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CASE REPORT WATANABE ET AL INTRAMURAL LEFT ATRIAL HEMATOMA
The presence of lead vegetations poses additional difficulties for explantation, as many methods cannot be used because of the potential hazard of pulmonary embolism. The real incidence of lead vegetations in pacemaker endocarditis is unclear because of the lack of routine transthoracic echocardiography. With transthoracic echocardiography, Klug and associates [4] observed vegetations in 30% of patients compared with 94% using transesophageal echocardiography. They managed these patients depending on the length of the vegetations: percutaneous technique when less than 10 mm long and open heart surgical intervention when longer than 10 mm. The first technique was used in 73% of patients in 30% of them, pulmonary embolus was found on scanning after the procedure. Of patients having open heart surgical procedures, only 1 had a fatal pulmonary embolic event. Many authors consider a surgical approach with sternotomy to be the safest method when leads have vegetations. Despite the potential risks associated with operation, the risk of death from sepsis or pulmonary embolism is higher if the leads are left in place or if other methods are used [11]. When cardiopulmonary bypass needs to be avoided, the electrodes can be removed through a pursestring in the right atrium, but it is very difficult to remove all material successfully without detachment of vegetations or substantial blood loss. Our procedure easily and safely resolves of these concerns. We think this technique is a good alternative for the management of pacemaker lead endocarditis.
References 1. Heimburger TS, Duma RJ. Infections of prosthetic valves and cardiac pacemakers. Infect Dis Clin North Am 1989;3: 221– 45. 2. Frame R, Brodman RF, Furman S, et al. Surgical removal of infected transvenous pacemaker leads. PACE 1993;16: 2343– 8. 3. Phibbs B, Marriott HJL. Complications of permanent transvenous pacing. N Engl J Med 1985;312:1428–32. 4. Klug D, Lacroix D, Savoye C, et al. Systemic infection related to endocarditis on pacemaker leads: clinical presentation and management. Circulation 1997;95:2098 –107. 5. Marrie TJ, Nelligan J, Costerton J. A scanning and transmission electron microscopic study of an infected endocardial pacemaker lead. Circulation 1982;66:1339– 41. 6. Kratz JM, Leman R, Gillette PC. Forceps extraction of permanent pacing leads. Ann Thorac Surg 1990;49:676–7. 7. Praeger P, Kay R, Somberg E, et al. Pacemaker removal— another source of infections. PACE 1984;7:763– 4. 8. Belott PH. Endocardial lead extraction. Armonk, NY: Futura, 1998:11–12 (introduction). 9. Byrd CL, Wilkoff B, Love C, et al. Clinical study of the laser sheath: results of the PLEXES trial. PACE 1997;20:1053. 10. Smith HJ, Fearnot NE, Byrd CL, Wilkoff BL, Love CJ, Sellers TD. Five-years experience with intravascular lead extraction. U.S. Lead Extraction Database. PACE 1994;17(11 Pt 2): 2016–20. 11. Brodman RF, Frame R, Andrews C, et al. Removal of infected transvenous leads requiring cardiopulmonary bypass or inflow occlusion. J Thorac Cardiovasc Surg 1992;103:649 –54. © 2001 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
Ann Thorac Surg 2001;72:2132– 4
Spontaneous Intramural Left Atrial Hematoma Associated With Systemic Amyloidosis Ko Watanabe, MD, Bruno Miguel, MD, Jean L. Kemeny, MD, Bernard Citron, MD, and Lionel F. Camilleri, MD Department of Cardiovascular Surgery, Pr Charles de Riberolles, Gabriel Montpied University Hospital, ClermontFerrand, France
Spontaneous intramural left atrial hematoma is very rare. We describe a case of spontaneous intramural left atrial hematoma that had to be semiurgently resected. Postoperatively, the patient was diagnosed as having systemic immunocyte-derived (AL) amyloidosis, because of rare manifestations of fatal bleeding. Though spontaneous intramural left atrial hematoma is one of the severe complications of systemic AL amyloidosis, we believe that amyloid deposits caused fragility of the left atrial wall. (Ann Thorac Surg 2001;72:2132– 4) © 2001 by The Society of Thoracic Surgeons
F
atal hemorrhage is a rare clinical problem in patients with systemic amyloidosis although focal or generalized hemorrhage is common. We encountered a spontaneous intramural left atrial hematoma as a manifestation of severe bleeding. A 70-year-old man was admitted to our hospital for acute pericarditis, complaining of dyspnea and chest pain. The patient had received an oral anticoagulant for suspected pulmonary embolism after an orthopedic operation. At admission a prothrombin test was performed with a result of 20% (International Normalized Ratio, 5.6). Two days after admission, the patient suffered a sudden heart failure. A transesophageal echocardiogram revealed a 5.7 ⫻ 7.0 cm left intraatrial mass that adhered to the atrial septum and occupied the left atrium. A pericardial effusion of some importance induced compression of the right ventricle. Magnetic resonance imaging revealed an intracardiac mass in the left atrium, more likely to be a thrombus than a tumor (Fig 1). The patient underwent a semiurgent operation. Fibrins were diffusely attached to the surface of the pericardium and the pericardial effusion contained 300 mL of blood. We approached the left atrium using transseptal superior exposure. The mass was located in the intramural space, not in the intracardiac cavity. The left atrial cavity was filled almost entirely by the mass, which was attached to the septal wall, and extended through the mitral annulus to the pulmonary veins within the intramural space. Though the pulmonary veins were not involved, and no Accepted for publication Feb 3, 2001. Address reprint requests to Dr Watanabe, Chirurgie Cardio-Vasculaire, Hoˆ pital Gabriel Montpied, Place Henri Dunant, BP 69, F-63003 ClermontFerrand Cedex 1, France; e-mail:
[email protected].
0003-4975/01/$20.00 PII S0003-4975(01)02653-4
Ann Thorac Surg 2001;72:2132– 4
CASE REPORT WATANABE ET AL INTRAMURAL LEFT ATRIAL HEMATOMA
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ing usually observed in patients suffering from systemic immunocyte-derived (AL) amyloidosis with heart involvement [1, 2]. Isolated factor X deficiency, which is one cause of the hemorrhage associated with amyloidosis, was not present [1, 3]. The patient was diagnosed as having systemic AL amyloidosis. We have concluded that the intramural left atrial hematoma occurred spontaneously as a severe bleeding manifestation of systemic AL amyloidosis, though the patient was under anticoagulation therapy, suggesting that amyloid deposits caused fragility of the left atrial walls. The patient has shown no signs of recurrence and remains well 9 months after the operation.
Comment Fig 1. Preoperative magnetic resonance imaging demonstrating the mass resulting in a decrease of the left atrial cavity (arrow).
tear of the left atrial wall was observed, the infiltrated tissue was very fragile. It seemed that the hematoma had enlarged and delacerated the intramural space. After a pathologic diagnosis of the mass as a thrombus, we enucleated it. We resected fragile tissues from the left pulmonary veins to the right pulmonary veins, down to the mitral annulus, and reconstructed the left atrial wall with a pericardial patch. Postoperative convalescence was uneventful except for atrial fibrillation. Pathologically, the mass was an encysted hematoma without proliferative cells. The atrial wall was infiltrated to the epicardium by amyloid, which was stained with Congo red and presented the characteristic apple-green birefringence when viewed under polarized light (Fig 2A). These deposits remained visible after they were treated with permanganate. Likewise, amyloid deposits were present in the thickened walls of some pericardial vessels (Fig 2B). Monoclonal immunoglobulin of IgG kappa was detected postoperatively in the serum by means of protein electrophoresis, though rectal biopsy proved negative. The patient had no family history of amyloidosis. An echocardiogram did not reveal ventricular wall thicken-
Spontaneous intramural left atrial hematoma is very rare. Intramural blood collection is thought to be caused by chest trauma, infectious endocarditis, mitral annular calcification, pericardial puncture, placement of a pacemaker, or complications after an operation, where anticoagulation therapy might be an additional factor [4, 5]. In spite of this, focal or generalized hemorrhage is a commonly encountered clinical problem in patients with amyloidosis [1, 2]. Yood and colleagues [3] reported that the frequency of bleeding problems in patients with amyloidosis was approximately 40%, with most cases being only mild hemorrhages. However, some cases were far more severe, to the point of being fatal, such as upper gastrointestinal bleeding and retroperitoneal bleeding. Furthermore, Yood and colleagues [3] stated that bleeding occurred frequently, even when patients had no abnormalities of coagulation tests, and they suggested that amyloid infiltration of blood vessels with consequent increased fragility contributed to hemorrhaging in amyloidosis. Our patient did not show an evident cause of preoperative hemorrhaging aside from the anticoagulation therapy. Postoperative diagnosis was systemic immunocyte-derived (AL) amyloidosis, without ventricular wall thickening, and electrocardiogram abnormality, although the rectal biopsy was negative.
Fig 2. Amyloid deposits presenting characteristic birefringence in Congo red stain viewed under polarized light in the left atrial wall (⫻ 140) (A), as well as in the thickened wall of epicardial vessels (arrow) (⫻ 350) (B).
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CASE REPORT MAUNEY ET AL INNOMINATE ARTERY PSEUDOANEURYSM
We concluded that amyloid deposition, which contributed to left atrial wall fragility, in addition to anticoagulation therapy, was responsible for the spontaneous intramural left atrial hematoma. Throughout our investigation, there has been no other reports of spontaneous intramural left atrial hematoma associated with systemic amyloidosis. We have experienced a very rare case of spontaneous intramural left atrial hematoma as one of the severe bleeding manifestations of systemic immunocytederived (AL) amyloidosis, implying that amyloid deposits induced the left atrial wall fragility. Nonetheless, hematoma resection, in the presence of a very fragile left atrial wall, followed by pericardial patch reconstruction, has proven to be successful.
References 1. Pepys MB. Amyloidosis, 4th ed, Vol 1. In: Samter M, ed. Immunological diseases. Boston/Toronto: Little, Brown and Company, 1988:631–74. 2. Dubrey SW, Cha K, Anderson J, et al. The clinical features of immunoglobulin light– chain (AL) amyloidosis with heart involvement. QJM 1998;91:141–57. 3. Yood RA, Skinner M, Rubinow A, Talarico L, Cohen AS. Bleeding manifestation in 100 patients with amyloidosis. JAMA 1983;249:1322– 4. 4. Jimenez JFD, Rufilanchas JJ, Pajuelo CG. Spontaneous left atrial haematoma. Int J Cardiol 1991;31:353– 6. 5. Schecter SO, Fyfe B, Pou R, Goldman ME. Intramural left atrial haematoma complicating mitral annular calcification. Am Heart J 1996;132:455–7.
Management of Innominate Artery Injury in the Setting of Bovine Arch Anomaly Michael M. Mauney, MD, David C. Cassada, MD, Aditya K. Kaza, MD, Stewart M. Long, MD, and John A. Kern, MD Department of Thoracic and Cardiovascular Surgery, University of Virginia Health System, Charlottesville, Virginia
Blunt injury to the aortic arch vessels is rare and can be life-threatening. Historically urgent repair of these injuries is emphasized. We describe the initial nonoperative management of a blunt injury to the brachiocephalic trunk in the setting of bovine arch anomaly, followed by delayed surgical management. (Ann Thorac Surg 2001;72:2134 – 6) © 2001 by The Society of Thoracic Surgeons
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e report the repair of an innominate artery injury in the setting of a bovine arch anomaly without the use of cardiopulmonary bypass. Although most series urge immediate repair, we describe the successful application of a delayed definitive treatment. Accepted for publication March 23, 2001. Address reprint requests to Dr Cassada, Department of Thoracic and Cardiovascular Surgery, University of Virginia Health System, MR4, Room 3111, PO Box 801359, Charlottesville, VA 22908-1359; e-mail:
[email protected].
© 2001 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
Ann Thorac Surg 2001;72:2134 – 6
A 39-year-old man was in a high-speed motor vehicle accident. Upon arrival his pulse was 115, blood pressure 130/80 mm Hg, and Glasgow Coma Score 3T (he was pharmacologically paralyzed and unresponsive on the ventilator). He had a large contusion over the left chest and shoulder, and his pulses were symmetric. A chest radiogram revealed widened mediastinum with a right pulmonary contusion and pneumothorax. After chest tube placement, the patient underwent a computed tomographic (CT) scan of the head which was negative for injury. Chest and abdominal CT revealed a large hematoma of the soft tissues of the neck and chest with extension into the superior mediastinum, a grade I splenic laceration, a right posterior acetabular fracture, and multiple right rib fractures. A thoracic arteriogram demonstrated a bovine arch (left common carotid artery taking origin from the brachiocephalic trunk), an avulsed left vertebral artery, and a pseudoaneurysm of the proximal brachiocephalic trunk. An initial plan of nonoperative therapy was chosen for several reasons. The pseudoaneurysm distal to the takeoff of the left common carotid combined with an occluded left vertebral artery placed his entire cerebral circulation at risk during application of a proximal clamp. Anticoagulation for a shunt to both distal common carotid arteries increased the risk of hemorrhage from the splenic laceration. Additionally, there was a risk of exacerbating brain injury given the initial uncertainty of his neurologic status, despite the normal head CT. Initial management consisted of blood pressure control to keep systolic blood pressure lower than 130 mm Hg, neurologic evaluations, and serial chest CT angiograms to follow the pseudoaneurysm. The patient was admitted and maintained on a labetalol drip. A CT angiogram of the chest obtained 12 hours after admission demonstrated a 11 ⫻ 17 mm pseudoaneurysm along the posterior aspect of the innominate artery just distal to the takeoff of the left common carotid artery (Fig 1A). The patient regained consciousness with a normal neurologic exam and was extubated. His blood pressure was controlled on oral -blockers. Repeat CT scans 5 days later and then 11 days postinjury showed no contrast extravasation or change in the pseudoaneurysm. He was discharged home 12 days postinjury on aspirin and -blockers. An outpatient chest CT scan 22 days postinjury demonstrated increasing size of the pseudoaneurysm to more than 20 mm (Fig 1B). Although the patient was normotensive and asymptomatic, it was decided to intervene surgically, given the risk for embolization or rupture. Median sternotomy was performed, and the pericardium was opened and suspended. The midline incision was extended onto the left neck, exposing the great vessels and allowing distal control of both common carotid arteries. Proximal control was obtained at the takeoff of the bovine trunk from the aorta. Pursestring sutures of 5-0 Prolene (Ethicon, Somerville, NJ) were placed in each common carotid artery. A pursestring pledget of 4-0 Prolene was placed in the proximal ascending aorta. Heparin was administered to achieve an activated clotting time of 250 seconds. A 10F wire-wound pediatric arterial cannula was secured in the ascending aorta. Each distal common carotid artery was cannulated with an 8F wire-wound cannula. Both were connected by a Y adapter to the aortic cannula. After careful removal of 0003-4975/01/$20.00 PII S0003-4975(01)02661-3
