1814
CASE REPORT CROSLAND ET AL PEA FOR CTEPH FROM SEPTIC EMBOLI
We express our deep thanks to Dr Cui Quan-Cai and Dr Shi Jie of the Pathological Department of Peking Union Medical College Hospital for their extraordinary pathological work.
References 1. Zhang Y, Li H, Zhang WQ. Malignant glomus tumor of the esophagus with mediastinal lymph node metastases. Ann Thorac Surg 2013;96:1464–6. 2. Zhu YZ, Li WP, Wang ZY, et al. Glomus tumor of uncertain malignant potential arising in the bronchus. J Cardiothorac Surg 2013;8:146. 3. Urdaneta AI, Yu JB, Wilson LD. Population based cancer registry analysis of primary tracheal carcinoma. Am J Clin Oncol 2011;34:32–7. 4. Folpe AL, Fanburg-Smith JC, Miettinen M, Weiss SW. Atypical and malignant glomus tumors: analysis of 52 cases, with a proposal for the reclassification of glomus tumors. Am J Surg Pathol 2001;25:1–12. 5. Honings J, van Dijck JA, Verhagen AF, van der Heijden HF, Marres HA. Incidence and treatment of tracheal cancer: a nationwide study in the Netherlands. Ann Surg Oncol 2007;14: 968–76.
FEATURE ARTICLES
Pulmonary Endarterectomy for Pulmonary Hypertension From Septic Emboli William Crosland, MD, Mustafa Ahmed, MD, Julian Booker, MD, Keith Wille, MD, Satinder Singh, MD, FCCP, Thomas Winokur, MD, and David McGiffin, MBBS, FRACS Departments of Medicine, Radiology, and Pathology, The University of Alabama at Birmingham, Birmingham, Alabama; and Department of Cardiothoracic Surgery and Transplantation, The Alfred Hospital and Monash University, Melbourne, Victoria, Australia
Pulmonary endarterectomy (PEA) can significantly increase long-term survival in patients with chronic thromboembolic pulmonary hypertension; however, the role of PEA for chronic thromboembolic pulmonary hypertension due to pulmonary valve endocarditis is controversial. A critically ill 61-year-old man with intractable right ventricular heart failure was found to have chronic thromboembolic pulmonary hypertension due to Streptococcus bovis pulmonary valve endocarditis and underwent successful pulmonary valve replacement and PEA. The successful outcome in this case suggests that PEA should be considered in patients with this condition. (Ann Thorac Surg 2015;99:1814–6) Ó 2015 by The Society of Thoracic Surgeons
C
hronic thromboembolic pulmonary hypertension (CTEPH) develops in 3.8% of all patients diagnosed with a pulmonary embolus [1]. This is a chronic progressive Accepted for publication June 11, 2014. Address correspondence to Mr McGiffin, The Alfred Hospital, 55 Commercial Rd, Melbourne VIC 3004 Australia; e-mail: d.mcgiffin@alfred. org.au.
Ó 2015 by The Society of Thoracic Surgeons Published by Elsevier
Ann Thorac Surg 2015;99:1814–6
disease characterized by fibrotic stenosis of the pulmonary vasculature, remodeling of the unobstructed distal pulmonary arteries (PAs), and subsequent right-sided heart failure [1]. Medical therapy is largely ineffective. Pulmonary endarterectomy (PEA) is the treatment of choice for CTEPH because surgical intervention has clearly demonstrated substantial survival benefit over the natural history of the disease [2–5]. CTEPH due to rightsided infective endocarditis typically occurs in chronically debilitated patients with protracted hospital courses, and surgical intervention is inherently high risk. Right-sided endocarditis predominantly involves the tricuspid valve in more than 80% of cases, typically due to intravenous drug use or indwelling catheter placement [6]. The incidence of septic embolism from tricuspid or pulmonary valve endocarditis is largely unknown, but it seems the systolic shear stress that develops across the infected pulmonary valve could increase the risk of septic emboli. The benefit of PEA for CTEPH due to right-sided infective endocarditis is unclear, with some opinion recommending against the procedure [7]. We present a case from the University of Alabama at Birmingham of a patient with CTEPH due to septic embolization from pulmonary valve endocarditis who underwent successful combined pulmonary valve replacement and PEA [3–4]. A 61-year-old man presented to the University of Alabama at Birmingham for management of bilateral pulmonary thromboemboli associated with pulmonary valve vegetations. The patient had had multiple admissions for pneumonia during the past year. Streptococcus bovis bacteremia had developed 3 months before presentation. The patient was critically ill with intractable right ventricular heart failure. His clinical condition remained unresponsive to multiple administrations of tissue plasminogen activator, and his fever and leukocytosis persisted despite prolonged antibiotic therapy. Echocardiography on admission noted a severely dilated right ventricle with reduced systolic function and pulmonary valve vegetations with severe pulmonary valvular regurgitation (Fig 1). Three-dimensional computed tomography revealed a severely dilated PA, complete occlusion of the right PA, and multiple occlusive defects within the left lung, including the left lower lobe segmental, left superior lingular, and left inferior lingular arteries (Fig 2). Right heart catheterization noted elevated right atrial pressures of 22/13 (mean 19) mm Hg and elevated right ventricular pressures of 56/12 (mean 22) mm Hg. The PA was not entered due to concern for further embolization and was measured directly in the operating room, noting elevated PA pressures of 53/18 (30) mm Hg. PEA was performed through a median sternotomy using the usual methods of cardiopulmonary bypass and myocardial protection. Deep hypothermia to 20 C and circulatory arrest facilitated visualization during the endarterectomy. Cerebral protection was augmented by intermittent cerebral perfusion. 0003-4975/$36.00 http://dx.doi.org/10.1016/j.athoracsur.2014.06.109
Ann Thorac Surg 2015;99:1814–6
CASE REPORT CROSLAND ET AL PEA FOR CTEPH FROM SEPTIC EMBOLI
1815
the superior vena cava and the ascending aorta, and full clearance was obtained. In contradistinction to the usual thromboembolic disease, where establishing the dissection plane is straightforward and it strips easily, the plane in this condition was not easy to establish and did not strip as easily. Success required persisting with a dissection plane that was quite adherent, tedious, and foreign from that encountered in the usual thromboembolic disease, and consequently, with a troubling degree of uncertainty about the correctness of the plane (Fig 3). The total circulatory arrest time was 85 minutes, including periods of intermittent antegrade cerebral perfusion, with a total bypass time of 176 minutes. The histologic analysis of the surgical specimen noted dense neutrophilic infiltrates consistent with acute inflammation in the native pulmonary valve (Fig 4A) and in the pulmonary emboli (Fig 4B). The patient’s postoperative course was uneventful. The postoperative PA pressure was 28/10 (16) mm Hg, with the pulmonary vascular resistance calculated to be 89 (dynes ∙ sec)/cm5. At the most recent outpatient followup, the patient had markedly improved exercise tolerance and had returned to work on a regular basis.
Comment
The pulmonary valve was essentially destroyed, with 1 leaflet completely replaced by vegetation and the other 2 leaflets with multiple large perforations. The valve was replaced with a 27-mm Freestyle stentless Xenograft aortic valve (Medtronic, Minneapolis, MN). The left PA was accessed through a longitudinal incision, the endarterectomy plane established, and full clearance of the left PA and branches achieved. The right PA was opened through a longitudinal incision between
Fig 2. Three-dimensional computed tomography in (A) axial and (B) coronal views demonstrates a large filling defect in right main pulmonary artery (red arrows) and a large intraluminal filling defect (white arrow) in the left lower lingular pulmonary artery extending into the lower lobe branches.
FEATURE ARTICLES
Fig 1. Preoperative transesophageal echocardiography displays severe pulmonary valvular regurgitation. (A) Color Doppler imaging. (B) Continuous-wave Doppler echocardiography.
Pathologic analysis of PEA specimens notes the rarity of acute inflammation in pulmonary emboli, which hallmarks the unique nature and severe acuity of the patient’s clinical condition [8]. The corresponding dense neutrophilic infiltrates in the PEA specimen and the native pulmonary valve are strongly suggestive that the emboli originated from the pulmonary valve endocarditis [5]. The benefits of PEA have been well established in patients with CTEPH, but concern exists regarding the role of PEA in patients with CTEPH due to pulmonary valve endocarditis. A previous report noted significant adherence of the thrombus to the pulmonary vessels, which undermined attempts at endarterectomy, and both cases were unsuccessful. The authors recommended against performing PEA for CTEPH due to infectious endocarditis secondary to technical difficulties [7].
1816
CASE REPORT VIAL ET AL DIAGNOSING PULMONARY TUMOR EMBOLI
Ann Thorac Surg 2015;99:1816–9
marked symptomatic and hemodynamic response. In our opinion, PEA in this condition is technically possible based on our experience with this patient. Future attempts in similar patients should anticipate difficult dissection planes and should expect difficult extrication of the septic emboli because this is an inherent aspect of the disease process. Therefore, patients with infective pulmonary endocarditis complicated by pulmonary emboli resulting in CTEPH should be considered for PEA.
References
Fig 3. Surgical specimen of thromboemboli after bilateral pulmonary endarterectomy.
FEATURE ARTICLES
The procedure reported in this patient met similar challenges, but persistent, careful dissection led to successful clearance of the pulmonary arteries, with a
1. Rahnavardi M, Yan TD, Cao C, et al. Pulmonary thromboendarterectomy for chronic thromboembolic pulmonary hypertension: a systematic review. Ann Thorac Cardiovasc Surg 2011;17:435–45. 2. Madani MM, Auger WR, Pretorius V, et al. Pulmonary endarterectomy: recent changes in a single institution’s experience of more than 2,700 patients. Ann Thorac Surg 2012;94: 97–103. 3. Jenkins D, Mayer E, Screaton N, Madani M. State-of-the-art chronic thromboembolic pulmonary hypertension diagnosis and management. Eur Respir Rev 2012;21:32–9. 4. Mandani MM, Jamieson SW. technical advances of pulmonary endarterectomy for chronic thromboembolic pulmonary hypertension. Semin Thorac Cardiovasc Surg 2006;18:243–9. 5. Jenkins DP, Madani M, Mayer E, et al. Surgical treatment of chronic thromboembolic pulmonary hypertension. Eur Respir J 2013;41:735–42. 6. Revilla A, Lopez J, Villacorta E, et al. Isolated right-sided valvular endocarditis in non-intravenous drug users. Rev Esp Cardiol 2008;61:1253–9. 7. Heiberg J, Ilkjaer LB. Pulmonary endarterectomy after pulmonary infectious embolisms. Interact Cardiovasc Thorac Surg 2013;16:556–7. 8. Bernard J, Eunhee SY. Pulmonary thromboendarterectomy: a clinicopathologic study of 200 consecutive pulmonary thromboendarterectomy cases in one institution. Hum Pathol 2007;38:871–7.
Endobronchial Ultrasound-Guided Diagnosis of Pulmonary Artery Tumor Embolus Macarena R. Vial, MD, Mona Sarkiss, MD, Donald R. Lazarus, MD, and George Eapen, MD Division of Pulmonary Medicine, Clinica Alemana de Santiago, Universidad del Desarrollo, Chile; Department of Anesthesiology and Perioperative Medicine, The University of Texas MD Anderson Cancer Center; Department of Pulmonary Medicine, Baylor College of Medicine; and Department of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas
A patient diagnosed with pulmonary embolism had persistent symptoms despite adequate therapy. Tissue sampling with endobronchial ultrasound-guided needle Accepted for publication June 24, 2014.
Fig 4. Neutrophilic infiltration (arrows) is seen in (A) the pulmonary valve leaflet (B) and in the pulmonary emboli (hematoxylin and eosin stain; original magnification 40). Ó 2015 by The Society of Thoracic Surgeons Published by Elsevier
Address correspondence to Dr Eapen, Division of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, 1400 Pressler St, Unit 1462, Houston, TX 77030; e-mail: [email protected].
0003-4975/$36.00 http://dx.doi.org/10.1016/j.athoracsur.2014.06.111
CASE REPORT CROSLAND ET AL PEA FOR CTEPH FROM SEPTIC EMBOLI
We express our deep thanks to Dr Cui Quan-Cai and Dr Shi Jie of the Pathological Department of Peking Union Medical College Hospital for their extraordinary pathological work.
References 1. Zhang Y, Li H, Zhang WQ. Malignant glomus tumor of the esophagus with mediastinal lymph node metastases. Ann Thorac Surg 2013;96:1464–6. 2. Zhu YZ, Li WP, Wang ZY, et al. Glomus tumor of uncertain malignant potential arising in the bronchus. J Cardiothorac Surg 2013;8:146. 3. Urdaneta AI, Yu JB, Wilson LD. Population based cancer registry analysis of primary tracheal carcinoma. Am J Clin Oncol 2011;34:32–7. 4. Folpe AL, Fanburg-Smith JC, Miettinen M, Weiss SW. Atypical and malignant glomus tumors: analysis of 52 cases, with a proposal for the reclassification of glomus tumors. Am J Surg Pathol 2001;25:1–12. 5. Honings J, van Dijck JA, Verhagen AF, van der Heijden HF, Marres HA. Incidence and treatment of tracheal cancer: a nationwide study in the Netherlands. Ann Surg Oncol 2007;14: 968–76.
FEATURE ARTICLES
Pulmonary Endarterectomy for Pulmonary Hypertension From Septic Emboli William Crosland, MD, Mustafa Ahmed, MD, Julian Booker, MD, Keith Wille, MD, Satinder Singh, MD, FCCP, Thomas Winokur, MD, and David McGiffin, MBBS, FRACS Departments of Medicine, Radiology, and Pathology, The University of Alabama at Birmingham, Birmingham, Alabama; and Department of Cardiothoracic Surgery and Transplantation, The Alfred Hospital and Monash University, Melbourne, Victoria, Australia
Pulmonary endarterectomy (PEA) can significantly increase long-term survival in patients with chronic thromboembolic pulmonary hypertension; however, the role of PEA for chronic thromboembolic pulmonary hypertension due to pulmonary valve endocarditis is controversial. A critically ill 61-year-old man with intractable right ventricular heart failure was found to have chronic thromboembolic pulmonary hypertension due to Streptococcus bovis pulmonary valve endocarditis and underwent successful pulmonary valve replacement and PEA. The successful outcome in this case suggests that PEA should be considered in patients with this condition. (Ann Thorac Surg 2015;99:1814–6) Ó 2015 by The Society of Thoracic Surgeons
C
hronic thromboembolic pulmonary hypertension (CTEPH) develops in 3.8% of all patients diagnosed with a pulmonary embolus [1]. This is a chronic progressive Accepted for publication June 11, 2014. Address correspondence to Mr McGiffin, The Alfred Hospital, 55 Commercial Rd, Melbourne VIC 3004 Australia; e-mail: d.mcgiffin@alfred. org.au.
Ó 2015 by The Society of Thoracic Surgeons Published by Elsevier
Ann Thorac Surg 2015;99:1814–6
disease characterized by fibrotic stenosis of the pulmonary vasculature, remodeling of the unobstructed distal pulmonary arteries (PAs), and subsequent right-sided heart failure [1]. Medical therapy is largely ineffective. Pulmonary endarterectomy (PEA) is the treatment of choice for CTEPH because surgical intervention has clearly demonstrated substantial survival benefit over the natural history of the disease [2–5]. CTEPH due to rightsided infective endocarditis typically occurs in chronically debilitated patients with protracted hospital courses, and surgical intervention is inherently high risk. Right-sided endocarditis predominantly involves the tricuspid valve in more than 80% of cases, typically due to intravenous drug use or indwelling catheter placement [6]. The incidence of septic embolism from tricuspid or pulmonary valve endocarditis is largely unknown, but it seems the systolic shear stress that develops across the infected pulmonary valve could increase the risk of septic emboli. The benefit of PEA for CTEPH due to right-sided infective endocarditis is unclear, with some opinion recommending against the procedure [7]. We present a case from the University of Alabama at Birmingham of a patient with CTEPH due to septic embolization from pulmonary valve endocarditis who underwent successful combined pulmonary valve replacement and PEA [3–4]. A 61-year-old man presented to the University of Alabama at Birmingham for management of bilateral pulmonary thromboemboli associated with pulmonary valve vegetations. The patient had had multiple admissions for pneumonia during the past year. Streptococcus bovis bacteremia had developed 3 months before presentation. The patient was critically ill with intractable right ventricular heart failure. His clinical condition remained unresponsive to multiple administrations of tissue plasminogen activator, and his fever and leukocytosis persisted despite prolonged antibiotic therapy. Echocardiography on admission noted a severely dilated right ventricle with reduced systolic function and pulmonary valve vegetations with severe pulmonary valvular regurgitation (Fig 1). Three-dimensional computed tomography revealed a severely dilated PA, complete occlusion of the right PA, and multiple occlusive defects within the left lung, including the left lower lobe segmental, left superior lingular, and left inferior lingular arteries (Fig 2). Right heart catheterization noted elevated right atrial pressures of 22/13 (mean 19) mm Hg and elevated right ventricular pressures of 56/12 (mean 22) mm Hg. The PA was not entered due to concern for further embolization and was measured directly in the operating room, noting elevated PA pressures of 53/18 (30) mm Hg. PEA was performed through a median sternotomy using the usual methods of cardiopulmonary bypass and myocardial protection. Deep hypothermia to 20 C and circulatory arrest facilitated visualization during the endarterectomy. Cerebral protection was augmented by intermittent cerebral perfusion. 0003-4975/$36.00 http://dx.doi.org/10.1016/j.athoracsur.2014.06.109
Ann Thorac Surg 2015;99:1814–6
CASE REPORT CROSLAND ET AL PEA FOR CTEPH FROM SEPTIC EMBOLI
1815
the superior vena cava and the ascending aorta, and full clearance was obtained. In contradistinction to the usual thromboembolic disease, where establishing the dissection plane is straightforward and it strips easily, the plane in this condition was not easy to establish and did not strip as easily. Success required persisting with a dissection plane that was quite adherent, tedious, and foreign from that encountered in the usual thromboembolic disease, and consequently, with a troubling degree of uncertainty about the correctness of the plane (Fig 3). The total circulatory arrest time was 85 minutes, including periods of intermittent antegrade cerebral perfusion, with a total bypass time of 176 minutes. The histologic analysis of the surgical specimen noted dense neutrophilic infiltrates consistent with acute inflammation in the native pulmonary valve (Fig 4A) and in the pulmonary emboli (Fig 4B). The patient’s postoperative course was uneventful. The postoperative PA pressure was 28/10 (16) mm Hg, with the pulmonary vascular resistance calculated to be 89 (dynes ∙ sec)/cm5. At the most recent outpatient followup, the patient had markedly improved exercise tolerance and had returned to work on a regular basis.
Comment
The pulmonary valve was essentially destroyed, with 1 leaflet completely replaced by vegetation and the other 2 leaflets with multiple large perforations. The valve was replaced with a 27-mm Freestyle stentless Xenograft aortic valve (Medtronic, Minneapolis, MN). The left PA was accessed through a longitudinal incision, the endarterectomy plane established, and full clearance of the left PA and branches achieved. The right PA was opened through a longitudinal incision between
Fig 2. Three-dimensional computed tomography in (A) axial and (B) coronal views demonstrates a large filling defect in right main pulmonary artery (red arrows) and a large intraluminal filling defect (white arrow) in the left lower lingular pulmonary artery extending into the lower lobe branches.
FEATURE ARTICLES
Fig 1. Preoperative transesophageal echocardiography displays severe pulmonary valvular regurgitation. (A) Color Doppler imaging. (B) Continuous-wave Doppler echocardiography.
Pathologic analysis of PEA specimens notes the rarity of acute inflammation in pulmonary emboli, which hallmarks the unique nature and severe acuity of the patient’s clinical condition [8]. The corresponding dense neutrophilic infiltrates in the PEA specimen and the native pulmonary valve are strongly suggestive that the emboli originated from the pulmonary valve endocarditis [5]. The benefits of PEA have been well established in patients with CTEPH, but concern exists regarding the role of PEA in patients with CTEPH due to pulmonary valve endocarditis. A previous report noted significant adherence of the thrombus to the pulmonary vessels, which undermined attempts at endarterectomy, and both cases were unsuccessful. The authors recommended against performing PEA for CTEPH due to infectious endocarditis secondary to technical difficulties [7].
1816
CASE REPORT VIAL ET AL DIAGNOSING PULMONARY TUMOR EMBOLI
Ann Thorac Surg 2015;99:1816–9
marked symptomatic and hemodynamic response. In our opinion, PEA in this condition is technically possible based on our experience with this patient. Future attempts in similar patients should anticipate difficult dissection planes and should expect difficult extrication of the septic emboli because this is an inherent aspect of the disease process. Therefore, patients with infective pulmonary endocarditis complicated by pulmonary emboli resulting in CTEPH should be considered for PEA.
References
Fig 3. Surgical specimen of thromboemboli after bilateral pulmonary endarterectomy.
FEATURE ARTICLES
The procedure reported in this patient met similar challenges, but persistent, careful dissection led to successful clearance of the pulmonary arteries, with a
1. Rahnavardi M, Yan TD, Cao C, et al. Pulmonary thromboendarterectomy for chronic thromboembolic pulmonary hypertension: a systematic review. Ann Thorac Cardiovasc Surg 2011;17:435–45. 2. Madani MM, Auger WR, Pretorius V, et al. Pulmonary endarterectomy: recent changes in a single institution’s experience of more than 2,700 patients. Ann Thorac Surg 2012;94: 97–103. 3. Jenkins D, Mayer E, Screaton N, Madani M. State-of-the-art chronic thromboembolic pulmonary hypertension diagnosis and management. Eur Respir Rev 2012;21:32–9. 4. Mandani MM, Jamieson SW. technical advances of pulmonary endarterectomy for chronic thromboembolic pulmonary hypertension. Semin Thorac Cardiovasc Surg 2006;18:243–9. 5. Jenkins DP, Madani M, Mayer E, et al. Surgical treatment of chronic thromboembolic pulmonary hypertension. Eur Respir J 2013;41:735–42. 6. Revilla A, Lopez J, Villacorta E, et al. Isolated right-sided valvular endocarditis in non-intravenous drug users. Rev Esp Cardiol 2008;61:1253–9. 7. Heiberg J, Ilkjaer LB. Pulmonary endarterectomy after pulmonary infectious embolisms. Interact Cardiovasc Thorac Surg 2013;16:556–7. 8. Bernard J, Eunhee SY. Pulmonary thromboendarterectomy: a clinicopathologic study of 200 consecutive pulmonary thromboendarterectomy cases in one institution. Hum Pathol 2007;38:871–7.
Endobronchial Ultrasound-Guided Diagnosis of Pulmonary Artery Tumor Embolus Macarena R. Vial, MD, Mona Sarkiss, MD, Donald R. Lazarus, MD, and George Eapen, MD Division of Pulmonary Medicine, Clinica Alemana de Santiago, Universidad del Desarrollo, Chile; Department of Anesthesiology and Perioperative Medicine, The University of Texas MD Anderson Cancer Center; Department of Pulmonary Medicine, Baylor College of Medicine; and Department of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas
A patient diagnosed with pulmonary embolism had persistent symptoms despite adequate therapy. Tissue sampling with endobronchial ultrasound-guided needle Accepted for publication June 24, 2014.
Fig 4. Neutrophilic infiltration (arrows) is seen in (A) the pulmonary valve leaflet (B) and in the pulmonary emboli (hematoxylin and eosin stain; original magnification 40). Ó 2015 by The Society of Thoracic Surgeons Published by Elsevier
Address correspondence to Dr Eapen, Division of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, 1400 Pressler St, Unit 1462, Houston, TX 77030; e-mail: [email protected].
0003-4975/$36.00 http://dx.doi.org/10.1016/j.athoracsur.2014.06.111
