Abstract

A 40-year-old African American man with a history of sickle cell disease (SCD), deep venous thrombosis and alcohol abuse was transferred to the medical intensive care unit for worsening agitation and stridor. Physical examination revealed a symmetrically swollen neck with large palpable veins over the anterior chest wall and abdomen. Figure 1 is an axial computed tomographic image of his chest which illustrates several large superficial collateral veins (arrows). A volume rendered computed tomographic image in Figure 2 depicts the extent of his chest and abdominal wall varicosities (arrows). The presence of extensive venous collateralization suggested that the thrombosis had been present for a prolonged period of time. Although SCD is a hypercoagulable state, a compelling causal link with venous thromboembolism is not well established. 1. Austin H. Key N.S. Benson J.M. et al. Sickle cell trait and the risk of venous thromboembolism among blacks. Blood. 2007; 110: 908-912 Crossref PubMed Scopus (169) Google Scholar , 2. Stein P.D. Beemath A. Meyers F.A. et al. Deep venous thrombosis and pulmonary embolism in hospitalized patients with sickle cell disease. Am J Med. 2006; 119: 897.e7-897.e11 Abstract Full Text Full Text PDF PubMed Scopus (148) Google Scholar However, a higher prevalence of pulmonary embolism and to a lesser extent deep venous thrombosis has been observed in African Americans with SCD. 2. Stein P.D. Beemath A. Meyers F.A. et al. Deep venous thrombosis and pulmonary embolism in hospitalized patients with sickle cell disease. Am J Med. 2006; 119: 897.e7-897.e11 Abstract Full Text Full Text PDF PubMed Scopus (148) Google Scholar A negative laboratory evaluation for a second hypercoagulable state suggested that SCD was the cause for the thrombosis. The patient was eventually discharged on subcutaneous enoxaparin twice daily. Figure 2 View Large Image Figure Viewer

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