Ann Thorac Surg 2014;98:1841–3
References 1. Fauci AS, Harley JB, Roberts WC, Ferrans VJ, Gralnick HR, Bjornson BH. NIH conference. The idiopathic hypereosinophilic syndrome. Clinical, pathophysiologic, and therapeutic considerations. Ann Intern Med 1982;97:78–92. 2. Epstein DM, Taormina V, Gefter WB, Miller WT. The hypereosinophilic syndrome. Radiology 1981;140:59–62. 3. Chusid MJ, Dale DC, West BC, Wolff SM. The hypereosinophilic syndrome: analysis of fourteen cases with review of the literature. Medicine (Baltimore) 1975;54:1–27. 4. Klion AD, Bochner BS, Gleich GJ, et al. Approaches to the treatment of hypereosinophilic syndromes: a workshop summary report. J Allergy Clin Immunol 2006;117:1292–302. 5. Sheikh J, Weller PF. Advances in diagnosis and treatment of eosinophilia. Curr Opin Hematol 2009;16:3–8. 6. Simon HU, Rothenberg ME, Bochner BS, et al. Refining the definition of hypereosinophilic syndrome. J Allergy Clin Immunol 2010;126:45–9. 7. Weller PF, Bubley GJ. The idiopathic hypereosinophilic syndrome. Blood 1994;83:2759–79.
Aneurysm of the Pulmonary Vein: An Unusual Cause of Stroke Alexander Emmert, MD, Ahmad Fawad Jebran, MD, Karsten Schmidt, MD, Marc Hinterthaner, MD, Hanibal Bohnenberger, MD, Mathias B€ ahr, MD, Friedrich A. Sch€ ondube, MD, and Bernhard C. Danner, MD Departments of Thoracic and Cardiovascular Surgery, Neurology, and Pathology, University Medical Center, Georg-August University, G€ ottingen, Germany
1841
P
ulmonary vein aneurysm (PVA) is a rare entity characterized by aneurysmal dilatation of the pulmonary vein. Clinical symptoms are usually absent, and the diagnosis is by chance. PVA can be of an acquired or a congenital origin. If acquired, PVA is usually associated with mitral valve disease or pulmonary hypertension. Pulmonary venous aneurysms are known to be a source of recurrent emboli. Therefore, symptomatic PVAs, especially those with complications, warrant surgical therapy. A 59-year-old man presented with a first session of acute onset of right-sided hemiparesis and dysphasia. He had been previously healthy, had not experienced any trauma, and had no prior history of cardiovascular disease or vasculitis. On admission, his vital signs and electrocardiographic findings were unremarkable, with sinus rhythm. The results of initial laboratory tests were within normal limits. The patient was given thrombolytic therapy, and his neurologic symptoms resolved. The standard chest roentgenogram revealed a left parasternal mass. Evaluation included contrast computed tomography of the thorax, which showed a giant aneurysm with thrombus formation of the left superior pulmonary vein, including absence of perfusion to the left apical and apicoposterior segment 1 and 2 of the upper lobe (Fig 1). Transthoracic echocardiography revealed normal left ventricular systolic and diastolic function and no abnormalities, especially no mitral valve stenosis or regurgitation. On the basis of the imaging findings, we decided for resection of the thrombosed aneurysm after complete neurologic convalescence. Inasmuch as there was a persistent thrombus (Fig 1), we decided to perform the operation immediately; nevertheless, we had extracorporeal circulation circuit on standby because of the unknown tissue fragility. The patient underwent an uncomplicated left anteroaxillary thoracotomy. The findings at operation included a saccular pulmonary venous aneurysm. There
This clinical report deals with a giant true pulmonary venous aneurysm, which was partially thrombosed. The overall incidence of pulmonary venous aneurysms is unknown, and they are reported only occasionally. We present the case of a previously healthy man with acute onset of ischemic cerebral stroke. The cause was a thrombus in a huge aneurysm of the left superior pulmonary vein. The patient subsequently underwent uncomplicated therapy for stroke, including thrombolysis followed by excision of the giant pulmonary venous aneurysm. As curative therapy we recommend complete resection of this rare entity. (Ann Thorac Surg 2014;98:1841–3) Ó 2014 by The Society of Thoracic Surgeons
Accepted for publication Dec 18, 2013. Address correspondence to Dr Emmert, Robert-Koch-Str 40, Department of Thoracic and Cardiovascular Surgery, University Medical Center, Georg-August University, D-37075, G€ ottingen, Germany; e-mail: [email protected].
Ó 2014 by The Society of Thoracic Surgeons Published by Elsevier
Fig 1. Computed tomographic image of pulmonary vein aneurysm (white arrows) and thrombus formation (black arrows). 0003-4975/$36.00 http://dx.doi.org/10.1016/j.athoracsur.2013.12.087
FEATURE ARTICLES
improved after diagnosis and subsequent treatment with corticosteroids. Although IHES is a rare disease, it should be on the list of differential diagnoses of pneumothorax and migratory pulmonary opacities, and peripheral blood tests and bone marrow biopsy should be performed to confirm the diagnosis.
CASE REPORT EMMERT ET AL ANEURYSM OF THE PULMONARY VEIN
1842
CASE REPORT EMMERT ET AL ANEURYSM OF THE PULMONARY VEIN
was no anomalous pulmonary venous connection, so that aneurysmectomy by anatomic anteroposterior segmentectomy (segment 1–3) of the left upper lobe (Fig 2) without the need for cardiopulmonary bypass could be performed. The aneurysm base was closed primarily. The surgical approach revealed a total resected pulmonary aneurysm with an organized red thrombus. Pathologic examination showed a mass of 10 7 2 cm with a macroscopically very fragile and thin venous wall encapsulating an organized thrombus of 5 4 2.5 cm inside the lumen. Histopathologically, it consisted of a true venous aneurysm. After the surgical intervention, the patient was completely asymptomatic. Because he was allergic to aspirin, we prescribed clopidogrel medication for 3 months.
Comment
FEATURE ARTICLES
A PVA is a rare venous abnormality characterized by aneurysmal dilatation of the pulmonary vein. The definition of a PVA has been controversial; it has been described in the literature under different names: pulmonary venous aneurysm, pulmonary venous pseudoaneurysm, pulmonary varix, or pulmonary venous ectasia. We suggest the term venous aneurysm, similar to arterial aneurysm because of dilatation of the pulmonary vein beyond normal limits. Since its first report in 1843 as an incidental postmortem finding in a newborn baby, a total of about 74 cases have been reported [1]. The quality of the reports is variable, and all necessary information is not given in every report. The incidence of PVA has been noted in both sexes and all age groups [2]. The ages of the patients range from neonate to 82 years [3]. It is typically observed near its
Fig 2. Macroscopic view of the pulmonary vein aneurysm (white arrow), opened within the thrombus mass (solid black arrow), adherent to segment 1–3 of the left upper lobe (open black arrow).
Ann Thorac Surg 2014;98:1841–3
point of entry into the left atrium. Previous studies have shown that pulmonary aneurysms are mostly located in the right lower lobe (60% of cases), left upper lobe (17%), and right upper lobe (8.5%) [3, 4]. Pulmonary aneurysm can be classified into three morphologic categories: saccular type, tortuous type, and confluent type [1, 3]. Patients with PVA are mostly asymptomatic. A few cases of hemoptysis, dyspnea, and rupture have been reported. A PVA can be either congenital or acquired [5]. In a study by Uyama and colleagues, it was found that 62% of aneurysms were associated with mitral valve disease [3, 5]. The same review by Uyama and colleagues showed that 62% of aneurysms of the confluent type and 19% of aneurysms of the tortuous type were associated with valve disease. An acquired PVA is associated with chronic pulmonary hypertension and regurgitation of the mitral valve. In our case, there were none of the abnormal changes that are usually seen secondary to disease of mitral valve. The presence of PVA in neonates suggests that some of the vascular lesions are congenital abnormalities. Congenital anomalies of the pulmonary veins, which cause dilatation, include scimitar syndrome, partial anomalous pulmonary venous return, pseudoscimitar syndrome and PVA [2]. The latest embryologic research shows that a congenital PVA probably results from dilatation of persistent embryologic venous drainage channels [2, 6]. The histologic findings of venous aneurysm may be loss of elastic layers and hypertrophy of the connective tissue, absence of the media and adventitia, endophlebosclerosis, endophlebohypertrophy, and thinning of the venous wall without congenital anomaly. Ferretti and colleagues have shown that less commonly, mitral stenosis is associated with pulmonary aneurysm in about 50% of cases and may reveal congenital weakness of the wall of the veins [4]. Shida and colleagues investigated PVA and suggested that there was no intrinsic defect in the structure of the vessel wall [7]. Computed tomographic angiography, echocardiography, and angiography are essential for an accurate diagnosis of pulmonary vein anomalies. The indication for operation on PVA has not been extensively studied. In a few cases, patients have undergone surgical exploration and treatment only for diagnostic purposes. Calligaro and collaborators describe in their review 5 patients with thoracic venous aneurysms who underwent attempted excision of the aneurysm, whereas 1 patient was treated by wrapping the aneurysm with polyethylene cellophane [8]. In most cases, patients with PVA are asymptomatic, and surgical treatment is necessary only in cases with complications like dysphagia, hemoptysis with bleeding into the bronchus, rupture, potential rupture, or embolism, which can be fatal. In another case a patient had to be operated on because of recurrent pulmonary infection. Occasionally, PVA can be associated with cerebral thromboembolism, but the real estimation is unknown. It is believed that our case is the third of a giant PVA to be recognized clinically and the first patient to be cured
Ann Thorac Surg 2014;98:1843–5
CASE REPORT LI ET AL EXTRAESOPHAGEAL SALINE DURING ESD IN ESOPHAGEAL CANCER
by thrombolytic therapy and surgical treatment. Our case is also an example of cerebral stroke caused by thrombosis in the pulmonary vein, and it is a reminder that PVA should be included in the differential diagnosis of ischemic stroke of unknown cause. Whenever possible, we recommend early surgical repair of symptomatic PVAs because they are associated with a risk of systemic embolism, especially when an intraaneurysmal thrombus mass is present. In conclusion, PVAs are rare but potentially serious because thrombotic material in the aneurysm can embolize, with a fatal outcome. However, further analyses of many more patients are needed to determine the precise causes and clinical complications of this rare disorder.
1843
Saline submucosal injection (SSI) is an indispensable procedure before endoscopic submucosal dissection (ESD) in patients with early esophageal squamous cell carcinoma. Successful SSI should create a saline cushion in the submucosa rather than elsewhere. However, saline outside the esophagus was detected incidentally by endoscopic ultrasonography during ESD in a patient with early esophageal cancer. In this case, saline separated the esophageal adventitia from adjacent tissues, and there were no complications during or after ESD. This finding indicates that it is possible to use interventional extraesophageal saline injection to help differentiate advanced esophageal cancer of Stage T3 from Stage T4 by endoscopic ultrasonography. (Ann Thorac Surg 2014;98:1843–5) Ó 2014 by The Society of Thoracic Surgeons
References
Extraesophageal Saline During Endoscopic Submucosal Dissection in a Patient With Early Esophageal Squamous Cell Carcinoma Jian-jun Li, MD, PhD,* Hong-bo Shan, MD, PhD,* Long-jun He, MD,* Guang-yu Luo, MD, Li-ming Chen, BA, Guo-liang Xu, MD, Yin Li, MD, and Rong Zhang, MD Department of Endoscopy, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangdong Esophageal Cancer Institute, Guangzhou, China Accepted for publication Dec 3, 2013. *Jian-jun Li, Hong-bo Shan, and Long-jun He contributed equally to this work. Address correspondence to Dr Jian-jun Li, Department of Endoscopy, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangdong Esophageal Cancer Institute, Guangzhou, China, 510060; e-mail: [email protected].
Ó 2014 by The Society of Thoracic Surgeons Published by Elsevier
E
sophageal squamous cell carcinoma (ESCC) is one of the most common carcinomas in southern China [1]. At present, the main method used to classify early ESCC is endoscopic ultrasonography (EUS) [2], and the usual treatment is endoscopic resection, including endoscopic mucosal resection (EMR) [3, 4] or endoscopic submucosal dissection (ESD) [5]. Submucosal saline injection (SSI) is routinely used before EMR or ESD to minimize damage to the adjacent tissues and organs [6]. SSI creates a salinefilled cushion in the loose connective tissue of the submucosa that separates the mucosa from the submucosa and adjacent tissues and organs. Successful SSI should create a saline cushion in the submucosa rather than elsewhere. However, saline outside the esophagus was detected incidentally by EUS during ESD in a patient with early ESCC. In April 2012, a 48-year-old woman with pathologically confirmed ESCC underwent ESD in Sun Yat-sen University Cancer Center, Guangzhou, China. The ESCC was staged as T1a by preoperative EUS. Before ESD, the patient had signed informed consent. Endoscopic ultrasonography was performed with the Fujinon 7000 endoscopy system (Fujinon Co Ltd, Japan) with a 7.5-MHz ultrasonic probe (EG-530UR). Single-use mucosal needles (22-G) for SSI were purchased from Endo-Flex Co (Germany). SSI was performed routinely as described previously. EUS was conducted simultaneously by an expert with more than 10 years’ experience. The procedure was performed with the patient under general anesthesia and took approximately 80 minutes. According to the Paris endoscopic classification of superficial neoplastic lesions in the esophagus [7], the mucosal lesion in the right and posterior wall of the lower thoracic esophagus was type II-a (Fig 1). Because this was a relatively large lesion of 2 cm 3 cm that extended over almost three-quarters of the circumference of the esophageal lumen, the patient consented to treatment by ESD. After SSI and before ESD, EUS visualized a thickened lesion in the right and posterior esophageal mucosa; no dark areas of liquid were detected (Fig 2A). However, 0003-4975/$36.00 http://dx.doi.org/10.1016/j.athoracsur.2013.12.058
FEATURE ARTICLES
1. Ben-Menachem Y, Kuroda K, Kyger R, Brest AN, Copeland OP, Coan JD. The various forms of pulmonary varices: report of three new cases and review of the literature. Am J Roetgenol 1975;125:881–9. 2. Berecova Z, Neuschl V, Boruta P, et al. A complex pulmonary vein varix: diagnosis with ECG gated MDCT, MRI and invasive pulmonary angiography. J Radiol Case Rep 2012;6:9–16. 3. Uyama T, Monden Y, Harada K, et al. Pulmonary varices: a case report and review of the literature. Jpn J Surg 1988;18: 359–62. 4. Ferretti GR, Arbib F, Bertrand B, et al. Haemoptysis associated with pulmonary varices: demonstration using computed tomographic angiography. Eur Respir J 1998;12:989–92. 5. Sellares J, Santos S, Ballester E, et al. Pulmonary varix inside a Bulla. Arch Bronconeumol 2006;42:39–41. 6. Shiraishi J, Tatsumi T, Kimata M, et al. Echocardiographic diagnosis of pulmonary vein varix. Circ J 2003;67:796–8. 7. Shida T, Ohashi H, Nakamura K, et al. Pulmonary varices associated with mitral valve disease: a case report and survey of the literature. Ann Thorac Surg 1982;24:452–6. 8. Calligaro KD, Ahmad S, Dandora R, et al. Venous aneurysms: surgical indications and review of the literature. Surgery 1995;117:1–6.
References 1. Fauci AS, Harley JB, Roberts WC, Ferrans VJ, Gralnick HR, Bjornson BH. NIH conference. The idiopathic hypereosinophilic syndrome. Clinical, pathophysiologic, and therapeutic considerations. Ann Intern Med 1982;97:78–92. 2. Epstein DM, Taormina V, Gefter WB, Miller WT. The hypereosinophilic syndrome. Radiology 1981;140:59–62. 3. Chusid MJ, Dale DC, West BC, Wolff SM. The hypereosinophilic syndrome: analysis of fourteen cases with review of the literature. Medicine (Baltimore) 1975;54:1–27. 4. Klion AD, Bochner BS, Gleich GJ, et al. Approaches to the treatment of hypereosinophilic syndromes: a workshop summary report. J Allergy Clin Immunol 2006;117:1292–302. 5. Sheikh J, Weller PF. Advances in diagnosis and treatment of eosinophilia. Curr Opin Hematol 2009;16:3–8. 6. Simon HU, Rothenberg ME, Bochner BS, et al. Refining the definition of hypereosinophilic syndrome. J Allergy Clin Immunol 2010;126:45–9. 7. Weller PF, Bubley GJ. The idiopathic hypereosinophilic syndrome. Blood 1994;83:2759–79.
Aneurysm of the Pulmonary Vein: An Unusual Cause of Stroke Alexander Emmert, MD, Ahmad Fawad Jebran, MD, Karsten Schmidt, MD, Marc Hinterthaner, MD, Hanibal Bohnenberger, MD, Mathias B€ ahr, MD, Friedrich A. Sch€ ondube, MD, and Bernhard C. Danner, MD Departments of Thoracic and Cardiovascular Surgery, Neurology, and Pathology, University Medical Center, Georg-August University, G€ ottingen, Germany
1841
P
ulmonary vein aneurysm (PVA) is a rare entity characterized by aneurysmal dilatation of the pulmonary vein. Clinical symptoms are usually absent, and the diagnosis is by chance. PVA can be of an acquired or a congenital origin. If acquired, PVA is usually associated with mitral valve disease or pulmonary hypertension. Pulmonary venous aneurysms are known to be a source of recurrent emboli. Therefore, symptomatic PVAs, especially those with complications, warrant surgical therapy. A 59-year-old man presented with a first session of acute onset of right-sided hemiparesis and dysphasia. He had been previously healthy, had not experienced any trauma, and had no prior history of cardiovascular disease or vasculitis. On admission, his vital signs and electrocardiographic findings were unremarkable, with sinus rhythm. The results of initial laboratory tests were within normal limits. The patient was given thrombolytic therapy, and his neurologic symptoms resolved. The standard chest roentgenogram revealed a left parasternal mass. Evaluation included contrast computed tomography of the thorax, which showed a giant aneurysm with thrombus formation of the left superior pulmonary vein, including absence of perfusion to the left apical and apicoposterior segment 1 and 2 of the upper lobe (Fig 1). Transthoracic echocardiography revealed normal left ventricular systolic and diastolic function and no abnormalities, especially no mitral valve stenosis or regurgitation. On the basis of the imaging findings, we decided for resection of the thrombosed aneurysm after complete neurologic convalescence. Inasmuch as there was a persistent thrombus (Fig 1), we decided to perform the operation immediately; nevertheless, we had extracorporeal circulation circuit on standby because of the unknown tissue fragility. The patient underwent an uncomplicated left anteroaxillary thoracotomy. The findings at operation included a saccular pulmonary venous aneurysm. There
This clinical report deals with a giant true pulmonary venous aneurysm, which was partially thrombosed. The overall incidence of pulmonary venous aneurysms is unknown, and they are reported only occasionally. We present the case of a previously healthy man with acute onset of ischemic cerebral stroke. The cause was a thrombus in a huge aneurysm of the left superior pulmonary vein. The patient subsequently underwent uncomplicated therapy for stroke, including thrombolysis followed by excision of the giant pulmonary venous aneurysm. As curative therapy we recommend complete resection of this rare entity. (Ann Thorac Surg 2014;98:1841–3) Ó 2014 by The Society of Thoracic Surgeons
Accepted for publication Dec 18, 2013. Address correspondence to Dr Emmert, Robert-Koch-Str 40, Department of Thoracic and Cardiovascular Surgery, University Medical Center, Georg-August University, D-37075, G€ ottingen, Germany; e-mail: [email protected].
Ó 2014 by The Society of Thoracic Surgeons Published by Elsevier
Fig 1. Computed tomographic image of pulmonary vein aneurysm (white arrows) and thrombus formation (black arrows). 0003-4975/$36.00 http://dx.doi.org/10.1016/j.athoracsur.2013.12.087
FEATURE ARTICLES
improved after diagnosis and subsequent treatment with corticosteroids. Although IHES is a rare disease, it should be on the list of differential diagnoses of pneumothorax and migratory pulmonary opacities, and peripheral blood tests and bone marrow biopsy should be performed to confirm the diagnosis.
CASE REPORT EMMERT ET AL ANEURYSM OF THE PULMONARY VEIN
1842
CASE REPORT EMMERT ET AL ANEURYSM OF THE PULMONARY VEIN
was no anomalous pulmonary venous connection, so that aneurysmectomy by anatomic anteroposterior segmentectomy (segment 1–3) of the left upper lobe (Fig 2) without the need for cardiopulmonary bypass could be performed. The aneurysm base was closed primarily. The surgical approach revealed a total resected pulmonary aneurysm with an organized red thrombus. Pathologic examination showed a mass of 10 7 2 cm with a macroscopically very fragile and thin venous wall encapsulating an organized thrombus of 5 4 2.5 cm inside the lumen. Histopathologically, it consisted of a true venous aneurysm. After the surgical intervention, the patient was completely asymptomatic. Because he was allergic to aspirin, we prescribed clopidogrel medication for 3 months.
Comment
FEATURE ARTICLES
A PVA is a rare venous abnormality characterized by aneurysmal dilatation of the pulmonary vein. The definition of a PVA has been controversial; it has been described in the literature under different names: pulmonary venous aneurysm, pulmonary venous pseudoaneurysm, pulmonary varix, or pulmonary venous ectasia. We suggest the term venous aneurysm, similar to arterial aneurysm because of dilatation of the pulmonary vein beyond normal limits. Since its first report in 1843 as an incidental postmortem finding in a newborn baby, a total of about 74 cases have been reported [1]. The quality of the reports is variable, and all necessary information is not given in every report. The incidence of PVA has been noted in both sexes and all age groups [2]. The ages of the patients range from neonate to 82 years [3]. It is typically observed near its
Fig 2. Macroscopic view of the pulmonary vein aneurysm (white arrow), opened within the thrombus mass (solid black arrow), adherent to segment 1–3 of the left upper lobe (open black arrow).
Ann Thorac Surg 2014;98:1841–3
point of entry into the left atrium. Previous studies have shown that pulmonary aneurysms are mostly located in the right lower lobe (60% of cases), left upper lobe (17%), and right upper lobe (8.5%) [3, 4]. Pulmonary aneurysm can be classified into three morphologic categories: saccular type, tortuous type, and confluent type [1, 3]. Patients with PVA are mostly asymptomatic. A few cases of hemoptysis, dyspnea, and rupture have been reported. A PVA can be either congenital or acquired [5]. In a study by Uyama and colleagues, it was found that 62% of aneurysms were associated with mitral valve disease [3, 5]. The same review by Uyama and colleagues showed that 62% of aneurysms of the confluent type and 19% of aneurysms of the tortuous type were associated with valve disease. An acquired PVA is associated with chronic pulmonary hypertension and regurgitation of the mitral valve. In our case, there were none of the abnormal changes that are usually seen secondary to disease of mitral valve. The presence of PVA in neonates suggests that some of the vascular lesions are congenital abnormalities. Congenital anomalies of the pulmonary veins, which cause dilatation, include scimitar syndrome, partial anomalous pulmonary venous return, pseudoscimitar syndrome and PVA [2]. The latest embryologic research shows that a congenital PVA probably results from dilatation of persistent embryologic venous drainage channels [2, 6]. The histologic findings of venous aneurysm may be loss of elastic layers and hypertrophy of the connective tissue, absence of the media and adventitia, endophlebosclerosis, endophlebohypertrophy, and thinning of the venous wall without congenital anomaly. Ferretti and colleagues have shown that less commonly, mitral stenosis is associated with pulmonary aneurysm in about 50% of cases and may reveal congenital weakness of the wall of the veins [4]. Shida and colleagues investigated PVA and suggested that there was no intrinsic defect in the structure of the vessel wall [7]. Computed tomographic angiography, echocardiography, and angiography are essential for an accurate diagnosis of pulmonary vein anomalies. The indication for operation on PVA has not been extensively studied. In a few cases, patients have undergone surgical exploration and treatment only for diagnostic purposes. Calligaro and collaborators describe in their review 5 patients with thoracic venous aneurysms who underwent attempted excision of the aneurysm, whereas 1 patient was treated by wrapping the aneurysm with polyethylene cellophane [8]. In most cases, patients with PVA are asymptomatic, and surgical treatment is necessary only in cases with complications like dysphagia, hemoptysis with bleeding into the bronchus, rupture, potential rupture, or embolism, which can be fatal. In another case a patient had to be operated on because of recurrent pulmonary infection. Occasionally, PVA can be associated with cerebral thromboembolism, but the real estimation is unknown. It is believed that our case is the third of a giant PVA to be recognized clinically and the first patient to be cured
Ann Thorac Surg 2014;98:1843–5
CASE REPORT LI ET AL EXTRAESOPHAGEAL SALINE DURING ESD IN ESOPHAGEAL CANCER
by thrombolytic therapy and surgical treatment. Our case is also an example of cerebral stroke caused by thrombosis in the pulmonary vein, and it is a reminder that PVA should be included in the differential diagnosis of ischemic stroke of unknown cause. Whenever possible, we recommend early surgical repair of symptomatic PVAs because they are associated with a risk of systemic embolism, especially when an intraaneurysmal thrombus mass is present. In conclusion, PVAs are rare but potentially serious because thrombotic material in the aneurysm can embolize, with a fatal outcome. However, further analyses of many more patients are needed to determine the precise causes and clinical complications of this rare disorder.
1843
Saline submucosal injection (SSI) is an indispensable procedure before endoscopic submucosal dissection (ESD) in patients with early esophageal squamous cell carcinoma. Successful SSI should create a saline cushion in the submucosa rather than elsewhere. However, saline outside the esophagus was detected incidentally by endoscopic ultrasonography during ESD in a patient with early esophageal cancer. In this case, saline separated the esophageal adventitia from adjacent tissues, and there were no complications during or after ESD. This finding indicates that it is possible to use interventional extraesophageal saline injection to help differentiate advanced esophageal cancer of Stage T3 from Stage T4 by endoscopic ultrasonography. (Ann Thorac Surg 2014;98:1843–5) Ó 2014 by The Society of Thoracic Surgeons
References
Extraesophageal Saline During Endoscopic Submucosal Dissection in a Patient With Early Esophageal Squamous Cell Carcinoma Jian-jun Li, MD, PhD,* Hong-bo Shan, MD, PhD,* Long-jun He, MD,* Guang-yu Luo, MD, Li-ming Chen, BA, Guo-liang Xu, MD, Yin Li, MD, and Rong Zhang, MD Department of Endoscopy, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangdong Esophageal Cancer Institute, Guangzhou, China Accepted for publication Dec 3, 2013. *Jian-jun Li, Hong-bo Shan, and Long-jun He contributed equally to this work. Address correspondence to Dr Jian-jun Li, Department of Endoscopy, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangdong Esophageal Cancer Institute, Guangzhou, China, 510060; e-mail: [email protected].
Ó 2014 by The Society of Thoracic Surgeons Published by Elsevier
E
sophageal squamous cell carcinoma (ESCC) is one of the most common carcinomas in southern China [1]. At present, the main method used to classify early ESCC is endoscopic ultrasonography (EUS) [2], and the usual treatment is endoscopic resection, including endoscopic mucosal resection (EMR) [3, 4] or endoscopic submucosal dissection (ESD) [5]. Submucosal saline injection (SSI) is routinely used before EMR or ESD to minimize damage to the adjacent tissues and organs [6]. SSI creates a salinefilled cushion in the loose connective tissue of the submucosa that separates the mucosa from the submucosa and adjacent tissues and organs. Successful SSI should create a saline cushion in the submucosa rather than elsewhere. However, saline outside the esophagus was detected incidentally by EUS during ESD in a patient with early ESCC. In April 2012, a 48-year-old woman with pathologically confirmed ESCC underwent ESD in Sun Yat-sen University Cancer Center, Guangzhou, China. The ESCC was staged as T1a by preoperative EUS. Before ESD, the patient had signed informed consent. Endoscopic ultrasonography was performed with the Fujinon 7000 endoscopy system (Fujinon Co Ltd, Japan) with a 7.5-MHz ultrasonic probe (EG-530UR). Single-use mucosal needles (22-G) for SSI were purchased from Endo-Flex Co (Germany). SSI was performed routinely as described previously. EUS was conducted simultaneously by an expert with more than 10 years’ experience. The procedure was performed with the patient under general anesthesia and took approximately 80 minutes. According to the Paris endoscopic classification of superficial neoplastic lesions in the esophagus [7], the mucosal lesion in the right and posterior wall of the lower thoracic esophagus was type II-a (Fig 1). Because this was a relatively large lesion of 2 cm 3 cm that extended over almost three-quarters of the circumference of the esophageal lumen, the patient consented to treatment by ESD. After SSI and before ESD, EUS visualized a thickened lesion in the right and posterior esophageal mucosa; no dark areas of liquid were detected (Fig 2A). However, 0003-4975/$36.00 http://dx.doi.org/10.1016/j.athoracsur.2013.12.058
FEATURE ARTICLES
1. Ben-Menachem Y, Kuroda K, Kyger R, Brest AN, Copeland OP, Coan JD. The various forms of pulmonary varices: report of three new cases and review of the literature. Am J Roetgenol 1975;125:881–9. 2. Berecova Z, Neuschl V, Boruta P, et al. A complex pulmonary vein varix: diagnosis with ECG gated MDCT, MRI and invasive pulmonary angiography. J Radiol Case Rep 2012;6:9–16. 3. Uyama T, Monden Y, Harada K, et al. Pulmonary varices: a case report and review of the literature. Jpn J Surg 1988;18: 359–62. 4. Ferretti GR, Arbib F, Bertrand B, et al. Haemoptysis associated with pulmonary varices: demonstration using computed tomographic angiography. Eur Respir J 1998;12:989–92. 5. Sellares J, Santos S, Ballester E, et al. Pulmonary varix inside a Bulla. Arch Bronconeumol 2006;42:39–41. 6. Shiraishi J, Tatsumi T, Kimata M, et al. Echocardiographic diagnosis of pulmonary vein varix. Circ J 2003;67:796–8. 7. Shida T, Ohashi H, Nakamura K, et al. Pulmonary varices associated with mitral valve disease: a case report and survey of the literature. Ann Thorac Surg 1982;24:452–6. 8. Calligaro KD, Ahmad S, Dandora R, et al. Venous aneurysms: surgical indications and review of the literature. Surgery 1995;117:1–6.
