eng Science and Education Publishing American Journal of Medical Case Reports 2374-216X 2020-06-18 8 10 332 334 10.12691/ajmcr-8-10-3 AJMCR20208103 article Hira Chaudhary 1 Peter Gillette 1 Michael Ashamalla 2 Angeleque Hartt 2 Moro Salifu 2 Samy I. McFarlane Samy.mcfarlane@downstate.edu 2 Department of Medicine, SUNY-Downstate Health Sciences University, 450 Clarkson Avenue, Brooklyn, New York 11203, USA Department of Internal Medicine, Donald and Barbara Zucker School of Medicine at Hofstra/ Northwell, 300 Community Drive, Manhasset, NY 11030, USA Acute chest syndrome (ACS) is associated with prolonged hospitalization and high mortality in sickle cell population. The etiology of ACS is often multifactorial. It is well known that any chest pain that limits ventilation, blood flow or oxygenation establishes the risk of ACS. The independent contributory mechanism is fluid overload, resulting in pulmonary edema. In this report, we present a case of compound heterozygous Hb S/¦Â+ thalassemia in a 32-year-old woman who presented with chest pain complicated by the development of pulmonary edema advancing to acute chest syndrome. We discuss the putative mechanisms might have led to pulmonary edema in this patient including hydration with underlying renal defect, along with a vicious cycle of vascular changes that resulted into pulmonary edema and consequently ACS. http://pubs.sciepub.com/ajmcr/8/10/3/ajmcr-8-10-3.pdf acute chest syndrome Sickle cell thalassemia Hb S/¦Â+ thalassemia pulmonary edema