6] The so-called Virchow trias, hypercoagulability, stasis, and endothelial damage, also serve as risk factors for livedoid vasculopathy microvascular thrombosis.

Furthermore, when paraproteinemia or solid organ cancers are suspected, tests for protein electrophoresis, Ig kappa and lambda chain levels, and immunofixation should be carried out.

Vasculitis, peripheral arterial vascular disease, and lower extremity chronic venous insufficiency are the most frequent conditions to be taken into account during the differential diagnosis process.

[16] UV light, compression, hyperbaric oxygen, and routine wound debridement are examples of local therapies for livedoid vasculopathy.

[4] Hyperbaric oxygen and compression therapy have been demonstrated to enhance fibrinolysis in addition to their respective roles in reducing edema and mitigating reperfusion injury.