Abstract: Case Reports |


Michael E. Ezzie, MD*; John Mastronarde, MD
Author and Funding Information

The Ohio State University Medical Center, Columbus, OH

Chest. 2006;130(4_MeetingAbstracts):332S-b-333S. doi:10.1378/chest.130.4_MeetingAbstracts.332S-b
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INTRODUCTION: There are multiple causes of hypoxia in patients with acute myeloid leukemia (AML). One of these is pulmonary leukostasis which is an oncologic emergency and can be difficult to diagnose and manage. We report a case of a patient with newly diagnosed AML and hypoxia secondary to pulmonary leukostasis that was successfully treated with chest irradiation.

CASE PRESENTATION: A 71-year-old white male with no past medical history presented to our medical center with three weeks of progressive dyspnea, fatigue, and a ten pound weight loss. He denied chest pain, orthopnea, or fevers. His only medicines were over-the-counter vitamins and he was a lifelong nonsmoker. On examination, he was tachycardic to 120 beats per minute and his SpO2 was 92% on 3 liters nasal cannula. There were faint crackles bilaterally on lung exam with no jugular venous distention or lower extremity edema. Labs revealed a white count of 208.9 K/ul with 60% blasts, hemoglobin of 6.9 g/dl, and platelet count of 26 K/ul. Bone marrow biopsy was hypercellular with 94% blasts and the patient was given a diagnosis of AML. His ejection fraction by MUGA was 51%. Chest CT demonstrated diffuse ground glass infiltrates. Blood cultures were negative for infection. Cytoreduction was attempted with hydroxyurea and 2 cycles of leukapheresis. Despite these therapies, his oxygen requirement increased and on 100% FIO2 his PaO2 was 134, with an SpO2 of 90%. Chest irradiation was then given at 100 cGy with a marked improvement in his oxygenation, eventually weaning to room air in 48 hours. He was then initiated on induction chemotherapy for his AML.

DISCUSSIONS: The differential diagnosis of hypoxia in patients with AML includes leukostasis, pneumonia, pulmonary emboli, congestive heart failure, alveolar hemorrhage, or spurious hypoxia. Spurious hypoxemia is found in patients with hyperleukocytosis and may be due to consumption of dissolved oxygen from the sample by the white cells or coating of the oxygen electrode by white cells. In these cases, pulse oximetry may be the most accurate method of assessing oxygenation. Leukostasis occurs due to an increased blast count that impedes blood flow in the microcirculation. In addition, there may be an adhesive interaction between the blasts and endothelium, and hypoxia due to leukostasis may be exacerbated by the high metabolic activity of the dividing cells. Making the diagnosis of pulmonary leukostasis can be difficult. A diffuse vascular occlusive pattern on perfusion lung scanning may be supportive. A bronchoalveolar lavage with a large number of blasts and no evidence of infection may also be supportive, but most diagnoses are retrospective after clinical improvement with cytoreduction. Cytoreduction is often initiated as, in some patients, leukostasis or other problems may lessen the response to chemotherapy or delay the initiation of chemotherapy. However, cytoreduction by leukapheresis or other means has not been shown to improve mortality. Rapid cytoreduction can be achieved with induction chemotherapy, hydroxyurea, leukapheresis, or less commonly, irradiation. The rationale for radiation is that it destroys established intravascular foci of blast cells. There are only a few case reports in the literature utilizing irradiation for pulmonary leukostasis with hypoxia. Three cases that have reported benefit were all in young patients ages 25-29. A case report of a 65-year-old patient cited no benefit.

CONCLUSION: This is a case of 71-year-old patient with hypoxia due to pulmonary leukostasis that responded to chest irradiation after being refractory to other therapies. When instituted early, chest irradiation may be of benefit in treating severe pulmonary leukostasis.

DISCLOSURE: Michael Ezzie, None.

Wednesday, October 25, 2006

2:00 PM - 3:30 PM


von Eyben FE, Siddiqui MZ, Spanos G.Acta Haematol.1987;77(3)180-2.
Rajkumar SV, Fonseca R, Letendre L.Leukemia.1999March;13(3):490.




von Eyben FE, Siddiqui MZ, Spanos G.Acta Haematol.1987;77(3)180-2.
Rajkumar SV, Fonseca R, Letendre L.Leukemia.1999March;13(3):490.
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