Article citationsMore >>

Nath, K. A., & Hebbel, R. P. (2015). Sickle cell disease: renal manifestations and mechanisms. Nature Reviews Nephrology, 11(3), 161

has been cited by the following article:

Article

Pulmonary Edema in Hb S/β+ thalassemia Patient Leading to Acute Chest Syndrome. A Case Report and Review of Literature

1Department of Medicine, SUNY-Downstate Health Sciences University, 450 Clarkson Avenue, Brooklyn, New York 11203, USA

2Department of Internal Medicine, Donald and Barbara Zucker School of Medicine at Hofstra/ Northwell, 300 Community Drive, Manhasset, NY 11030, USA


American Journal of Medical Case Reports. 2020, Vol. 8 No. 10, 332-334
DOI: 10.12691/ajmcr-8-10-3
Copyright © 2020 Science and Education Publishing

Cite this paper:
Hira Chaudhary, Peter Gillette, Michael Ashamalla, Angeleque Hartt, Moro Salifu, Samy I. McFarlane. Pulmonary Edema in Hb S/β+ thalassemia Patient Leading to Acute Chest Syndrome. A Case Report and Review of Literature. American Journal of Medical Case Reports. 2020; 8(10):332-334. doi: 10.12691/ajmcr-8-10-3.

Correspondence to: Samy  I. McFarlane, Department of Medicine, SUNY-Downstate Health Sciences University, 450 Clarkson Avenue, Brooklyn, New York 11203, USA. Email: Samy.mcfarlane@downstate.edu

Abstract

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/β+ 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.

Keywords