American Journal of Medical Case Reports
ISSN (Print): 2374-2151 ISSN (Online): 2374-216X Website: Editor-in-chief: Samy, I. McFarlane
Open Access
Journal Browser
American Journal of Medical Case Reports. 2020, 8(10), 332-334
DOI: 10.12691/ajmcr-8-10-3
Open AccessCase Report

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

Hira Chaudhary1, Peter Gillette1, Michael Ashamalla2, Angeleque Hartt1, Moro Salifu1 and Samy I. McFarlane1,

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

Pub. Date: June 18, 2020

Cite this paper:
Hira Chaudhary, Peter Gillette, Michael Ashamalla, Angeleque Hartt, Moro Salifu and 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


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.

acute chest syndrome Sickle cell thalassemia Hb S/β+ thalassemia pulmonary edema

Creative CommonsThis work is licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license, visit


Figure of 3


[1]  Piel, F. B., Steinberg, M. H., & Rees, D. C. (2017). Sickle cell disease. New England Journal of Medicine, 376(16), 1561-1573.
[2]  Pathak, M. S., Borah, M. S., & Kalita, D. (2014). Haemoglobin S Interaction with Beta Thalassaemia-A Case Report from Assam, India. Journal of clinical and diagnostic research: JCDR, 8(9), FD15.
[3]  Farara, N. (2015). Sickle cell thalassemia: a case report and review of literature. IJMPCR, 5, 1-4
[4]  Pham, P. T. T., Pham, P. C. T., Wilkinson, A. H., & Lew, S. Q. (2000). Renal abnormalities in sickle cell disease. Kidney international, 57(1), 1-8.
[5]  Jones, J., & Quinn, R. (2017). Fluid Replacement Strategies in Sickle Cell Disease. Proceedings of UCLA Healthcare, 21
[6]  Nath, K. A., & Hebbel, R. P. (2015). Sickle cell disease: renal manifestations and mechanisms. Nature Reviews Nephrology, 11(3), 161
[7]  Mack AK, Kato GJ. Sickle cell disease and nitric oxide: a paradigm shift?. Int J Biochem Cell Biol. 2006;38(8):1237-1243.
[8]  Morris, C. R. (2008). Mechanisms of vasculopathy in sickle cell disease and thalassemia. ASH Education Program Book, 2008(1), 177-185.
[9]  Jain S, Bakshi N, Krishnamurti L. Acute Chest Syndrome in Children with Sickle Cell Disease. Pediatrics Allergy Immunol Pulmonol. 2017;30(4):191–201.
[10]  Iqbal, M. H., Abe, O., Popilevsky, F., Garewal, V., Gillette, P., Jamaleddine, G., & Zein, J. G. (2008). HEMATOLOGIC PARAMETERS ASSOCIATED WITH WORSE OUTCOME IN CRITICALLY ILL SICKLE CELL DISEASE PATIENTS. Chest, 134(4), 61P.
[11]  Siddiqui, A. K., & Ahmed, S. (2003). Pulmonary manifestations of sickle cell disease. Postgraduate medical journal, 79(933), 384-390.