Carol Wu;
University of Texas MD Anderson Cancer Center
Girish Shroff;
University of Texas MD Anderson Cancer Center
Marcelo Benveniste;
University of Texas MD Anderson Cancer Center
Myelene Truong;
University of Texas MD Anderson Cancer Center
Sanjana Dhakshinamoorthy;
No Affiliation
Jitesh Ahuja;
University of Texas MD Anderson Cancer Center
Background
In-situ pulmonary artery thrombosis (PAT) is a well-described complication in the pulmonary artery (PA) stump after pneumonectomy or lobectomy. Recently in-situ PAT has also been described as a complication of radiation therapy (RT), specifically in patients receiving radiation therapy for chest malignancies. It is important to distinguish this entity from other causes of filling defects in the PA, specifically acute pulmonary embolism (PE), as management and prognosis differ.
Educational Goals / Teaching Points
In this educational exhibit, we will describe proposed pathophysiology of in-situ PAT, illustrate imaging findings, and discuss the differential diagnosis of PAT.
Key Anatomic/Physiologic Issues and Imaging Findings/Techniques
In-situ PAT pathophysiology is different from that of acute PE. Acute PE is related to thrombi formed in a distal deep vein that dislodge and travel to the pulmonary arteries. In comparison, PAT forms within the pulmonary artery. The essential pathophysiology of in-situ PAT following lung surgery or radiation therapy is based on Virchow’s triad (hypercoagulability, stasis, endothelial damage). Both lung surgery and RT result in inflammation and endothelial injury of PA. PA stump after pneumonectomy or lobectomy causes blood stasis. Similarly, fibrotic changes in the lungs from RT cause stasis of blood in PA supplying the fibrotic lung. The patient’s malignancy induces a hypercoagulable state that completes Virchow’s triad within the PA. In-situ PAT has distinctive imaging features that help to distinguish it from acute PE. Acute PE is typically described as a central filling defect surrounded by the contrast and may cause bulging of the affected vessel. PE often forms an acute angle to the vessel wall. In contrast, PAT is eccentric and forms an obtuse angle to the vessel wall. It is often solitary, seen in the PA stump or within the radiation therapy plan. The differential diagnosis for PAT, other than acute PE, includes tumor embolism and pulmonary artery sarcoma. Sarcoma, breast, hepatocellular, or renal cell carcinoma are common tumors that can lead to tumor emboli. Vascular dilation, beaded appearance, contrast enhancement, and FDG avidity on PET-CT help differentiate tumor emboli from bland thromboembolic diseases. Pulmonary artery sarcoma, an extremely rare cause of PA filling defects, shows the lobulated border, vessel expansion, extraluminal extension, heterogenous soft tissue with hemorrhage or necrosis, and contrast enhancement. Hypermetabolism on fluoro-2-deoxy-D-glucose PET-CT, typically seen with sarcomas and tumor emboli and not with bland thromboembolism, can help narrow the differential diagnosis.
Conclusion
In-situ PAT can be seen after lung surgery and radiation therapy. Understanding and accurately diagnosing PAT may assist in an appropriate treatment strategy.
