DESCRIPTION
A macular, bluish/purple discolouration of the skin that has a net- or lace-like
appearance.
CAUSES:
• Primary or idiopathic livedo reticularis (LR)
• Elderly people
• Secondary LR
• Hypercoagulable/haematological states
• Antiphospholipid syndrome
• Snedden’s syndrome
• Cryoglobulinaemia
• Multiple myeloma
• Polycythaemia
• DVT
• TTP
• Vasculitis
• Connective tissue disorders (e.g. SLE, Sjögren’s)
• Embolisation (e.g. cholesterol embolisation syndrome)
• Vessel wall deposition (e.g. calciphylaxis)
• Amantadine adverse effect
• Quinine adverse
LR is essentially increased visibility of the venous plexus of the skin. Venodilatation of the vessels and deoxygenation of blood in the plexus are the two main factors. The venous plexus of the skin is
formed when arterioles arising from the dermis, perpendicular to the skin, divide to form a capillary bed. These capillaries then drain into venules and the venous plexus at the periphery of the bed.
In general, venodilatation is caused by altered autonomic nervous system function; circulating factors that cause venodilatation; or in response to local hypoxia. Venodilatation allows more venous blood to be present in engorged venules, making them larger and easier to see through the skin.
Deoxygenation is principally caused by decreased cutaneous perfusion,50 which can be as a result of decreased arteriolar inflow or decreased venous outflow.
These changes in flow are caused by:
• decreased arteriolar inflow – vasospasm due to cold, ANS activity, arterial thrombosis or increased blood
viscosity
• decreased venous outflow – venous thrombosis, increased blood viscosity.
Primary or idiopathic LR:
LR without the presence of underlying disease is thought to be caused by spontaneous arteriolar vasospasm, which decreases oxygenated blood inflow, causing tissue hypoxia and increased deoxygenation
of venous blood.
SIGN VALUE:
Despite the many potential causes, LR is still a valuable sign. Primary or idiopathic LR is a diagnosis of
exclusion and other causes should be ruled out first.
• LR has been shown to have a significant relationship with anti-phospholipid syndrome in the absence of SLE, with up to 40% of patients having LR as the first sign of the underlying prothrombotic disorder.
• LR in a patient with SLE has been shown to be a significant predictor of the development of neuropsychiatric symptoms of SLE.
A macular, bluish/purple discolouration of the skin that has a net- or lace-like
appearance.
CAUSES:
• Primary or idiopathic livedo reticularis (LR)
• Elderly people
• Secondary LR
• Hypercoagulable/haematological states
• Antiphospholipid syndrome• Snedden’s syndrome
• Cryoglobulinaemia
• Multiple myeloma
• Polycythaemia
• DVT
• TTP
• Vasculitis
• Connective tissue disorders (e.g. SLE, Sjögren’s)
• Embolisation (e.g. cholesterol embolisation syndrome)
• Vessel wall deposition (e.g. calciphylaxis)
• Amantadine adverse effect
• Quinine adverse
LR is essentially increased visibility of the venous plexus of the skin. Venodilatation of the vessels and deoxygenation of blood in the plexus are the two main factors. The venous plexus of the skin is
formed when arterioles arising from the dermis, perpendicular to the skin, divide to form a capillary bed. These capillaries then drain into venules and the venous plexus at the periphery of the bed.
In general, venodilatation is caused by altered autonomic nervous system function; circulating factors that cause venodilatation; or in response to local hypoxia. Venodilatation allows more venous blood to be present in engorged venules, making them larger and easier to see through the skin.
Deoxygenation is principally caused by decreased cutaneous perfusion,50 which can be as a result of decreased arteriolar inflow or decreased venous outflow.
These changes in flow are caused by:
• decreased arteriolar inflow – vasospasm due to cold, ANS activity, arterial thrombosis or increased blood
viscosity
• decreased venous outflow – venous thrombosis, increased blood viscosity.
Primary or idiopathic LR:
LR without the presence of underlying disease is thought to be caused by spontaneous arteriolar vasospasm, which decreases oxygenated blood inflow, causing tissue hypoxia and increased deoxygenation
of venous blood.
SIGN VALUE:
Despite the many potential causes, LR is still a valuable sign. Primary or idiopathic LR is a diagnosis of
exclusion and other causes should be ruled out first.
• LR has been shown to have a significant relationship with anti-phospholipid syndrome in the absence of SLE, with up to 40% of patients having LR as the first sign of the underlying prothrombotic disorder.
• LR in a patient with SLE has been shown to be a significant predictor of the development of neuropsychiatric symptoms of SLE.
