Correct!
5. Pulmonary leukostasis
Pulmonary edema secondary to fluid administration is unlikely because the patient was clinically dehydrated and at this juncture had received only 2 liters of fluid. An opportunistic infection is possible but he is afebrile and his history is more consistent with a slowly evolving process. There is nothing at this juncture to suggest alveolar hemorrhage or granulomatosis with polyangitis which is the new name for Wegener’s granulomatosis. However, pulmonary leukostasis is likely in this situation (2,3).
Pulmonary leukostasis can occur with hyperleukocytosis of any type. The critical leukocyte level for development of pulmonary leukostasis depends on the type of leukemia and the size of the cell. Generally, leukostasis does not occur until the white blood count excess 100,000 cells/mm3 for acute myelocytic leukemia, 150,000 cells/mm3 for acute lymphocytic leukemia and 400,000 cells for chronic lymphocytic leukemia. Myelocytes and myeloblasts are the largest cell becoming progressively smaller with the lymphocytes in acute lymphocytic leukemia and even smaller with chronic lymphocytic leukemia. Multiple organs can be involved including the central nervous system and kidneys as well as the lungs.
There are 2 main theories of pulmonary leukostasis. One is that increased blood viscosity leads to sludging of blood in the pulmonary circulation. Leukemic blasts are less deformable than mature leukocytes. With high blast counts, plugs of cells develop in microcirculation, impeding blood flow. The other theory is that local hypoxemia and cytokine release result in pulmonary injury. The cells have high metabolic activity and release cytokines. The cytokines may lead to endothelial damage, resulting in hemorrhage and migration of leukemic cells into the tissue.
The patient was begun on cytoreduction therapy. Which of the following have not been proven to be beneficial in cytoreduction?