Discussion

CML is a malignant neoplasm, which is characterized by the expansion of the erythroid, myeloid, and platelets in the peripheral blood and myeloid hyperplasia of the bone marrow. It is associated with the BCR/ABL1 fusion gene. This gene encodes an abnormal protein which leads to the constitutive activation of tyrosine kinase, which eventually results in neoplastic proliferation(5). CML accounts for 15-20% of leukemias in adults(6) and Ionization radiation exposure is the only known risk factor(1, 7).
The average diagnostic age ranges from 60 to 65 years(8). About 50% of cases are asymptomatic and are identified incidentally by routine complete blood count tests(2). Anemia, splenomegaly, fatigue, weight loss, and night sweats are the commonest initial manifestations(5). Extramedullary involvement such as the lymph nodes, skin, and soft tissues can be seen in patients with blast crises(9). very rarely, soft tissue hematoma can be the first manifestation of CML. The soft tissue hematoma may be explained by platelet dysfunction, acquired Von Willebrand disease, or acquired Glanzmann’s thrombasthenia(3).
The clonal expansion of dysfunctional megakaryocytes can explain platelet dysfunction in CML, which explains the anticipated improvement in their function following the initiation of tyrosine kinase inhibitors(3, 10-12).
The Morel‐Lavallée lesion is a closed traumatic soft‐tissue degloving injury, first described by the French physician, Dr. Victor‐Auguste‐François Morel‐Lavallée in 1863. This damage is the result of the separation of the hypodermis from the fascial tissue due to a shearing force. Hematoma collection forms due to disruption of the soft tissue’s perforating blood and lymphatic vessels(3, 13). The subcutaneous tissues beside the greater trochanter are the most frequently affected areas by the Morel‐Lavallée lesion(13). We were able to find three case reports in which the Morel Lavallee lesion was the initial manifestation of CML. The first patient was a 16-year-old male athlete who presented with swelling on his knee, confirmed to be CML after investigation, and was managed both surgically and with a tyrosine kinase inhibitor(14).
The second patient was a 55-year-old male who came with left thigh swelling and was also diagnosed with CML after workup and treated with imatinib and conservatively(4). The third case was a Morel Lavallee lesion affecting the posterior chest wall, he was treated conservatively and started on dasatinib(3). Our case is the fourth CML patient presenting with Morel Lavallee lesion, and the first case that involved the anterior abdominal wall. She was managed conservatively.
platelet dysfunction, acquired Glanzmann’s thrombasthenia, acquired Von Willebrand deficiency, were attributed to the spontaneous hematoma in the previous case reports(10-12).
Even though it’s not clear why this patient developed hematoma in unusual site without any prior trauma, platelet dysfunction is the likely etiology.