This is the unique case of a hemodynamically stable 77-year-old man with significant cardiac history who underwent an uneventful extraction of a Citrobacter-infected and eroded pacemaker lead. The patient’s wife gave written consent after the procedure for publication of any aspect of his case. His postoperative course was acutely complicated by a sudden turn of events that began with respiratory failure and quickly progressed into disseminated intravascular coagulation (DIC), acute renal failure, shock liver, and ventricular tachycardic arrest. The acute release of endotoxins and purulent material into the bloodstream during the procedure led to an unfortunate course, which culminated with his eventual demise. This is the first case report of such a drastic turn of events after a routine pacemaker lead extraction.
A 77-year-old man with medical history significant for hypertension, diabetes mellitus, breast cancer, chronic renal insufficiency, sick-sinus syndrome, and myocardial infarction presented for extraction of pacemaker leads. The patient had developed a pacemaker pocket infection that was unresponsive to antibiotic therapy (ciprofloxacin 400 mg IV every 12 hours). He was afebrile, and his white blood cell count remained elevated at 15,300 cells/mm3 of blood. Cultures were positive for Citrobacter.
Preoperatively the patient was hemodynamically stable. Vital signs on presentation were 164/62 mm Hg, pulse 64 bpm, and oxygen saturation 96% on room air. On examination, he was awake and alert, oriented to person, place, and time. The patient had no murmurs noted on physical examination. Electrocardiogram showed normal sinus rhythm with an old inferior infarct.
General anesthesia was delivered using an induction regimen consisting of etomidate/fentanyl/midazolam and cis-atracurium for muscle relaxation. A radial arterial line was placed preinduction, and the case proceeded without complication. IV antibiotics consisting of vancomycin and gentamicin were dosed intraoperatively. The patient remained hemodynamically stable throughout the uneventful case. The patient was extubated at the end of the procedure after meeting all extubation criteria. Estimated blood loss was minimal. Fluid resuscitation was 1200 mL, and urine output was 350 mL over 3 1/2 hours.
En route to the recovery area, the patient became acutely agitated. He was transferred to the postoperative recovery room on 4 L nasal cannula. Approximately 1 hour postoperatively, he demonstrated increased agitation and tachypnea. The arterial blood gas showed a Po2 of 61 mm Hg despite 100% O2 by facemask and a developing metabolic acidosis. He was reintubated and placed on ventilatory support. Serial arterial blood gases showed a worsening metabolic acidosis with a pH of 7.27, bicarbonate 19 mmol/L, and base excess of −6. Profuse oozing was noted from his left chest surgical extraction site. The patient was transferred to the cardiac care unit for continued postoperative care.
In the cardiac care unit, hypotension ensued with a systolic blood pressure noted to be 65 mm Hg. The patient was started on pressor support including phenylephrine and vasopressin. Coagulation studies showed an elevated international normalized ratio of 2.3, prothrombin time (PT) 54 seconds, partial prothromboplastin time (PTT) 25.5 seconds, fibrinogen 61 mg/dL, fibrin split products >40 μg/dL, and a d-dimer >3999 μg/L requiring multiple transfusions. Laboratory values representative of shock liver demonstrated aspartate aminotransferase and alanine transaminase >1000 IU/L and acute renal failure with an increase of creatinine to 5.71 mg/dL. On postoperative day 1, a head computerized tomogram showed a right temporoparietal hypodensity and pontine lacunar stroke possibly because of an embolic event. Over the next few days, his clinical picture deteriorated with worsening renal failure requiring hemodialysis and unstable cardiac rhythms requiring increasing inotropic and pressor support, cardioversion, and even cardiopulmonary resuscitation. The patient died on postoperative day 6.
Over 250,000 pacemakers are inserted each year in the United States, and approximately 500,000 Americans are currently living with such a device implanted in their chest wall.1 Most of these procedures occur uneventfully, and insertion has been shown to be a low-risk procedure. However, in a small percentage, leads and/or devices must be removed because of infection or mechanical failure.2–4
Pacemaker infections are rare, and according to reports, infections develop in 0.13% to 19.9% of cases.4 The most prominent pathogens responsible for pacemaker infections are coagulase-negative staphylococci, Staphylococcus epidermidis, and Staphylococcus aureus. For those pacemakers that get infected, the appropriate management is removal of pacemaker device and leads, antibiotic therapy, and implantation of a permanent pacemaker in another location.2,4–6 Current management of lead extraction is guided by the Heart Rhythm Society’s North American Society of Pacing and Electrophysiology (NASPE) 2000 recommendations, which call for extraction in class 1 infections or those in which the lead cannot be severed in clean tissue.7 Although overall it has been shown to be a rather safe and effective procedure with reported clinical success rates of up to 97.6%, it is not without the risk of severe morbidity and mortality. In 1 large single-center study, a complication rate of 0.9% was reported with 1 postoperative death because of endocarditis in a total of 647 lead extractions.7
Although lead extraction has previously been shown to carry some inherent risk such as bleeding, perforation, valvular insufficiency, and thrombosis, there was no documentation of acute DIC leading to such a sudden demise after such a procedure.8 This was a particularly dangerous complication with an extremely fast onset. One should be aware that such events are possible whenever a patient with an infected lead presents for extraction and that aggressive efforts to minimize this outcome should be pursued.
In this case, extraction of infected pacemaker leads led to serious consequences and an untimely patient demise. The operative team should be aware that severe DIC can happen even after routine pacemaker lead extraction.
1. Maisel W, Moynahan M, Zuckerman B, Gross TP, Tovar OH, Tillman DB, Schultz DB. Pacemaker and ICD generator malfunctions: analysis of Food and Drug Administration annual reports. JAMA 2006;295:19016.
2. Buch E, Boyle NG, Belott PH. Pacemaker and defibrillator lead extraction. Circulation 2011;123:e37880.
3. Bracke F. Complications and lead extraction in cardiac pacing and defibrillation. Neth Heart J 2008;16(suppl 1):S2831.
4. Sohail MR, Uslan DZ, Khan AH, Friedman PA, Hayes DL, Wilson WR, Steckelberg JM, Jenkins SM, Baddour LM. Infective endocarditis complicating permanent pacemaker and implantable cardioverter-defibrillator infection. Mayo Clin Proc 2008;83:4653.
5. Farooqi FM, Talsania S, Hamid S, Rinaldi CA. Extraction of cardiac rhythm devices: indications, techniques and outcomes for the removal of pacemaker and defibrillator leads. Int J Clin Pract 2010;64:11407.
6. Sohail MR, Uslan DZ, Khan AH, Friedman PA, Hayes DL, Wilson WR, Steckelberg JM, Stoner S, Baddour LM. Management and outcome of permanent pacemaker and implantable cardioverter-defibrillator infections. J Am Coll Cardiol 2007;49:18519.
7. Kennergren C, Bjurman C, Wiklund R, Gäbel J. A single-centre experience of over one thousand lead extractions. Europace 2009;11:6127.
8. Malecka B, Kutarski A, Pietura R, Lelakowski J, Zabek A, Bednarek J, Szczerbo-Trojanowska M. Complications of dual-chamber pacing such as late purulent pacemaker pocket infection with broken and looped atrial lead, complicated by pulmonary embolism after transvenous lead removal: a case report. Polski Arch Med Wew J 2008;118:3225.