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Sarah Kerkla

Posted Date

May 5, 2022, 5:30 AM


Mr. Darrin Lancaster is a 28-year-old male who presents to the ER after experiencing an acute onset of shortness of breath lasting for the past two hours. He has an associated cough that has led to pleuritic chest pain and is exacerbated by deep breathing or coughing. The dyspnea is constant, but is worse with exertion. He has no active medical problems; he reports renal caliculi two years ago. The only medication he takes is Ibuprofen PRN for sports related injuries. He does have a significant family history for cardiac and vascular disease with premature death in his parents. My differential diagnoses were: pulmonary embolism, spontaneous pneumothorax, and ACS.

I obtained basic laboratories that were significant for leukocytosis, negative troponin, and an elevated d-dimer. The first imaging modality I used was a chest x-ray which demonstrated blunting of the right costophrenic angel. A CXR is not diagnostic of a PE; however, abnormalities are usually present, such as with Mr. Lancaster, with a pleural effusion (Matinez Licha et al., 2020). Because of this abnormality and normal renal function, I chose to do a chest CTA, which is the gold standard for PE diagnosis (Matinez Licha et al., 2020). Mr. Lancaster’s showed “intraarterial filling defects in multiple vessels and the segmental peripheral areas of consolidation involving the right lower lobe”. The most common risk factor for a PE is a DVT, so it is appropriate to evaluate the extremities using venous duplex (Matinez Licha et al., 2020). Mr. Lancaster has “fresh thrombus of the right common iliac and right common femoral vein”.  The major risk for thrombus is explained by Virchow’s triad: venous stasis, endothelial damage, and hypercoagulability (Matinez Licha et al., 2020). He does not have obvious risks for clotting such as long travel, immobility, obesity, older age or smoking. His family history of cardiovascular disease led me to believe he may have a genetic disorder. His hypercoagulability work-up shows protein C deficiency. I also did an EKG, as this places his him at risk for other thrombotic events, which showed tachycardia with PACs and no ST changes. I also checked a troponin with was negative. His echocardiogram showed no abnormalities and no RV strain in the setting of an acute PE (Matinez Licha et al., 2020).

His protein C level was 40% which indicates it is likely he has a genetic mutation and not an acquired form of the condition (Bauer, 2021).  It is suggested that his first-degree relatives be tested for the condition as well. Treatment consideration for thrombosis with protein C deficiency is generally to avoid warfarin. With the initiation of warfarin therapy, there is a transient decrease in protein c leading to a hypercoagulable state (Bauer, 2021). Patients with protein c deficiency are predisposed to warfarin-induced skin necrosis due to vascular occlusion (Bauer, 2021). Warfarin may still be used if patients have factors that would preclude them from other therapies. Most patients with protein c deficiency and an unprovoked thromboembolic event need indefinite anticoagulation (Bauer, 2021).


Bauer, K. A. (2021). Protein C deficiecny. UpToDate. Retrieved May 3, 2022, from

Matinez Licha, C. R., McCurdy, C. M., Maldanado, S. M., & Lee, L. S. (2020). Current management of acute pulmonary embolism. Annals of Thoraci and Cardiovascular Surgery26(2), 65–71.

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