Blast crisis is diagnosed if any of the following are present in a patient with CML:
>20% blasts in the blood or bone marrow
The presence of an extramedullary proliferation of blasts

Treatment
The only curative treatment for CML is a bone marrow transplant or an allogeneic stem cell transplant. Other than this there are four major mainstays of treatment in CML: treatment with tyrosine kinase inhibitors, myelosuppressive or leukopheresis therapy (to counteract the leukocytosis during early treatment), splenectomy and interferon alfa-2b treatment. Due to the high median age of patients with CML it is relatively rare for CML to be seen in pregnant women, despite this, however, chronic myelogenous leukemia can be treated with relative safety at any time during pregnancy with the cytokine Interferon-alpha. Chronic phase
In the past, antimetabolites (e.g., cytarabine, hydroxyurea), alkylating agents, interferon alfa 2b, and steroids were used as treatments of CML in the chronic phase, but since the 2000s have been replaced by Bcr-Abl tyrosine-kinase inhibitors drugs that specifically target BCR-ABL, the constitutively activated tyrosine kinase fusion protein caused by the Philadelphia chromosome translocation. Despite the move to replacing cytotoxic antineoplastics (standard anticancer drugs) with tyrosine kinase inhibitors sometimes hydroxyurea is still used to counteract the high leukocyte counts encountered during treatment with tyrosine kinase inhibitors like imatinib; in these situations it may be the preferred myelosuppressive agent due to its relative lack of leukemogenic effects and hence the relative lack of potential for secondary haematologic malignancies to result from treatment.
The WHO criteria are perhaps most widely used, and define the accelerated phase by the presence of ≥1 of the following haematological/cytogenetic criteria or provisional criteria concerning response to tyrosine kinase inhibitor (TKI) therapy

Haematological/cytogenetic criteria
Persistent or increasing high white blood cell count (> 10 × 109/L), unresponsive to therapy
Persistent or increasing splenomegaly, unresponsive to therapy
Persistent thrombocytosis (> 1000 × 109/L), unresponsive to therapy
Persistent thrombocytopenia (< 100 × 109/L), unrelated to therapy
≥ 20% basophils in the peripheral blood
10―19% blasts in the peripheral blood and/or bone marrow
Additional clonal chromosomal abnormalities in Philadelphia (Ph) chromosome-positive (Ph+) cells at diagnosis, including so-called major route abnormalities (a second Ph chromosome, trisomy 8, isochromosome 17q, trisomy 19), complex karyotype, and abnormalities of 3q26.2
Any new clonal chromosomal abnormality in Ph+ cells that occurs during therapy
Provisional response-to-TKI criteria
Haematological resistance (or failure to achieve a complete haematological response d) to the first TKI
Any haematological, cytogenetic, or molecular indications of resistance to two sequential TKIs
Occurrence of two or more mutations in the BCR-ABL1 fusion gene during TKI therapyThe patient is considered to be in the accelerated phase if any of the above are present. The accelerated phase is significant because it signals that the disease is progressing and transformation to blast crisis is imminent. Drug treatment often becomes less effective in the advanced stages. Blast crisis
Blast crisis is the final phase in the evolution of CML, and behaves like an acute leukemia, with rapid progression and short survival.