Calfee uses biomarkers to investigate the development, ability to detect and impact of treatment on acute lung injury and acute respiratory distress syndrome (ARDS).[3] In critically ill patients, ARDS is a frequent cause of acute respiratory failure, and has mortality rates of up to 40%.[4] Calfee studies different phenotypes of ARDS in an effort to identify novel treatments. By understanding unrecognised subphenotypes of people who suffer from ARDS, Calfee looks to test more targeted interventions.[5] She identified that around one third of ARDS patients have a hyper-inflammatory phenotype, which may be more responsive to mechanical ventilation and pharmacotherapy.[4] This particular phenotype is associated with elevated levels of proinflammatory biomarkers in plasma as well as an increase in organ dysfunction.[6]
During the COVID-19 pandemic Calfee studied why SARS-CoV-2 patients experienced such different symptoms; ranging from mild to life-threatening.[7][13] Her research identified that the infection attacks the alveolar epithelium, small air sacs that usually prevent fluid entering the lungs.[7] When the barrier between the air sacs and blood becomes leaky, fluid starts to pour into the lungs.[13] This damage can be so severe that it takes a long time to heal, which means that the time for ventilation is longer than expected.[7] In this specific type of RNA virus, a human's immune system response can be so intense that it damages the lungs.[7] Calfee analyses the fluid and blood samples to understand what factors cause the most extreme responses of coronavirus disease. At the time, Calfee served as an intensive care physician, and remarked that “the scale and severity of this epidemic is like nothing any of us have experienced,”.[7]
