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Case Report |
1
Department of Radiology, Jefferson Medical College and Thomas Jefferson
University Hospital, 111 S. 11th St., Ste. 3390 Gibbon, Philadelphia, PA
19107.
2
Present address: Weill Medical College of Cornell University and New York
Presbyterian Hospital, 525 E. 68th St., New York, NY 10021.
Received February 2, 2000;
accepted after revision November 6, 2000.
Address correspondence to R. J. Wechsler.
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CT is beginning to play a more important role in examining patients with suspected complications of pulmonary resection. At our institution, it is the practice of thoracic surgeons and oncologists to obtain a chest CT scan after surgery that will serve as a baseline for subsequent surveillance studies. Recognition of the imaging appearance of true pathology and normal variants after surgery is essential to correctly interpret these studies. We report a patient with a persistent filling defect within the pulmonary artery stump that appeared on CT after right middle and lower lobectomies.
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In situ thrombosis of the pulmonary artery is thought to be rare. Most of the reported cases are from necropsy studies. However, there is no clear method at autopsy to separate old, organized pulmonary emboli from in situ thrombosis [4]. In situ pulmonary artery thrombosis has been reported after right heart failure (particularly failure that is due to mitral stenosis), obstructive lung disease, nephrotic syndrome, primary pulmonary hypertension, right heart catheterization, and congenital heart disease [5]. In 1966, Chuang et al. [6] described two cases of pulmonary artery thrombosis with lethal embolization to the contralateral lung in patients after right pneumonectomy. These researchers conducted a subsequent survey [6] of 600 experienced thoracic surgeons who reported 64 additional cases of this complication among their patients. However, with the increasing use of postoperative CT, vascular stump thromboses may be an incidental finding after surgery in asymptomatic patients.
In 1856, Virchow [7] postulated that intravascular thrombosis was caused by endothelial injury resulting from local trauma or inflammation of the vessel wall, stasis of blood flow, and hypercoagulability. These postulates have since been known as Virchow's triad of thrombolic pathogenesis, and all three apply to patients who have undergone pulmonary resection. Endothelial damage and inflammation at the vascular stump arise from surgery. Resulting stasis in the pulmonary vascular stump is caused by the surgical procedure itself and the resulting postoperative condition of the patients. These patients may also be hypercoagulable because of such factors as cancer and smoking, postoperative state, and sepsis. Ichinose et al. [8] described thrombosis-inducing activity in the peripheral blood of 13 of 19 patients undergoing pulmonary resection for lung cancer. None of these patients had thrombosis-inducing activity before their surgery. The patients with increased thrombosis had a significant elevation of plasma fibrinogen levels and peripheral platelet counts compared with those without thrombosis-inducing activity. Therefore, discovery of either pulmonary embolic events or vascular stump thrombosis in a subset of patients after pulmonary resection for cancer would not be unexpected.
Our patient had undergone radiation therapy, and, although most research on radiation-induced injury to the thorax concentrates on lung injury, thrombus resulting in partial or complete obstruction of the lumina of small arteries has been reported [9]. Histopathologically, blood vessels show intimal and medial edema and intramural infiltration of both neutrophils and lymphocytes. This intimal thickening can progress to obliterate the vessel lumen and may predispose the patient to the formation of luminal thrombus. The obliteration does not typically occur in larger second- or third-order pulmonary arteries, but vascular stumps are end arteries and may be more vulnerable to in situ thrombosis from irradiation.
As with the autopsy findings, separating in situ thrombosis of the pulmonary artery from pulmonary emboli on CT is difficult. We presume that the vascular stump intraluminal defect in this patient was in situ thrombosis for the following reasons. First, it occurred at the surgical site only and was stable on subsequent examinations. Pulmonary emboli tend to change on subsequent studies. Second, no other pulmonary thrombi were found in areas remote from the stump site. Approximately 75% of the emboli were multifocal in the two studies involving unsuspected or incidental pulmonary emboli detected on scans that had been originally obtained for other reasons [2, 3]. Finally, we found no evidence of systemic clots that could lead to pulmonary thromboembolism. We have subsequently seen three other patients with a filling defect at the vascular stump site with no other evidence of pulmonary emboli. We presume these filling defects to be stump thromboses, although we lack the confirmation of pathology findings.
The importance of vascular stump thrombosis remains open to question. We saw no untoward effect in our patient attributable to the condition, and the pulmonary artery thrombi did not evolve into clinically apparent pulmonary embolic disease.
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