A 29‐year old previously healthy white male patient presented with 1 day of shortness of breath, left‐sided pleuritic chest pain, cough, and hemoptysis. The patient had been on a trip a week prior to presentation where he had driven for eight hours. He had mild pain without swelling in bilateral calves. Family history was negative for VTE. Physical exam showed a heart rate 125/minute, respiratory rate 26/minute, room air oxygen saturation 92% and a blood pressure 125/70 mm Hg. Chest exam revealed diminished vesicular breathing in the left base and calves were tender to palpation but no swellings. Laboratory investigation revealed elevated serum D‐dimer level (4054 ng/mL). EKG showed sinus tachycardia. Chest x‐ray showed atelactatic changes at left lung base. To rule out pulmonary embolism CT of the chest done and confirmed the presence of bilateral acute pulmonary emboli. Doppler ultrasound of lower extremities showed bilateral DVT of popliteal veins. Mildly elevated RVSP at 47 mm Hg was noted on echocardiogram without right ventricle strain. Patient age and presentation suggested thrombophilic etiology. Hypercoagulable screening panel was positive for factor V Leiden (FVL) mutation (heterozygous type). Standard regimen anticoagulation was initiated and later was discharged home to continue his warfarin for 6 months at a therapeutic INR.
The pathogenesis of venous thromboembolism is complex and multifactorial. It frequently reflects the interplay between environmental, clinical and genetic factors. Among genetic factors, factor V Leiden is the most common inherited cause of thrombophilia. Heterozygous FVL increases the risk of developing a first DVT by 5‐ to 7‐fold, and the risk for isolated PE increases approximately 3‐fold. Thus, even though the relative risk of developing a VTE seems high, the absolute risk of having a VTE is still quite low with heterozygous FVL. We herein describe a case of a 29‐year‐old man with FVL mutation (heterozygote) who developed extensive PE with concomitant bilateral DVT, likely provoked by a prolonged travel and emphasizes that very often; people with FVL have additional risk factors that contribute to the development of blood clots. These factors may include age, surgery, obesity, immobility, hospitalization, oral contraceptive use, hormonal replacement therapy, pregnancy, and malignancy. Establishing the diagnosis of FVL is critically important indicating that carriers should be counseled about eliminating these factors or they may require temporary anticoagulation during periods of particularly high risk.
This case is intended to increase hospitalists' general awareness of heterozygous FVL alone is a relatively mild thrombophilic defect and carriers are at higher risk to develop VTE if they become exposed to additional risk factors. Recognition is the key to appropriate counseling and treatment.
Computed tomography of the chest showed numerous filling defects are present within the pulmonary artery upper and lower branches (white arrows); right and left sides suggestive of extensive acute pulmonary embolism. Main portions of the right and left main pulmonary artery and main central pulmonary artery are patent without embolus.
To cite this abstract:Shaheen K, Alrayies A, Alraies M. Travel Trouble — Unexpected Finding. Abstract published at Hospital Medicine 2013, May 16-19, National Harbor, Md. Abstract 399. Journal of Hospital Medicine. 2013; 8 (suppl 2). https://www.shmabstracts.com/abstract/travel-trouble-unexpected-finding/. Accessed May 26, 2019.