A previously healthy 61‐year‐old woman presented with three weeks of progressive shortness of breath, bilateral lower extremity swelling, fatigue, fevers, chills and nonproductive cough. On physical exam, vitals were notable for tachycardia to 116 bpm. HEENT, heart and lung exams were unremarkable. No lymphadenopathy was palpated. Edema extending to the calves was noted along with bilateral calf tenderness. Laboratory studies were remarkable for WBC count of 11.8 thousand/ul, platelet count of 170 thousand/ul and hemoglobin of 12.6 g/dL. Liver function tests showed AST at 92 U/L and ALT at 58 U/L. D‐dimer level was markedly elevated. On imaging, a pulmonary embolus was found in the right posterior basal segmental artery. Upper and lower extremity venous doppler studies were negative. Serological tests for HIV and hepatitis were negative. CMV IgG and IgM were elevated and EBV DNA was detected, although the EBV PCR quantitative was lower than the lowest detectable limit. Cardiolipin IgG was normal but IgM was markedly elevated. Tests for genetic hypercoagulability were negative. A diagnosis of CMV mononucleosis‐like illness was made. Anticoagulation treatment was initiated and the patient was discharged with hematology follow‐up.
First of all, this case demonstrates the initial algorithm in diagnosing a pulmonary embolism (PE). The patient was deemed to have a low probability of PE as she lacked identifiable risk factors. A D‐dimer was thus checked, which prompted the CT scan that led to the diagnosis. Furthermore, the case presented above illustrates the relationship between a common viral infection and venous thromboembolism (VTE). The literature about this relationship is limited to animal studies and case reports. Animal studies have shown that mice immunized with viral antigens such as a CMV peptide generate antiphospholipid (aPL) antibodies that have binding characteristics and functional properties similar to those found in the serum of patients with antiphospholipid syndrome. Molecular mimicry has been implicated in the mechanism of this process. In case reports, a number of viral infections, including HCV, HIV, CMV, varicella zoster, EBV, adenovirus and parvovirus B have been associated with induced production of aPL antibodies, leading to a hypercoagulable state and subsequent VTE. These cases have been reported predominantly in immunocompromised patients or in those with a genetic hypercoagulability syndrome. As such, although rare, this case demonstrates the potential for VTE in an immunocompetent patient in the setting of acute viral syndrome and elevated aPL antibodies. This finding leads to treatment implications as such an occurrence would be considered a provoked thrombosis and would thus require a shorter duration of anticoagulation therapy if the aPL antibodies resolve with the infection.
The case above emphasizes the use of the initial algorithm to diagnose pulmonary embolism in a low‐risk patient and the importance of considering uncommon causes of venous thromboembolism depending on the clinical situation. This concept is illustrated here with the involvement of viruses such as CMV in the induction of venous thromboembolism through production of antiphospholipid antibodies in an immunocompetent individual without predisposing risk factors. Thus it becomes essential to screen for such viral syndromes in the setting of spontaneous thrombosis and fever as there may be implications for length of anticoagulation therapy.
To cite this abstract:Baig J, Czaja M. An Unusual Case of Pulmonary Embolism. Abstract published at Hospital Medicine 2014, March 24-27, Las Vegas, Nev. Abstract 332. Journal of Hospital Medicine. 2014; 9 (suppl 2). https://www.shmabstracts.com/abstract/an-unusual-case-of-pulmonary-embolism/. Accessed November 17, 2019.