PV stump thrombus formation after lung resection has been recently studied and recognized as a cause of cerebral infarction and embolism to vital organs. In 2013, Ohtaka et al. found PV stump thrombus on CECT in 3.6% of 193 patients within 2 years after lung lobectomy. Importantly, all patients with a thrombus had undergone left upper lobectomy, and these comprised 13.5% of all patients that underwent left upper lobectomy . A PV stump thrombus other than that of the left superior PV is very rare, and there are only a few reports [8, 9]. The higher frequency of thrombus formation in the left superior PV stump could be because LUL leaves a longer PV stump than other types of lobectomy, which may lead to stagnant blood flow in the PV stump .
Dividing the PV to form a PV stump as short as possible has been suggested to prevent PV stump thrombus formation. However, it remains unclear if that will reduce the risk of thrombus formation or thromboembolism; PV stump formation has been reported even when the left superior PV was divided in the pleural space to make the stump as short as possible . If the PV was divided in the pericardium, the PV stump could be even shorter. However, it is not practical to perform this complicated and invasive maneuver in all patients .
Prophylactic anticoagulation has also been considered but has not been established because of the risk of bleeding, which can be fatal after lobectomies. Moreover, PV stump thrombosis can occur with anticoagulant therapy . Reported durations from lung resection to PV stump thrombus confirmation or arterial embolism occurrence vary from 1 day to 7 years . This suggests that further investigation is needed to determine the appropriate period and duration for prophylactic anticoagulation. AF causes thrombus formation by blood stagnation in the left atrium; the risk of thromboembolic complication is very low when cardioversion is performed within 48 h of AF onset . Conversely, a recent study has shown that cerebral infarction after pulmonary lobectomy tends to occur very early during the postoperative phase. Hattori et al. reported that 60% of their 10 cases of cerebral infarction after pulmonary lobectomy or more extensive intervention occurred within 2 postoperative days . Similarly, in our case, thromboembolism occurred within 48 h of the operation. This indicates that factors other than blood stagnation may cause PV stump thrombus-related embolism. According to the pathological findings, not only blood stagnation, but also inflammation at the PV stump possibly contributes to PV stump thrombus formation .
Left upper lobectomy, operative time, elderly age, and advanced stages of lung cancer (pathological stage II or more) have been indicated as risk factors for PV stump thrombus formation [1, 2]. Elderly age may be related to the fragility of the endothelium, while the advanced stage of lung cancer may be related to a hyper-thrombotic state.
From an anesthetic viewpoint, Kitajima et al. reported the implementation of routine intravenous systemic heparinization following LUL after encountering a patient who developed cerebral infarction post-LUL. Along with this postoperative anticoagulant therapy, they changed the postoperative analgesia from epidural analgesia to intercostal nerve blocks with intravenous patient-controlled analgesia . In this way, other methods of postoperative analgesia, such as continuous nerve blocks, may be utilized instead of epidural anesthesia if the risk factors for PV stump thrombus formation and prophylactic anticoagulation are established in the future. Therefore, it is important that these rare cases be reported.
This case provides crucial evidence linking LLL, thrombus formation in the pulmonary vein stump, and systemic embolism. It is important for medical caregivers to recognize that embolism caused by a PV stump thrombus may occur in lobectomies other than LUL. The patient may present with varied symptoms, as the target site may be systemic. Since the prophylactic prevention of PV stump thrombus formation has not been established thus far, early detection and treatment are the keys to minimize complications. Anesthesiologists should be aware of this complication to detect it as early as possible if it happens and to seek the safe and effective methods of postoperative analgesia.