A vascular malformation is a blood vessel or lymph vessel abnormality. Vascular malformations are one of the classifications of vascular anomalies, the other grouping is vascular tumors. They may cause aesthetic problems as they have a growth cycle, and can continue to grow throughout life. Vascular malformations of the brain (VMBs) include those involving capillaries, and those involving the veins and arteries. Capillary malformations in the brain are known as cerebral cavernous malformations or capillary cavernous malformations (CCMs). Those involving the mix of vessels are known as cerebral arteriovenous malformations (AVMs or cAVMs). The arteriovenous type is the most common in the brain. Types
A simple division of the vascular malformations is made into low-flow and high-flow types. Low-flow malformations involve a single type of blood or lymph vessel, and are known as simple vascular malformations; high-flow malformations involve an artery. There are also malformations that are of mixed-flow involving more than one type of vessel, such as an arteriovenous malformation.Low-flow vascular malformations include capillary malformations, venous malformations, and lymphatic malformations. Capillary malformation
Capillary malformations involve the capillaries, and are the most common type. They used to refer only to port-wine stains but now include others. Capillary malformations are limited to the superficial layers of the skin but they can thicken, become nodular, and sometimes become disfiguring.
Warfarin, a vitamin K antagonist discussed above, should be discontinued if possible.Other acceptable treatments may include one or more of the following:

Clot-dissolving agents (tissue plasminogen activator)
Maggot larval debridement
Correction of the underlying plasma calcium and phosphorus abnormalities (lowering the Ca x P product below 55 mg2/dL2)
Avoiding further local tissue trauma (including avoiding all subcutaneous injections, and all not-absolutely-necessary infusions and transfusions)
Patients who receive kidney transplants also receive immunosuppression. Considering lowering the dose of or discontinuing the use of immunosuppressive drugs in people who have received kidney transplants and continue to have persistent or progressive calciphylactic skin lesions can contribute to an acceptable treatment of calciphylaxis. A group has reported plasma exchange effective and propose a serum marker and perhaps mediator (calciprotein particles)

Prognosis
Overall, the clinical prognosis for calciphylaxis is poor. The 1-year mortality rate in patients who have end-stage kidney disease is 45-80%. Median survival in patients who do not have end-stage kidney disease is 4.2 months. Response to treatment is not guaranteed. The most common cause of death in calciphylaxis patients is sepsis, severe infection originating from a non-healing ulcer. Epidemiology
Calciphylaxis most commonly occurs in patients with end-stage renal disease who are on hemodialysis or who have recently received a kidney transplant. When reported in patients without end-stage renal disease (such as in earlier stages of chronic kidney disease or in normal kidney function), it is called non-uremic calciphylaxis by Nigwekar et al.