Ann Thorac Surg 2000;69:946-948
© 2000 The Society of Thoracic Surgeons
Case Reports
Septic paradoxical embolus through a patent foramen ovale after pacemaker implantation
David E. Allie, MDa,
Mitchell D. Lirtzman, MDa,
Charles H. Wyatt, MDa,
Dennis A. Vitrella, MAa,
Craig M. Walker, MDa
a Cardiovascular Institute of the South, Medical Center of Southwest Louisiana, Lafayette, Louisiana, USA
Address reprint requests to Dr Allie, Cardiovascular Institute of the South, South Louisiana Clinical Research Foundation, 4212 W Congress St, Suite 2100, Lafayette, LA 70506
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Abstract
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A case of a septic paradoxic embolus due to an infected pacemaker lead associated with a patent foramen ovale (PFO) is described. Treatment consisted of immediate intracardiac embolectomy, pericardial patch closure of the PFO, total removal of the infected pacemaker lead and generator, and placement of a new permanent epicardial lead pacemaker system.
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Introduction
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Autopsy reports suggest that a patent foramen ovale (PFO) may occur in 11% to 35% of the normal population, with a 34.3% age-related incidence for ages 0 to 29 years, 25.4% for ages 30 to 79 years, and 20.2% for ages 80 to 99 years [1, 2]. Thompson and Evans [2] consecutively examined 1,100 autopsies and described a probe-patent foramen ovale (measuring 0.2 to 0.5 cm) in 29% and a pencil-patent foramen ovale (measuring 0.6 to 1.0 cm) in 6%. Infection remains the most common and serious complication after pacemaker implantation. Complete surgical removal of all hardware, including pacemaker leads, is required for total eradication of infection [3]. We describe a case in which a septic paradoxical embolus, due to an infected pacemaker lead and associated with a PFO, presented as a cerebrovascular accident (CVA).
A 61-year-old diabetic male presented with confusion and fever 6 weeks after dual-chamber mode, permanent pacemaker implantation. A transthoracic echocardiogram, performed 3 years previously, was normal. The pacemaker pocket showed no evidence of infection. The white blood cell count was 18,000 with a left shift. A chest roentgenogram revealed the leads to be in satisfactory position.
Twenty-four hours after presentation, the patient became lethargic, developed a right hemiplegia, and his temperature spiked to 39.5°C. A carotid ultrasound was normal.
A computed tomographic scan of the head, with and without contrast, revealed a left frontal hemispheric attenuation consistent with an embolic event. An echocardiogram revealed a normal functioning pacemaker. A transesophageal echocardiogram (TEE) revealed a long, freely mobile snake-like biatrial thrombus that appeared to be contiguous at the level of the atrial septum (Fig 1). There was no demonstrable atrial septal defect or PFO by TEE and the ejection fraction was 0.50. All cardiac valves were functioning normally, and there was no evidence of valvular vegetation. Vancomycin (1 g IV q 12 hours) and tobramycin (90 mg IV q 8 hours) were started along with intravenous heparin therapy. The patient was then transferred to our institute for evaluation.
Within 12 hours, the patient’s hemiplegia was nearly resolved, and a coronary angiogram revealed moderate coronary artery disease. A right heart catheterization and left ventriculogram were not performed. The patient was taken for immediate surgical exploration. Through median sternotomy, cardiopulmonary bypass (CPB), bicaval cannulation, and antegrade cold blood cardioplegia, the right and left atria were opened revealing a pacemaker lead attached to the lateral right atrial wall with a large friable sausage-shaped thrombus traversing a PFO into the left atrium where the thrombus became more cylindrical and friable (Figs 2–4 ). The entire thrombus was removed intact and cultured. The edges of the PFO were excised and the septal defect closed with a pericardial patch. Both pacemaker leads and generator were explanted and the wound irrigated, debrided, and closed primarily. A new dual-chamber pacemaker generator with permanent epicardial atrial and ventricular leads was placed.
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Fig 3. Transesophageal echocardiogram showing a biatrial thrombus extending through a patent foramen ovale.
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The patient was easily weaned off CPB, and an intraoperative TEE revealed no evidence of a PFO and normal valvular function. The postoperative course was uneventful and the patient was discharged on postoperative day 6. The operative cultures from both leads and thrombus were positive for staphylococcus epidermis. Blood cultures were negative on day 6, and a 6-week course of appropriate intravenous antibiotics was continued. The patient remains asymptomatic 18 months postoperatively.
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Comment
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Paradoxic embolism was first described by Cohnheim [4] in 1877, and refers to an arterial embolus through a right-to-left shunt at the cardiac level [5]. A PFO accounts for 70% of all right-to-left cardiac shunts. Other reported sources include a ventricular septal defect, Ebstein’s anomaly, pulmonary arteriovenous malformation, and a patent ductus arteriosis [5, 6].
With the introduction of TEE the ability to recognize intracardiac shunting has increased, leading to the description of a new clinical diagnosis of impending paradoxic embolus. It has been estimated that the incidence of cerebrovascular accidents in the United States exceeds 400,000 and several reports have shown that as high as 36% meeting the criteria for an embolic stroke had no demonstrable arterial or cardiac source [4].
A 1998 review article estimates that paradoxic emboli may account for as many as 47,000 strokes in the United States annually [1]. In 1985 Nellessen and associates [7] reported the first case of an impending paradoxic embolus diagnosed by TEE, and successfully corrected with operation. In an extensive English literature search from 1983 to 1997 by Meacham and colleagues [1], only 30 antemortum cases of impending paradoxic emboli were found reported without association with sepsis or infected pacemaker leads. In this report, we describe a case of an infected pacemaker lead presenting as a septic paradoxic embolus through a PFO and its surgical management.
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References
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Meacham R.R., III, Headly A.S., Bronze M.S., Lewis J.B., Rester M.M. Impending paradoxical embolism. Arch Intern Med 1998;158:438-448.[Abstract/Free Full Text]
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Thompson T., Evans W. Paradoxical embolism. QJM 1930;23:135-150.
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Wilhelm M.J., Schmid C., Hammel D., et al. Cardiac pacemaker infection. Ann Thorac Surg 1997;64:1707-1712.[Abstract/Free Full Text]
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AbuRahma A.F., Lucente F.C., Boland J.P. Paradoxical embolism. J Cardiovasc Surg 1990;31:685-692.[Medline]
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Loscalzo J. Paradoxical embolism. Am Heart J 1986;112:141-145.[Medline]
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Ward R., Jones D., Haponik E.F. Paradoxical embolism. Chest 1995;108:549-558.[Abstract/Free Full Text]
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Nellessen U., Daniel W.G., Matheis G., Oelert H., et al. Impending paradoxical embolism from atrial thrombus. J Am Coll Cardiol 1985;5:1002-1004.[Abstract]
Accepted for publication July 16, 1999.
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Abstract
Introduction
