Phlegmasia Cerulea Dolens, literally translated as painful blue edema, is a rare complication of Deep Vein Thrombosis. Deep Vein Thrombosis itself is defined as a blood clot in a deep vein in your body, commonly in the lower extremities. If left untreated, it may progress along a continuum from deep vein thrombosis, to Phlegmasia Alba Dolens (PAD), into Phlegmasia Cerulean Dolens, finally ending in gangrene. Phelgmasia Alba Dolens is extensive thrombosis occluding major deep venous channels. Subsequent compromise of arterial flow causes edema, pain, and a white appearance (alba) of the extremity. What differentiates PCD from PAD is occlusion extending into collateral veins. This results in worsening venous congestion, leading to acute significant edema. Blood pools in the lower extremity as venous return is diminished. Intravascular fluid dwindles and the patient becomes hypotensive, tachycardic, and urine output is decreased. Ischemia persists and the affected limb becomes cyanotic. With progression, cyanosis increases and the patient begins to form bullae, paresthesia, weakness, and compartment syndrome. In 40% - 60% of cases, there is arterial and venous capillary
Phlegmasia Cerulea Dolens, literally translated as painful blue edema, is a rare complication of Deep Vein Thrombosis. Deep Vein Thrombosis itself is defined as a blood clot in a deep vein in your body, commonly in the lower extremities. If left untreated, it may progress along a continuum from deep vein thrombosis, to Phlegmasia Alba Dolens (PAD), into Phlegmasia Cerulean Dolens, finally ending in gangrene. Phelgmasia Alba Dolens is extensive thrombosis occluding major deep venous channels. Subsequent compromise of arterial flow causes edema, pain, and a white appearance (alba) of the extremity. What differentiates PCD from PAD is occlusion extending into collateral veins. This results in worsening venous congestion, leading to acute significant edema. Blood pools in the lower extremity as venous return is diminished. Intravascular fluid dwindles and the patient becomes hypotensive, tachycardic, and urine output is decreased. Ischemia persists and the affected limb becomes cyanotic. With progression, cyanosis increases and the patient begins to form bullae, paresthesia, weakness, and compartment syndrome. In 40% - 60% of cases, there is arterial and venous capillary