In Situ Pulmonary Artery Thrombosis and Low Flow Stasis Artifact in Parenchymal Lung Disease: An Under-Recognized...

Pulmonary emboli (PE) are a common clinical problem seen when a peripheral deep vein thrombosis (DVT) migrates to the pulmonary arteries. However, emerging literature suggests that not all filling defects in the pulmonary arteries are the result of embolism, and that in situ pulmonary arterial thrombus (ISPAT) or low-flow stasis artifact (LFSA) within the pulmonary arteries can mimic acute PE. The proposed mechanism for ISPAT is chronic stasis due to abnormal perfusion in areas of parenchymal lung disease leading to in situ thrombosis. Similarly, LFSA occurs when stasis leads to persistent visualization of intravenous contrast which is then mistaken for thrombus. The clinical scenarios in which ISPAT and LFSA develop are not yet fully defined. We report here a series of patients with parenchymal lung disease leading to ventilation-perfusion mismatch who likely had ISPAT or LFSA and not acute PE. Our aim is to further define parenchymal lung disease as a subgroup of patients who are at high risk for ISPAT. Cases initially diagnosed as acute PE leading to activation of the UCLA pulmonary embolism response team (PERT) were reviewed. Inclusion criteria were all cases of PE that led to PERT activation. Inclusion criteria included absence of DVT, previously diagnosed pulmonary disease, and presence of thrombus only in areas of abnormal parenchyma. Cases were reviewed with radiology to identify cases in which ISPAT was the likely diagnosis, and five representative cases were selected to be discussed. These cases were then analyzed qualitatively for commonalities which are described below. The five representative cases described represent patients with known chronic lung disease who were diagnosed and initially managed as acute PE but, on review, met criteria for either ISPAT or stasis artifact. These cases, which were all rediagnosed as ISPAT or LFSA, were all seen in the absence of DVT, with thrombus specifically located in areas of significant parenchymal lung disease with suspected decrease in ventilation and perfusion in these areas. ISPAT or LFSA have been described in the literature, though its presence specifically in parenchymal lung disease has yet to be described. The authors recommend considering this diagnosis in patient's diagnosed with acute PE when the following are present: significant parenchymal lung disease, absence of DVT, absence of thrombus in the areas of the lung relatively spared of parenchymal lung disease, and suspected baseline decrease in both ventilation and perfusion to the affected areas of the lung. As this phenomenon may be physiologically beneficial, the authors suggest that not all cases of ISPAT or LFSA need anticoagulation, and that treatment should be considered on a case-by-case basis.