December 2016 Case Cedars-Sinai Skip to content Close Select your preferred language English عربى 简体中文 繁體中文 فارسي עִברִית 日本語 한국어 Русский Español Tagalog English English عربى 简体中文 繁體中文 فارسي עִברִית 日本語 한국어 Русский Español Tagalog Translation is unavailable for Internet Explorer Cedars-Sinai Home 1-800-CEDARS-1 1-800-CEDARS-1 Close Find a Doctor Locations Programs & Services Health Library Patient & Visitors Community My CS-Link Education clear Go Close Academics Academics Faculty Development Community Engagement Calendar Research Research Areas Research Labs Departments & Institutes Find Clinical Trials Research Cores Research Administration Basic Science Research Clinical & Translational Research Center (CTRC) Technology & Innovations News & Breakthroughs Education Graduate Medical Education Continuing Medical Education Graduate School of Biomedical Sciences Professional Training Programs Medical Students Campus Life Office of the Dean Simulation Center Medical Library Program in the History of Medicine About Us All Education Programs Departments & Institutes Faculty Directory Anatomic and Clinical Pathology Residency Back to Anatomic and Clinical Pathology Residency Application Information Explore the Residency Training Curriculum Autopsy Pathology Rotation Bone and Soft Tissue Head and Neck Pathology Rotation Breast Pathology Rotation Cardiovascular Pathology Rotation Clinical Chemistry Rotation Coagulation Rotation Cytopathology Rotation Dermatopathology Rotation Forensic Pathology Rotation Frozen Section Rotation Gastrointestinal and Liver Pathology Genitourinary Pathology Rotation Genomic Pathology Rotation Gynecologic Pathology Rotation Hematopathology Rotation Laboratory Management Rotation Microbiology Rotation Neuropathology Rotation Pulmonary and Mediastinal Pathology Rotation Renal Pathology Rotation Transfusion Medicine Rotation Surgical Pathology Pathology Physician Scientist Training Program Residents Graduates Case of the Month Archive Publications Leadership Frequently Asked Questions December 2016 Case Authors Angelica Vivero MD, Chelsea Hayes MD, Holli Mason MD, Ellen Klapper MD Subject Transfusion Medicine Clinical History A 53-year-old male with a past medical history of esophageal cancer, status post partial esophagectomy, coronary artery disease and hypertension presented to the emergency department with acute onset of abdominal pain following a fall sustained at home. Imaging revealed a left upper quadrant fluid collection suspicious for splenic hematoma. Vital signs were within normal limits and he was found to be anemic with a hemoglobin of 6.8 g/dL. One unit of red blood cells was transfused while the patient was transported to interventional radiology for splenic artery embolization. During the procedure he developed respiratory distress, became acutely hypoxic with an oxygen saturation of 75% and required emergent intubation. His temperature rose to 39.1C while blood pressure and heart rate remained unchanged. A chest x-ray is pictured below. The patient was transferred to the intensive care unit for management of acute respiratory failure. A complete blood count revealed leukopenia with a decrease in white blood cell count from a pre-procedure value of 7.0 x 1000/UL to a post-procedure value of 1.5 x 1000/UL. A transfusion reaction workup did not reveal evidence of hemolysis and an acute hemolytic transfusion reaction was ruled out. Within 72 hours the patient’s respiratory status improved, and he was discharged home in stable condition on hospital day 11. Diagnosis Transfusion-related acute lung injury (TRALI) Discussion Transfusion-related acute lung injury (TRALI) is a syndrome characterized by acute respiratory distress and hypoxemia, evidenced by SpO2 < 90% or PaO2/FiO2 ratio ≤ 300, as well as new-onset bilateral pulmonary edema, occurring within 6 hours of transfusion. These findings are present in the absence of preexisting acute lung injury, circulatory overload, and cardiogenic pulmonary edema. Additional symptoms include fever, chills, hypertension followed by hypotension, and transient leukopenia. Symptoms typically present within the first 1 to 2 hours following blood transfusion, but by definition must be present within 6 hours of transfusion. Treatment of TRALI is supportive and ranges from supplemental oxygen to ventilator support. The use of diuretics and corticosteroids are not indicated. Although symptom resolution usually occurs within 72 to 96 hours, TRALI can be life threatening and is currently the leading cause of transfusion-related mortality reported in the United States1. The mechanism of TRALI is not clearly understood. One hypothesis suggests that infusion of donor anti-HLA antibodies, anti-neutrophil antibodies, or biologic response modifiers (BRMs) interact with recipient neutrophils and/or pulmonary vascular endothelial cells resulting in neutrophil trapping and activation. This process results in endothelial damage, capillary leakage and pulmonary edema1-2. BRMs are substances that accumulate in blood products during storage, which are thought to enhance the neutrophil oxidative burst following transfusion. The second hypothesis postulates that TRALI is caused by two independent events. First, a physiologic stressor, such as sepsis, surgery, or massive transfusion, results in priming and sequestration of neutrophils in the pulmonary microvasculature. The second event occurs following transfusion of antibodies or BRMs, and the subsequent activation of primed neutrophils results in endothelial damage and pulmonary edema1-2. The patient in this case developed acute respiratory distress, hypoxemia and bilateral pulmonary edema within 6 hours of transfusion of a single unit of blood. Additional findings included fever and leukopenia. In the absence of preexisting acute lung injury or evidence of cardiogenic pulmonary edema, a diagnosis of TRALI was considered. Further investigation revealed that the blood donor was a multiparous female and therefore at increased risk of developing HLA antibodies. An anti-B8 HLA Class 1 antibody was identified in the donor plasma and subsequent HLA typing of the recipient revealed the presence of the cognate HLA B8 antigen, supporting the diagnosis of TRALI. References 1. Fung, M.K. (2014) Technical Manual. Bethesda, Maryland: AABB. 2. Silliman CC, Ambruso DR, Boshkov LK. Transfusion-related acute lung injury. Blood. 2005;15;105(6):2266-73. Have Questions or Need Help If you have questions or would like to learn more about the Anatomic and Clinical Pathology Residency Program at Cedars-Sinai, please call or send a message to Academic Program Coordinator, LeeTanya Marion-Murray. Department of Pathology and Laboratory Medicine 8700 Beverly Blvd., Room 8709 Los Angeles, CA 90048-1804 310-423-6941 send a message Please ensure Javascript is enabled for purposes of website accessibility