Successful management of multiple permanent pacemaker complications – infection, 13 year old silent lead perforation and exteriorisation following failed percutaneous extraction, superior vena cava obstruction, tricuspid valve endocarditis, pulmonary embolism and prosthetic tricuspid valve thrombosis
© Kaul et al; licensee BioMed Central Ltd. 2009
Received: 14 October 2008
Accepted: 24 February 2009
Published: 24 February 2009
A 59 year old man underwent mechanical tricuspid valve replacement and removal of pacemaker generator along with 4 pacemaker leads for pacemaker endocarditis and superior vena cava obstruction after an earlier percutaneous extraction had to be abandoned, 13 years ago, due to cardiac arrest, accompanied by silent, unsuspected right atrial perforation and exteriorisation of lead. Postoperative course was complicated by tricuspid valve thrombosis and secondary pulmonary embolism requiring TPA thrombolysis which was instantly successful. A review of literature of pacemaker endocarditis and tricuspid thrombosis along with the relevant management strategies is presented. We believe this case report is unusual on account of non operative management of right atrial lead perforation following an unsuccessful attempt at percutaneous removal of right sided infected pacemaker leads and the incidental discovery of the perforated lead 13 years later at sternotomy, presentation of pacemaker endocarditis with a massive load of vegetations along the entire pacemaker lead tract in superior vena cava, right atrial endocardium, tricuspid valve and right ventricular endocardium, leading to a functional and structural SVC obstruction, requirement of an unusually large dose of warfarin postoperatively occasioned, in all probability, by antibiotic drug interactions, presentation of tricuspid prosthetic valve thrombosis uniquely as vasovagal syncope and isolated hypoxia and near instantaneous resolution of tricuspid prosthetic valve thrombosis with Alteplase thrombolysis.
Pacemaker system infections can be generator pocket or lead infections and complicate 0.5 – 2 percent permanent pacemaker implantations . The usual predisposing causes of infection include haematoma, erosion, long duration of procedure, operator's inexperience and reexploration . Early infections are most commonly caused by staphylococcus aureus and late infections most commonly by staphylococcus epidermidis, although infections by staphylococcus lugudensis  streptococcus bovis, mitis and sanguis, pseudomonas , enterococci and fungi and even Mycobacterium fortuitum  have been described. Pacemaker infections present as local discharge, inflammation or abscess, erosion of part of the pacemaker system with secondary infection, or, more rarely, with endocarditis, sepsis and positive blood cultures. Pacemaker endocarditis refers to the presence of infective material in relation to the pacemaker system, in the veins leading up to the heart, or the chambers or the valves of the right heart. Pacemaker endocarditis is most commonly complicated by tricuspid valve vegetations , tricuspid regurgitation and occasionally by secondary pulmonary embolism . Rare complications include SVC thrombosis  tricuspid stenosis  and paradoxical emboli .
Our patient presented 18 years subsequent to his first pacemaker implantation with bilateral pacemaker pocket and lead infection with staphylococcus epidermidis, complicated by tricuspid valve and right ventricular endocarditis and further complicated by SVC obstruction due to partly the sheer load of huge vegetations surrounding the 4 pacemaker leads in the SVC and partly by the stenotic changes in the vena cava as evidenced by the extensive backfilling of the azygous system on the contrast CT. The infection of the pacemaker pocket and the lead and the subsequent endocarditis could have been predicted on the basis of previous three reexplorations on the right side, one for slipped lead, the second for erosion and the last for unsuccessful percutaneous lead extraction, and one on the left side for elective pulse generator change.
There is general consensus that once there is pacemaker pocket or lead infection, removal of the whole pacemaker system followed by a course of appropriate antibiotics results in the best prospect for long term eradication of infection [11–14, 7]. When pacemaker lead or pocket infection is complicated by vegetations on the leads, heart valves or chamber endocardium or when there is secondary pulmonary embolism, removal of the entire device is more urgently indicated. Pacemaker leads can be extracted percutaneously or after median sternotomy with cardiopulmonary bypass. Percutaneous extraction is preferably done under TOE guidance when there are no complicating factors like vegetations or endocarditis. Percutaneous lead extraction has been advanced by techniques initially described by Byrd [15, 16] and perfected by other operators later [12, 17, 18]. The technique essentially involves counter traction to the myocardium by a plastic sheath passed over the lead while traction is applied to the lead tip by a stylet which passes to the tip of the lead through a central channel in it and which locks it by uncoiling it. Percutaneous extraction can fail, or may be complicated by non fatal pulmonary embolism , avulsion of tricuspid valve leaflet  or lead tip fracture with resulting vegetation . TOE has been of value not only to diagnose the above complications, with the exception of PE, before the patient leaves the catheterization lab, but also to guide the mode of pacemaker lead removal. Generally lead removal by percutaneous traction in the presence of vegetations less than 1 cm is considered relatively safe, although one study described successful percutaneous traction in 9 out of 12 patients, with vegetations larger than 1 cm, with pacemaker endocarditis, with no post procedure secondary pulmonary embolism . Authors of one study of 53 patients with pacemaker endocarditis, out of which 29 had transvenous extraction with locking stylets and sheaths, reported one surgical conversion, no tamponade and no major pulmonary embolism. They recommended that those patients who have vegetations that might obstruct main pulmonary artery should have removal under cardiopulmonary bypass .
As a general rule, however, in pacemaker endocarditis complicated by lead, tricuspid valve or RA or RV vegetations, removal of pacemaker leads is best done through median sternotomy, employing cardiopulmonary bypass and debriding the right heart chambers and the tricuspid valve, under direct vision, of the infected vegetations and debris. This offers the best method of achieving long term eradication of infection from the chambers of heart. Although removal of infected pacemaker system without employing cardiopulmonary bypass, under inflow occlusion, has been described , the authors would not advocate this procedure except under exceptional circumstances. However, the author (PK) has removed a stuck right ventricular lead, in a different patient, through a purse string in the right atrial appendage, without taking recourse to cardiopulmonary bypass, in the absence of lead, chamber or valve vegetations, and with TOE monitoring. There has been one report of removal of a pacemaker lead sticking out of right atrium without cardiopulmonary bypass by using a purse string around the projecting lead .
Pacemaker endocarditis only rarely involves the tricuspid valve to the extent of destroying it and mostly debridement of vegetations from the valve and preservation of the valve itself suffices. However, occasionally excision of the tricuspid valve with or without valve replacement , tricuspid valve reconstruction with PTFE chordae  and balloon dilatation 4 years after pacemaker endocarditic tricuspid stenosis  have been described. Taira reported tricuspid valve stenosis related to subvalvar adhesion of a non infected loop of an excessively long ventricular lead  and Hagers reported acquired tricuspid stenosis in a patient with recurrent pacemaker lead endocarditis, further complicated by a paradoxical septic embolism through a PFO . Surgery for pacemaker endocarditis may be accompanied by additional procedures  apart from tricuspid valve surgery, including pulmonary embolectomy . Hong et al described removal of 6 entrapped endocardial pacemaker leads with concomitant redo coronary artery bypass grafting .
Lead perforation during implantation is a recognised but rare complication of transvenous pacemaker implantation. It may present by a rising stimulation threshold, an RBBB pattern from an RV lead, intercostal muscle or diaphragmatic contraction, friction rub after implantation, pericarditis, pericardial effusion, cardiac tamponade or rarely, no symptoms .
It was only at median sternotomy after dissecting the large granulomatous mass found adherent to the under surface of the sternum near the manubrium that it was realised that there had been a perforation of the right atrium with one of the right atrial leads, the lead having exited the right atrial appendage, and then migrated a considerable distance to lie adherent to the under surface of the sternum. This could only have happened at the time of the previous unsuccessful attempt at percutaneous extraction of the pacemaker leads which had been complicated by cardiac arrest after which the extraction was abandoned and a new pacemaker system implanted from the left side. Since these leads were not connected to the pulse generator which had been removed, the lead would have got further exteriorised with cardiac contractions without at the same time giving rise to frank bleeding into pericardial cavity. Obliteration of pericardial cavity by adhesions at sternotomy confirms this presumed course of events.
Presence of huge vegetations along the entire tract of the leads including right atrial and right ventricular endocardium and the tricuspid valve as well as the entangling of the tricuspid valve chordae with the RV leads mandated excision and replacement of tricuspid valve with a prosthetic valve.
There has been a tremendous improvement in prosthetic valve thrombosis in tricuspid position since Thorburn reported 20% incidence in monoleaflet models . Subsequent reports, corresponding to a mixture of newer valve models, showed incidence lower than 0.7% per patient year [30, 31]. Presentation may include fatigue, syncope, distended neck veins, signs of fluid retention, muffled valve clicks and middiastolic or pansystolic murmurs in tricuspid area. Confirmation by TTE requires presence of the following criteria: 1) high transvalvular gradients – mean of 6 mm Hg or higher, and peak of 15 mm Hg or higher 2) transvalvular gradients 50% or higher than observed before 3) visible thrombus on the prosthetic valve 4) inability to demonstrate 2 different mobile echoes representing the valve leaflets in a high quality image. Inability of the valve leaflets to either fully open or close on fluoroscopy employing multiple acquisition angles including the side view, with the disks parallel to the beam is generally considered indicative of a stuck valve. The diagnostic criteria for thrombosis on TOE were limited leaflet motion and/or visible thrombus .
The low velocity of blood across the tricuspid valve prosthesis makes it especially prone to thrombosis. There are well documented conditions that predispose to thrombosis. Probably the commonest is a sub therapeutic INR, with the mechanical tricuspid prosthesis requiring an INR in the range of 3 to 4. A change to low molecular weight heparin in place of heparin prior to surgery is yet another common predisposing cause . Hypercoagulable states like pregnancy , hypereosinophilic syndromes , malignancy , low flow states like Ebstein's anomaly  and use of Biomedicus Centrifugal Pump , drugs like Rifampicin, Dicloxacillin , HRT , Phenytoin , mechanical rather than bioprosthetic valves , all predispose to a greater likelihood of developing prosthetic valve thrombosis.
Our patient, who was continued on vancomycin and rifampicin postoperatively, required doses of warfarin in excess of 15 mg daily, in all probability due to the known facilitation of the induction of warfarin degradation by rifampicin. He presented with intermittent syncope and profound hypoxia responsive to increasing inspired fio2. TTE, TOE and fluoroscopy were clearly confirmatory. In addition, contrast CT scan demonstrated secondary pulmonary embolism and residual SVC obstruction. Clinical, radiological and echocardiographic resolution after Alteplase thrombolysis was instantaneous after one week of aggressive anticoagulation failed.
Although tricuspid valve thrombosis may occasionally respond to high intensity anticoagulation, thrombolysis should be the first line of treatment in these patients and is almost always successful. Failure of thrombolysis in symptomatic patients, particularly when both leaflets are stuck, is an indication of surgery  which shall usually involve re-replacement, and rarely, thrombectomy with or without rotation of the disk.
We believe this case report is unusual on account of the following: 1. The fact that a perforated right atrial lead lying more than an inch outside right atrial appendage was discovered 13 years after the attempted unsuccessful removal 2. Presentation of pacemaker endocarditis with a massive load of vegetations along the entire pacemaker lead tract in SVC, right atrial endocardium, tricuspid valve and right ventricular endocardium, leading to a functional and structural SVC obstruction 3. Requirement of an unusually large dose of warfarin postoperatively occasioned, in all probability, by antibiotic drug interactions 4. Presentation of tricuspid prosthetic valve thrombosis uniquely as vasovagal syncope and isolated hypoxia and near instantaneous resolution of tricuspid prosthetic valve thrombus with Alteplase thrombolysis.
Written informed consent was obtained from the patient for publication of this case report and the accompanying images. A copy of the written consent is available for review by Editor-in Chief of the journal.
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