- Email: [email protected]
Recurrent systemic embolization caused by aortic thrombi
CASE REPORTS
Recurrent S stemic Embolization Caused by ortic Thrombi
1
Harry R. Aldrich, MD, Leonard Girardi, MD, Harry L. Bush, Jr, MD, Richard B. Devereux, MD, and Todd K. Rosengart, MD Departments of Medicine and Surgery, The New York Hospital-Cornell University Medical Center, New York, New York
The aorta is a commonly unrecognized source of systemic embolization. Transesophageal echocardiography is a reliable method for visualization of the intima of the thoracic aorta and identification of aortic thrombi. Balloon embolectomy of the aorta can be used to remove thrombi and prevent further embolic events. (Ann Thorac Surg 1994;57:466-8)
T
he heart has long been identified as a major source of cerebral and peripheral emboli [l].Protruding atheromas and thrombi in the aorta have been recognized in some patients with systemic embolic events. However, the recent development of transesophageal echocardiography, which provides noninvasive reliable visualization of the thoracic aorta, has led to the identification of intraaortic atherosclerotic debris in a much higher proportion of patients with arterial embolization than previously appreciated [24]. This report will detail the diagnosis and contrast the management of 2 patients with large mobile intraaortic thrombi who had recurrent embolization.
Case Reports Patient 1 A 70-year-old man with prostate cancer presented 2 weeks after a radical perineal prostatectomy for evaluation of abdominal pain and fever. His examination was remarkable for a temperature of 39.3"C and mild generalized abdominal pain with a white blood cell count of 18,00O/pL. Peripheral pulses were intact. An abdominal computed tomographic scan showed new bilateral renal infarcts and thickening and hyperemia of the jejunum consistent with infarction. A transthoracic echocardiogram was normal. Transesophageal echocardiography revealed a large 3 x 1.5-cm mobile mass at the distal aortic arch, which extended into the descending aorta from its attachment point on the posterior aortic wall (Fig 1A). The aortic intima was not markedly thickened. Left ventricular wall motion and function were normal with no valve disease. There was a patent foramen ovale. The patient was anticoagulated with heparin. Three days later, severe abdominal pain developed. The patient underwent an exploratory laparotomy with resection of 90 cm of gangrenous small bowel and an embolectomy of the superior mesenteric artery. A repeat transesophageal Accepted for publication May 3, 1993. Address reprint requests to Dr Aldrich, Division of Cardiology, Department of Medicine, Allegheny General Hospital, 320 East North Ave, Pittsburgh, PA 15212.
0 1994 by The Society of Thoracic Surgeons
echocardiogram revealed a residual mass 0.2 cm in diameter at the site of the previous large mass (Fig 1B). Three weeks later, the patient was discharged on a regimen of warfarin and has had no subsequent embolic events during 16 months of follow-up.
Patient 2 A 60-year-old woman was admitted to her local hospital with a 4-day history of abdominal pain and fever. An abdominal computed tomographic scan identified bilateral renal infarcts, a splenic infarct, and massive edema of the small bowel and colon. She then began to experience bilateral leg weakness, calf pain, and loss of posterior tibia1 pulses. She was transferred to our hospital for further treatment. Physical examination was remarkable for a distended abdomen and cool, pulseless extremities. Her feet were anesthetic to touch without motor function. The white blood cell count was 31,OOO/pL. Serum creatinine level, which had previously been normal, was 3.5 mg/mL. An angiogram of the thoracic and abdominal aorta and lower extremities identified occlusion of the right renal artery, upper left renal artery, right hypogastric artery, bilateral superficial femoral artery, profunda artery, and popliteal artery at the knee. There was reduced flow in the superior mesenteric arcade consistent with partial occlusion. She underwent small bowel resection with bilateral profunda and superficial femoral artery embolectomies. Transesophageal echocardiography revealed a large, mobile, irregularly shaped mass that occupied up to half of the lumen of the descending aorta (Fig 2A). At its proximal end, 8 cm below the aortic arch, the mass was attached to the posterior and lateral aortic wall, and at its distal end it had several mobile fronds (Fig 2B). The remaining intima of the aorta was normal. There were normal left ventricular wall motion and function, a patent foramen ovale, and no valvular disease or vegetations. Due to the risk of subsequent peripheral emboli, it was thought that it would be beneficial to remove the presumed intraaortic thrombus. Through a standard left posterolateral thoracotomy incision, the aorta was dissected out from surrounding tissue. Intraoperative transesophageal echocardiography was used to ensure that the proximal cross-clamp position was above the mass. Because the thrombus extended below the diaphragm and would be disrupted by a distal clamp, a deflated Foley balloon catheter was passed into the thoracic aorta via a longitudinal aortotomy and then inflated. However, the thrombus was not visible through the aortotomy and could not be readily scooped out of the aorta. The thrombus was removed by withdrawing the slightly deflated Foley catheter similar to an embolectomy procedure and a 2.5 x 4 cm well-organized thrombus was recovered (Fig 3). The patient's postoperative course was notable for rapid improvement of renal function with a creatinine level of 1.3 mg/mL before discharge. There were no prothrombotic hematologic disorders. A repeat transesophageal echocardiogram revealed no residual thoracic aortic thrombi. The patient was discharged on a regimen of warfarin and has had no further thrombotic events. 0003-4975/94/$7.00
CASE REPORT
Ann Thorac Surg 1994;57:m
ALDRICH ET AL AORTIC THROMBI
467
Comment The aorta can be an unsuspected source of peripheral emboli [ 5 ] .Postmortem series have identified the aorta as the source of emboli in fewer than 5% of patients with peripheral emboli. Recent series have identified intraaortic atherosclerotic debris in up to 10% of patients referred for transesophageal echocardiography [4]. Elderly patients are more likely to have protruding aortic atheromas [2, 3, 61. An aortic atherosclerotic plaque may serve as a nidus for thrombus formation. A calcified plaque at the site of insertion of the ligamentum arteriosum has been reported as an attachment point for a thrombus [7]. The aorta may not have uniform intimal thickening and calcification. Both patients in this report had an otherwise normalappearing aortic intima, supporting the hypothesis that a
A
B Fig 2. (A) Transesophageal echocardiograms of patient 2 showing the large thrombus which at its proximal end filled over half the area of the mid-thoracic aorta. (B)A t the distal end of the thrombus, the mass had irregular mobile fronds.
B Fig 1 . (A) Transesophageal echocardiogram of the aortic arch of patient 1 showing the mobile thrombus attached to the posterior wall of the aorta. (B)After the large mass embolized, a small residual mass indicated by the arrow was seen by transesophageal echocardiography.
localized atherosclerotic plaque, perhaps ulcerated, may serve as the origin of the thrombus. Transesophageal echocardiography is superior to aortography and computed tomography for visualization of the aortic intima. The aortic thrombus in patient 2 of this report was not visualized by aortography and could not be retrospectively identified even with the knowledge of the thrombus location by transesophageal echocardiography. Transesophageal echocardiography characterizesthe mobility of the mass, which has been associated with an increased incidence of embolization [ 2 ] . Additionally, intraoperative transesophageal echocardiography can assist in the Precise localization of the thrombus and thus facilitate embolectomy. Therapy for intraaortic thrombi remains undefined. The
468
CASE REPORT ISHIGAMI ET AL EXTRACTION OF A VSD PATCH
Ann Thorac Surg 1994;57468-9
arteriosum: an unreported origin of peripheral emboli diagnosed by transesophageal echocardiography. Am Heart J 1992;124:222-3. 8. Hausmann D, Gulba D, Bargheer K, Niedermeyer J, Comess KA, Daniel WG. Successful thrombolysis of an aortic arch thrombus in a patient after mesenteric embolis. N Engl J Med 1992;327500-1.
Unexpected Extraction of a Ventricular Septa1 Defect Patch Without an Interventricular Shunt Fig 3. The thrombus that was removed from the aorta of patient 2. Its irregular shape was accurately imaged by transesophageal echocardiography.
natural history of asymptomatic patients with protruding aortic atheromas and thrombi is not known. Several treatment modalities have been reported for symptomatic patients with aortic debris and systemic embolization. Routine anticoagulation was not effective in patient 1 of this report. Recombinant tissue plasminogen activator was recently reported to successfully resolve an aortic thrombus in 1 case [8]. However, dissolution of the attachment point between the aorta and thrombus could cause a large distal embolization. Others have performed endarterectomy of the ascending aorta [3]. In patient 2, balloon embolectomy was used to successfully remove the aortic thrombus from an inaccessible position at the transdiaphragmatic portion of the aorta. In conclusion, these cases illustrate that the aorta may be a source of clinically severe systemic embolization. Transesophageal echocardiography of the heart and aorta should be performed on patients with systemic emboli to identify aortic pathology and assist in determining therapy. Balloon embolectomy of the aorta may be a beneficial surgical therapy for patients with recurrent systemic emboli due to aortic thrombi.
References 1. Elliott JP, Hageman JH, Szilagy DE, Ramatcrishnan V, Bravo IJ, Smith RF. Arterial embolization: problems of source, multiplicity, recurrence, and delayed treatment. Surgery 1980;88: 833-45. 2. Karalis DG, Chandrasekaran K, Victor MF, Ross JJ, Mintz GS. Recognition and embolic potential of intraaortic atherosclerotic debris. J Am Coll Cardiol 1991;1773-8. 3. Tunick PA, Culliford AT, Lamparello PJ, Kronzon I. Atheromatosis of the aortic arch as an occult source of multiple systemic emboli. Ann Intern Med 1991;114:391-2. 4. Tunick PA, Perez JC, Kronzon I. Protruding atheromas in the thoracic aorta and systemic embolization. Ann Intern Med 1991;115:423-7. 5. Heiskell CA, Conn J. Aortoarterial emboli. Am J Surg 1976; 132:4-7. 6. Tobler HG, Edwards JE. Frequency and location of atherosclerotic plaques in the ascending aorta. J Thorac Cardiovasc Surg 1988;96:304-6. 7. Laperche T, Sarkis A, Monin JL, et al. The ligamentation
Naoyuki Ishigami, MD, Yukifusa Yokoyama, MD, Masanao Osawa, MD, Kimitoshi Horiba, MD, Makoto Takinami, MD, and Yukio Harada, MD First Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan
We report the case of a mediastinocutaneous fistula, 13 years after the total correction of tetralogy of Fallot. During a fistula curettage operation, we unexpectedly extracted a ventricular septal defect patch. An interventricular shunt was not detected after the operation. The patient is well 3 years after the last operation. (Ann Thoruc Surg 2994;57:468-9)
T
he total correction of tetralogy of Fallot (TOF) consists of closing the ventricular septal defect (VSD) with a patch and relieving the right ventricular outflow tract (RVOT) stenosis with or without a patch [l-31. Detachment of these patches is one of the serious complications of using prosthetic materials. For the VSD patch, however, there are few reports of complete detachment. We report here the rare case of a completely excluded VSD patch from the right ventricle, which was the cause of a mediastinocutaneous fistula. A 16-year-old boy was referred to our hospital for the treatment of an extremely refractory mediastinocutaneous fistula on September 21, 1989. The total correction of TOF by median sternotomy had been performed on the patient at another hospital in 1975 when he was 2 years of age. The RVOT stenosis was relieved without a patch, and the large VSD was closed with a Teflon patch. He was discharged with an uneventful postoperative course, and his subsequent growth was normal. Thirteen years later, skin swelling and pus discharge were noted in the xiphisternal legion. Despite an operation to remove the wire with sternal resection and curettage, pus discharge recurred. Cultures of the pus were all negative during this period. During physical examinations, a granulation projecting over an area of about 3 cm around a central fistula was Accepted for publication May 5, 1993 Address reprint requests to Dr Ishigami, First Department of Surgery, Hamamatsu University School of Medicine, 3600 Handa-cho, Hamamatsu, 431-31, Japan.
Recurrent S stemic Embolization Caused by ortic Thrombi
1
Harry R. Aldrich, MD, Leonard Girardi, MD, Harry L. Bush, Jr, MD, Richard B. Devereux, MD, and Todd K. Rosengart, MD Departments of Medicine and Surgery, The New York Hospital-Cornell University Medical Center, New York, New York
The aorta is a commonly unrecognized source of systemic embolization. Transesophageal echocardiography is a reliable method for visualization of the intima of the thoracic aorta and identification of aortic thrombi. Balloon embolectomy of the aorta can be used to remove thrombi and prevent further embolic events. (Ann Thorac Surg 1994;57:466-8)
T
he heart has long been identified as a major source of cerebral and peripheral emboli [l].Protruding atheromas and thrombi in the aorta have been recognized in some patients with systemic embolic events. However, the recent development of transesophageal echocardiography, which provides noninvasive reliable visualization of the thoracic aorta, has led to the identification of intraaortic atherosclerotic debris in a much higher proportion of patients with arterial embolization than previously appreciated [24]. This report will detail the diagnosis and contrast the management of 2 patients with large mobile intraaortic thrombi who had recurrent embolization.
Case Reports Patient 1 A 70-year-old man with prostate cancer presented 2 weeks after a radical perineal prostatectomy for evaluation of abdominal pain and fever. His examination was remarkable for a temperature of 39.3"C and mild generalized abdominal pain with a white blood cell count of 18,00O/pL. Peripheral pulses were intact. An abdominal computed tomographic scan showed new bilateral renal infarcts and thickening and hyperemia of the jejunum consistent with infarction. A transthoracic echocardiogram was normal. Transesophageal echocardiography revealed a large 3 x 1.5-cm mobile mass at the distal aortic arch, which extended into the descending aorta from its attachment point on the posterior aortic wall (Fig 1A). The aortic intima was not markedly thickened. Left ventricular wall motion and function were normal with no valve disease. There was a patent foramen ovale. The patient was anticoagulated with heparin. Three days later, severe abdominal pain developed. The patient underwent an exploratory laparotomy with resection of 90 cm of gangrenous small bowel and an embolectomy of the superior mesenteric artery. A repeat transesophageal Accepted for publication May 3, 1993. Address reprint requests to Dr Aldrich, Division of Cardiology, Department of Medicine, Allegheny General Hospital, 320 East North Ave, Pittsburgh, PA 15212.
0 1994 by The Society of Thoracic Surgeons
echocardiogram revealed a residual mass 0.2 cm in diameter at the site of the previous large mass (Fig 1B). Three weeks later, the patient was discharged on a regimen of warfarin and has had no subsequent embolic events during 16 months of follow-up.
Patient 2 A 60-year-old woman was admitted to her local hospital with a 4-day history of abdominal pain and fever. An abdominal computed tomographic scan identified bilateral renal infarcts, a splenic infarct, and massive edema of the small bowel and colon. She then began to experience bilateral leg weakness, calf pain, and loss of posterior tibia1 pulses. She was transferred to our hospital for further treatment. Physical examination was remarkable for a distended abdomen and cool, pulseless extremities. Her feet were anesthetic to touch without motor function. The white blood cell count was 31,OOO/pL. Serum creatinine level, which had previously been normal, was 3.5 mg/mL. An angiogram of the thoracic and abdominal aorta and lower extremities identified occlusion of the right renal artery, upper left renal artery, right hypogastric artery, bilateral superficial femoral artery, profunda artery, and popliteal artery at the knee. There was reduced flow in the superior mesenteric arcade consistent with partial occlusion. She underwent small bowel resection with bilateral profunda and superficial femoral artery embolectomies. Transesophageal echocardiography revealed a large, mobile, irregularly shaped mass that occupied up to half of the lumen of the descending aorta (Fig 2A). At its proximal end, 8 cm below the aortic arch, the mass was attached to the posterior and lateral aortic wall, and at its distal end it had several mobile fronds (Fig 2B). The remaining intima of the aorta was normal. There were normal left ventricular wall motion and function, a patent foramen ovale, and no valvular disease or vegetations. Due to the risk of subsequent peripheral emboli, it was thought that it would be beneficial to remove the presumed intraaortic thrombus. Through a standard left posterolateral thoracotomy incision, the aorta was dissected out from surrounding tissue. Intraoperative transesophageal echocardiography was used to ensure that the proximal cross-clamp position was above the mass. Because the thrombus extended below the diaphragm and would be disrupted by a distal clamp, a deflated Foley balloon catheter was passed into the thoracic aorta via a longitudinal aortotomy and then inflated. However, the thrombus was not visible through the aortotomy and could not be readily scooped out of the aorta. The thrombus was removed by withdrawing the slightly deflated Foley catheter similar to an embolectomy procedure and a 2.5 x 4 cm well-organized thrombus was recovered (Fig 3). The patient's postoperative course was notable for rapid improvement of renal function with a creatinine level of 1.3 mg/mL before discharge. There were no prothrombotic hematologic disorders. A repeat transesophageal echocardiogram revealed no residual thoracic aortic thrombi. The patient was discharged on a regimen of warfarin and has had no further thrombotic events. 0003-4975/94/$7.00
CASE REPORT
Ann Thorac Surg 1994;57:m
ALDRICH ET AL AORTIC THROMBI
467
Comment The aorta can be an unsuspected source of peripheral emboli [ 5 ] .Postmortem series have identified the aorta as the source of emboli in fewer than 5% of patients with peripheral emboli. Recent series have identified intraaortic atherosclerotic debris in up to 10% of patients referred for transesophageal echocardiography [4]. Elderly patients are more likely to have protruding aortic atheromas [2, 3, 61. An aortic atherosclerotic plaque may serve as a nidus for thrombus formation. A calcified plaque at the site of insertion of the ligamentum arteriosum has been reported as an attachment point for a thrombus [7]. The aorta may not have uniform intimal thickening and calcification. Both patients in this report had an otherwise normalappearing aortic intima, supporting the hypothesis that a
A
B Fig 2. (A) Transesophageal echocardiograms of patient 2 showing the large thrombus which at its proximal end filled over half the area of the mid-thoracic aorta. (B)A t the distal end of the thrombus, the mass had irregular mobile fronds.
B Fig 1 . (A) Transesophageal echocardiogram of the aortic arch of patient 1 showing the mobile thrombus attached to the posterior wall of the aorta. (B)After the large mass embolized, a small residual mass indicated by the arrow was seen by transesophageal echocardiography.
localized atherosclerotic plaque, perhaps ulcerated, may serve as the origin of the thrombus. Transesophageal echocardiography is superior to aortography and computed tomography for visualization of the aortic intima. The aortic thrombus in patient 2 of this report was not visualized by aortography and could not be retrospectively identified even with the knowledge of the thrombus location by transesophageal echocardiography. Transesophageal echocardiography characterizesthe mobility of the mass, which has been associated with an increased incidence of embolization [ 2 ] . Additionally, intraoperative transesophageal echocardiography can assist in the Precise localization of the thrombus and thus facilitate embolectomy. Therapy for intraaortic thrombi remains undefined. The
468
CASE REPORT ISHIGAMI ET AL EXTRACTION OF A VSD PATCH
Ann Thorac Surg 1994;57468-9
arteriosum: an unreported origin of peripheral emboli diagnosed by transesophageal echocardiography. Am Heart J 1992;124:222-3. 8. Hausmann D, Gulba D, Bargheer K, Niedermeyer J, Comess KA, Daniel WG. Successful thrombolysis of an aortic arch thrombus in a patient after mesenteric embolis. N Engl J Med 1992;327500-1.
Unexpected Extraction of a Ventricular Septa1 Defect Patch Without an Interventricular Shunt Fig 3. The thrombus that was removed from the aorta of patient 2. Its irregular shape was accurately imaged by transesophageal echocardiography.
natural history of asymptomatic patients with protruding aortic atheromas and thrombi is not known. Several treatment modalities have been reported for symptomatic patients with aortic debris and systemic embolization. Routine anticoagulation was not effective in patient 1 of this report. Recombinant tissue plasminogen activator was recently reported to successfully resolve an aortic thrombus in 1 case [8]. However, dissolution of the attachment point between the aorta and thrombus could cause a large distal embolization. Others have performed endarterectomy of the ascending aorta [3]. In patient 2, balloon embolectomy was used to successfully remove the aortic thrombus from an inaccessible position at the transdiaphragmatic portion of the aorta. In conclusion, these cases illustrate that the aorta may be a source of clinically severe systemic embolization. Transesophageal echocardiography of the heart and aorta should be performed on patients with systemic emboli to identify aortic pathology and assist in determining therapy. Balloon embolectomy of the aorta may be a beneficial surgical therapy for patients with recurrent systemic emboli due to aortic thrombi.
References 1. Elliott JP, Hageman JH, Szilagy DE, Ramatcrishnan V, Bravo IJ, Smith RF. Arterial embolization: problems of source, multiplicity, recurrence, and delayed treatment. Surgery 1980;88: 833-45. 2. Karalis DG, Chandrasekaran K, Victor MF, Ross JJ, Mintz GS. Recognition and embolic potential of intraaortic atherosclerotic debris. J Am Coll Cardiol 1991;1773-8. 3. Tunick PA, Culliford AT, Lamparello PJ, Kronzon I. Atheromatosis of the aortic arch as an occult source of multiple systemic emboli. Ann Intern Med 1991;114:391-2. 4. Tunick PA, Perez JC, Kronzon I. Protruding atheromas in the thoracic aorta and systemic embolization. Ann Intern Med 1991;115:423-7. 5. Heiskell CA, Conn J. Aortoarterial emboli. Am J Surg 1976; 132:4-7. 6. Tobler HG, Edwards JE. Frequency and location of atherosclerotic plaques in the ascending aorta. J Thorac Cardiovasc Surg 1988;96:304-6. 7. Laperche T, Sarkis A, Monin JL, et al. The ligamentation
Naoyuki Ishigami, MD, Yukifusa Yokoyama, MD, Masanao Osawa, MD, Kimitoshi Horiba, MD, Makoto Takinami, MD, and Yukio Harada, MD First Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan
We report the case of a mediastinocutaneous fistula, 13 years after the total correction of tetralogy of Fallot. During a fistula curettage operation, we unexpectedly extracted a ventricular septal defect patch. An interventricular shunt was not detected after the operation. The patient is well 3 years after the last operation. (Ann Thoruc Surg 2994;57:468-9)
T
he total correction of tetralogy of Fallot (TOF) consists of closing the ventricular septal defect (VSD) with a patch and relieving the right ventricular outflow tract (RVOT) stenosis with or without a patch [l-31. Detachment of these patches is one of the serious complications of using prosthetic materials. For the VSD patch, however, there are few reports of complete detachment. We report here the rare case of a completely excluded VSD patch from the right ventricle, which was the cause of a mediastinocutaneous fistula. A 16-year-old boy was referred to our hospital for the treatment of an extremely refractory mediastinocutaneous fistula on September 21, 1989. The total correction of TOF by median sternotomy had been performed on the patient at another hospital in 1975 when he was 2 years of age. The RVOT stenosis was relieved without a patch, and the large VSD was closed with a Teflon patch. He was discharged with an uneventful postoperative course, and his subsequent growth was normal. Thirteen years later, skin swelling and pus discharge were noted in the xiphisternal legion. Despite an operation to remove the wire with sternal resection and curettage, pus discharge recurred. Cultures of the pus were all negative during this period. During physical examinations, a granulation projecting over an area of about 3 cm around a central fistula was Accepted for publication May 5, 1993 Address reprint requests to Dr Ishigami, First Department of Surgery, Hamamatsu University School of Medicine, 3600 Handa-cho, Hamamatsu, 431-31, Japan.