Prevention and Management of Procedural Complications

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25 Prevention and Management of Procedural Complications

Oussama Wazni, Bruce L. Wilkoff

The cardiac implantable electronic device (CIED) has become an integral part of both cardiology and the overall practice of medicine. The indications for CIED implantation have expanded in particular as a result of the documented mortality benefit from implantable defibrillators and cardiac resynchronization therapy (CRT) in complementary population studies in multicenter, randomized clinical trials. With the increasing number of indications for CIED implantation, the need to recognize the adverse effects associated with these devices and to develop methods to minimize complications and patient morbidity are greater than ever. This chapter addresses the issues surrounding implantation techniques and proposes strategies to reduce CIED-related morbidity. The acute management of implant complications is also addressed.

image Choice of Physician

A primary issue regarding morbidity associated with CIED implantation is which medical professional should implant and follow up in these patients. As the indications for CIEDs have broadened, and an increasing number of patients are considered for implantation, physicians of various specialties are being called on to implant the devices and manage the postimplantation care of these patients. Curtis et al.,1 using data from the National Cardiovascular Device ICD Registry, found that the rates of overall complications and major complications were lowest among procedures carried out by electrophysiologist (EP) physicians (3.5% and 1.3%, respectively) and highest among those performed by thoracic surgeons (5.8% and 2.5%). Importantly, EP physicians had the lowest rates of major complications, including cardiac arrest, lead dislodgment, and pneumothorax. In this study, the choice of device was also influenced by the specialty of the physician performing the procedure. Non–EP physicians failed to recommend implantation of an indicated cardiac resynchronization implantable cardioverter-defibrillator (ICD) device (CRT-D).1 In a different study, Al-Khatib et al.2 also identified implantation by non–EP physicians as being associated with an increased incidence of complications.2

image Implantation-Related Complications

Implantation technique is an important determinant of subsequent complications. In most centers a pocket for the generator is made, after which venous access is obtained. However, the formation of the pocket is a crucial part of the procedure, and several principles are useful to prevent future device complications. Through this venous access, a lead is placed, then connected to a device placed in the pocket. Some implantation techniques result in excessive stress on the lead and premature lead failure.

Depending on the physical characteristics of the lead, in terms of both materials and construction, certain approaches to subclavian vein access have been associated with subclavian crush, where the lead is compressed in the space between the clavicle and the first rib. This entrapment of the lead in the subclavius muscle, in the periosteum of the clavicle, or just through the very narrow space that occurs with medial subclavian vein puncture is completely dependent on the proceduralist’s approach to accessing the central circulation. In addition, management of suture tie-down sleeves with overly tight ligatures can damage the outer insulation, inner insulation, or conductor coils, particularly in coaxial leads with a polyurethane inner insulation.3,4

In response to the concerns about medial access of the subclavian system, physicians began to use more lateral access techniques. Unfortunately, extreme lateral access places different stresses on the lead body. Recently popularized implantation techniques within the last 10 years employ access to the subclavian venous system at the point where the axillary vein crosses the first rib, immediately lateral to the clavicle. However, if a more lateral approach into the axillary vein over the second or third rib stresses the leads by a different mechanism. The extreme angle of the lead on entry to the axillary vein at this lateral but also more posterior position, as well as the resultant acute anterior bend following the trajectory of the vein, exacerbated by the suture tie-down sleeve fixing the lead to the muscle, places a torque and compression fatigue stress on the lead conductors. This is most often observed with leads constructed with a thin body, coaxial construction, and active-fixation inner coils (Figs. 25-1 and 25-2).

image

Figure 25-1 Intrathoracic (thoracic inlet) introducer approaches.

Two introducer approaches, medial and lateral, demonstrate the issues associated with inserting introducers in the intrathoracic portion of the subclavian vein. The medial approach is safe, but the leads are subjected to crush (insulation failure) and binding (conductor coil fracture). The lateral approach is free from lead crush and binding, and it is safe when the needle is properly directed. Because of variation in chest wall anatomy, extensive experience is needed to avoid misdirection with the introducer needle and potentially lethal complications (e.g., transpulmonary vein implantation).

image

Figure 25-2 Lead stress and fracture.

A, With a turning radius less than 0.5 inches (R1), there is increased cyclic bending stress on the lead compared with a turning radius greater than 0.5 cm (R2). B, Note vein and medial access causing fracture of lead.

The more medial axillary vein puncture, over the first anterior rib, avoids both subclavian crush and second-rib fatigue fractures.5 The axillary vein can be accessed under fluoroscopy over the first rib and the area probed posterolaterally until the vein is punctured. Alternatively, venography or ultrasound can be used to guide lead implantation6 (see Chapter 21).

At implantation, the lead must be treated gently, and any mechanical stress should be avoided. Even overuse of the helical screw mechanism can place additional stress on the conductor. It is usually difficult to nail down the precise trauma that later causes a lead failure, but the time of implantation is a relatively dangerous time for a lead and is often a contributor to the ultimate failure. Prolapsing of the lead on itself should not be performed unless absolutely necessary. Again, although difficult to prove, this practice has been implicated in early lead failure, particularly with lower-profile ICD leads.7–12

In addition to placing the lead in the heart and affixing the suture sleeve, making the connections to the CIED is another potential problem. Utmost vigilance should be exercised when the leads are connected to the device, to avoid the need for surgical revision, reentering the pocket and increasing the risk of infection. In the Replace trial, five patients needed revision because of generator-lead interface problem, such as loose set screw or misconnected leads.13 With the introduction of the DF-4 ICD leads, in which the two DF-1 and one IS-1 connectors are replaced with a single connector, the incidence of connection error should be significantly reduced.14 Currently, an SJ-4 lead is available and is in clinical use (Fig. 25-3).

image

Figure 25-3 ICD lead connector.

Single DF-4 connector replaces three-pole connector of an ICD lead.

image Procedural Complications

Lead Dislodgment

Lead dislodgment is the most common complication associated with CIEDs (1.6%-4.4% of cases), with atrial lead dislodgment accounting for most cases. In the MOST trial of more than 2000 patients, Ellenbogen et al.15 found atrial dislodgment in 1.7% of patients in the first 30 postimplant days.15 To prevent dislodgment, it is important to have an adequate intrinsic signal and to ensure contact to the myocardial wall. This is partly assessed by viewing a modest current of injury in the unfiltered electrogram, in addition to the appearance on fluoroscopy. This has the appearance of a QRS complex with ST-segment elevation before fixation of the active helix into the myocardium. Appropriate slack on the lead is also important, to allow for settling of the device when the patient is upright. There may be micro- or macro-dislodgment. Micro-dislodgment has been defined as when there is loss of capture and sensing without radiographic evidence of dislodgment. Macro-dislodgment can be detected by radiography. Lead dislodgment requires reopening the pocket and repositioning of the dislodged lead to ascertain satisfactory function. However, it is best to reaccess the vein, remove the dislodged lead, and ensure that there is no clot or tissue or damage to the lead before reinsertion.

Pneumothorax

Inadvertent entrance into the pleural space, especially with the introducer access technique, can lead to pneumothorax (0.7%-2% of cases).1,2 This is related to the experience of the implanter and also the level of difficulty obtaining access. This complication can be mitigated by using an extrathoracic approach with the introducer technique, accessing the axillary vein over the first rib, which acts as a barrier against entering the lung. Pneumothorax should not occur when using the cephalic vein cutdown technique. Most patients with pneumothorax are asymptomatic and are diagnosed on the postimplant chest radiograph. In patients with a sizable pneumothorax, cardiothoracic surgery should be consulted for possible chest tube insertion, in addition to administering high-flow oxygen. Tension pneumothorax should be recognized as a potential cause of sudden hemodynamic compromise during device implantation. Tension pneumothorax should be treated immediately with a chest tube.

Hemothorax

Hemothorax is rare and is usually caused by injury to the great vessels. If arterial access is obtained, pressure should be applied for several minutes. Advancing the wire into the inferior vena cava (IVC) below the diaphragm before enlarging the defect in the vessel with the introducer ensures that the artery is not cannulated. Surgical intervention will depend on the degree of injury and hemodynamic instability. Axillary access is always extrathoracic and therefore amenable to manual compression. A more medial needle stick, especially if arterial, can cause uncontrollable bleeding, especially if the site is intrathoracic. This is another reason that the extrathoracic approach to access is recommended.

Perforation

Perforation of the great vessels is very rare during implantation and is more common with lead extraction. Ventricular perforation is rare and reported to occur in 0.3% to 1% of CIED cases7,11,16,17 (Fig. 25-4). Most are self-limited with no sequelae. Acute tamponade is extremely rare but should be quickly recognized as a cause of hemodynamic compromise and easily diagnosed by bedside echocardiography or with fluoroscopy; the enlarged cardiac silhouette is associated with minimal contraction. Immediate pericardiocentesis should be performed and surgical intervention sought if bleeding does not stop.

image

Figure 25-4 ICD lead perforation.

The tip is in the epicardial fat.

Most cases of perforation manifest after the procedure with complaints of chest pain, pleurisy, and at times extracardiac pacing. Perforation also may manifest as a change in sensing and pacing characteristics. Delayed perforation has been a concern with the small-profile ICD and pacemaker leads, although careful analysis did not confirm the incidence of perforation.11,17–19 However, when there is a delayed perforation, days to months after implantation, the lead should be extracted with surgical backup in the unlikely event of acute tamponade. According to most reported cases and from experience at our institution, extraction of such perforating leads is uneventful, and reimplantation can be performed at the same time.18 Implantation at the right ventricular septum is associated with less risk of perforation.20 This can be achieved using a stylet with a posteriorly angulated bend.21

Pocket Hematoma

Pocket hematoma usually occurs acutely after implantation. The source of bleeding may be the pocket itself or backbleeding from the vein around the lead entry site. Hemostasis may be achieved using electrocautery while creating the pocket. Digital pressure at the lead entry site usually controls backbleeding; otherwise, purse-string or figure-of-eight suture placement may be needed.

The risk of hematoma is higher in anticoagulated patients, especially when heparin is restarted after the procedure. The use of antiplatelet therapy and anticoagulation may increase the risk of hematoma. In one study, only 4.2% of patients with no antiplatelet or anticoagulation developed hematoma, whereas up to 18% of patients with uninterrupted clopidogrel developed hematoma at the pocket site. Patients taking warfarin (Coumadin) only had a 6.9% risk. Combinations of these increased the risk drastically;22 24% of patients with ongoing aspirin and clopidogrel treatment developed hematoma.23 The use of periprocedural heparin (enoxaparin) was associated with increased risk of bleeding compared with continuation of warfarin (INR >1.5).24 The use of dual-antiplatelet therapy presents a challenge, particularly in that it is difficult to stop these agents in patients with drug eluting stents. Warfarin use seems to be less of an issue. Giudici et al revealed that discontinuation of warfarin was associated with same risk as continuation of anticoagulation with a mean international normalized ratio (INR) of 2.5.25 Most hematomas are treated conservatively. Evacuation of hematoma may be needed with continued bleeding, severe tension, and pain. The optimal approach to patients undergoing therapy with the new factor X antagonists, such as dabigatran, has not been directly approached in those with planned device procedures, but it may provide an alternative pathway to a bridging anticoagulation approach.

Vein Thrombosis

Symptomatic venous thrombosis occurs in up to 5% of patients.26,27 However, the incidence of superior vena cava (SVC) obstruction with symptomatic SVC syndrome is rare, approximating 2 per 1000 implants. Treatment is usually based on symptom relief. Acute deep vein thrombosis (DVT) after implantation can occur in up to 40% of cases, but most are asymptomatic. When subclavian occlusions have not presented with symptoms, they are usually detected when a new lead is required because of lead dysfunction or mode-upgrade procedures. In patients with symptoms, arm elevation is advised and, depending on the severity, anticoagulation started with either warfarin alone or with heparin. Again, the use of factor X antagonists has not been explored.

image Pain

Occasionally, patients complain of pain in or near the implant pocket. History and physical examination are the only diagnostic tools available. Regardless of the cause, pain is a difficult complication to manage. Acutely, some patients heal with no complaints of pain; others have severe pain. The cause of pain may be nerve entrapment, inflammation of the scar tissue, migration, or injury to the musculoskeletal system. Pain associated with no physical signs may be related to nerve entrapment; the best approach for successful treatment is to remove the generator and leads, abandon the site, and reimplant on the opposite side. Chronic pain or pain that starts after implantation is often an indication of infection and should be treated accordingly.

image Infection

Increased implantation of CIEDs has led to a greater awareness of implant infection. The increasing incidence of CIED infections, now reported at 1% to 7%, presumably is a result of the increasing number of nonprimary implantations (e.g., generator changes, upgrades). Infection occurs in 1.9 to 2.11 per 1000 device-years, with most infections being pocket infections.28 CIED infection is a serious problem with high morbidity and mortality. In the LExICon study the all-cause in-hospital mortality in infected patients was 3%, with the highest mortality associated with device-related endocarditis (4.3%).29 Tarakji et al.30 demonstrated all-cause mortality as high as 4.6% in infected patients. After extraction of the infected device, mortality remained high in that cohort, with 1-year mortality after removal of 17%. One-year mortality was significant in both the pocket infection group (12%) and the endovascular infection group (25%).

Risk Factors

Patient-associated risk factors for infection include diabetes mellitus, renal failure, and heart failure. In one study, oral anticoagulation with the development of pocket hematoma increased the risk of infection, although this has not been confirmed in larger studies.31

Procedural factors associated with infection are reoperation, prolonged procedure time, and previous temporary pacing. In the long term, generator changes and device upgrades continue to pose significant risk for increasing rates of infection.28

Prevention

Because of the high morbidity and mortality associated with CIED infection, especially in the heart failure population, who also tend to have comorbidities, prevention of infection is probably the most important aspect of device therapy. Universal infection prevention techniques, including hand scrubbing, procedure room and instrument preparation, and double gloving should be observed during CIED implantation. Skin preparation is crucial, but even with skin preparation and periprocedural antibiotics, the overall infection rate during replacement procedures was 1.4% in the Replace Registry.13 Preimplantation antibiotic administration is standard care and has been recently reinforced. In a randomized double-blind study of 649 patients, de Oliveira et al.32 demonstrated that 1.0 g of cefazolin given before CIED implantation was associated with an 80% decrease in infections at 6-month follow-up. The infection rate was 0.64% in the cefazolin group and 3.28% in the control group (P = .016). All infections were caused by Staphylococcus species, with about two-thirds being S. aureus.32

The choice of antibiotic agent depends on the patterns of infections and antibiotic resistance in individual treatment centers. Approximately half of all device-related infections are caused by methicillin-resistant S. aureus (MRSA). At our institution, we recommend the use of vancomycin for preoperative antibiotic prophylaxis. We also screen patients for MRSA using nasal swabs and, if the test is positive, pretreat patients with mupirocin. Although not proven in the literature on CIED use, several studies of patients undergoing cardiac surgery have shown that treatment of carriers of MRSA with mupirocin decreases the rate of postoperative infection.33 No matter what antibiotic is used, it is important to have the infusion completed by the time of the surgical incision and initiated within 1 hour if agent is not vancomycin and within 2 hours if vancomycin.34–36 Not only is this important to reduce the incidence of postsurgical infections. but it is a U.S. national quality measure.37

Presentation

The most common presentation of infection continues to be pocket infection with a variety of appearances (Figs. 25-5 to 25-9). In a recent study by Tarakji et al.,30 89% of patients presented with pocket infection compared to patients with systemic signs of infection with an intact pocket. This is in line with historical data. Patients with pocket infection tend to present earlier, whereas patients with systemic infection have more comorbidities, such as heart failure, renal failure, diabetes, or previous episodes of endocarditis.

image

Figure 25-5 Erythema and fluctuance.

These are signs of infection, not an allergic reaction.

image

Figure 25-6 Fat necrosis.

This presentation of infection occurs even in the absence of erythema or discharge. Compromised blood supply to the subcutaneous tissue and skin causes a decrease in the supply of nutrients to the cells. In the early stages (pre-erosion), the fatty tissue begins to lose mass.

image

Figure 25-7 Tissue pocket erosion.

During the latter pre-erosion stages, the tissue becomes ischemic, and skin changes occur. The last stage before erosion is adhesion of the skin to the fibrous tissue pocket. Complete loss of blood supply to the skin results in gangrene of the skin before erosion.

image

Figure 25-8 Erosion of leads through the implant pocket.

image

Figure 25-9 Purulent discharge from implant-induced infection.

Pocket infection has a diverse and continuum of presentation. Although frank, purulent discharge is the obvious presentation, pocket infection should be considered present with warmth, erythema, dehiscence, and skin adherence. Erosion of the overlying skin is by definition a pocket infection. It is important to recognize that patients with pocket infection can also harbor endovascular vegetations (Fig. 25-10), Tarakji et al.30 reported that vegetations were detected in almost half the patients (56) in whom transesophageal echocardiography (TEE) was performed in a group of 241 patients with pocket infection. Klug et al.35,38,39 reported evidence of intravascular system involvement in at least 88% of patients with pocket infection. As such, as deduced by the Cleveland Clinic group, pocket infections should be considered a manifestation of an infected system encompassing endovascular infection, rather than only a localized phenomenon.30 CIED infection can also have systemic manifestations, including fever, chills, endocarditis, and persistent bacteremia.

image

Figure 25-10 Transesophageal echo revealing a large vegetation.

Bacteriology

Staphylococcus species cause most implant infections, with some series reporting 80%. In cases of coagulase-negative staphylococcal infection, it is important to rule out contamination by repeat cultures. Organisms such as Pseudomonas, Klebsiella, Proteus, and Enterococcus are seen less frequently (8%). Fungi and acid-fast mycobacteria are present on rare occasions. Some of these organisms may have caused the infection, and some may be secondary contaminants (e.g., yeast). Infections caused by a mycobacterium are rare, dangerous, and difficult to treat.40–47

Patterns of antibiotic resistance differ among patient situations or series, with up to 50% of Staphylococcus spp. being methicillin resistant. Infection with gram-negative bacteria, Candida, and fungi is rare compared to Staphylococcus spp. The most plausible pathogenesis is introduction of the microorganisms during the procedure, whether during the primary implantation or subsequent instrumentation. The most likely source is the patients’ skin flora.

Management

Superficial infection usually presents as a stitch abscess or a superficial incisional infection that does not seem to involve the device. This may be treated with oral antibiotics that cover staphylococci, for 1 week to 10 days.

Staphylococcal bacteria are the most common pathogen on entering the pocket and form a protective biofilm that adheres to the insulation and metal of the devices. This makes these infections resistant to the patients’ immune system and antibiotics. In certain cases, when a patient is not a candidate for extraction, long-term suppression with antibiotics may be warranted. In most patients the definitive treatment of CIED infection is extraction of all the CIED system. Treatment with antibiotics according to susceptibility is necessary but is not sufficient. Because most infections are caused by staphylococci, empiric therapy with vancomycin should be started until antibiotic susceptibility on blood cultures are available. If there is only pocket erosion with no frank purulence, treatment for 1 week to 10 days may be sufficient. All other cases should be treated with parenteral antibiotics for at least 2 weeks. Treatment with antibiotics alone may pose significant risk to patients, since this would expose them to longer periods of uncontrolled infection, spread, and possible seeding of distant structures.

image Measuring Outcomes and Quality Improvement

Clearly, it is essential that every EP laboratory have a practical quality assurance program in place. This program will help in tracking and measuring outcomes. The program could entail a procedural database that will capture complications and possibly a registry that will follow the patients after discharge. Also, such a program should include the capability of remote monitoring of the implanted devices. The goal should be continuing quality improvement in procedures and in follow-up of patients with implantable cardiac devices. Attention to detail, measuring outcomes, and continuous improvement in techniques are the fundamentals that ensure consistent quality care.

References

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23 Kutinsky IB, Jarandilla R, Jewett M, et al. Risk of hematoma complications after device implant in the clopidogrel era. Circ Arrhythm Electrophysiol. 2010;3:312-318.

24 Tompkins C, Cheng A, Dalal D, et al. Dual antiplatelet therapy and heparin “bridging” significantly increase the risk of bleeding complications after pacemaker or implantable cardioverter-defibrillator device implantation. J Am Coll Cardiol. 2010;55:2376-2382.

25 Giudici MC, Paul DL, Bontu P, et al. Pacemaker and implantable cardioverter-defibrillator implantation without reversal of warfarin therapy. Pacing Clin Electrophysiol. 2004;27:358-360.

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27 Oginosawa Y, Abe H, Nakashima Y. The incidence and risk factors for venous obstruction after implantation of transvenous pacing leads. Pacing Clin Electrophysiol. 2002;25:1605-1611.

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29 Wazni O, Epstein LM, Carrillo RG, et al. Lead extraction in the contemporary setting: the LExICon study: an observational retrospective study of consecutive laser lead extractions. J Am Coll Cardiol. 2010;55:579-586.

30 Tarakji KG, Chan EJ, Cantillon DJ, et al. Cardiac implantable electronic device infections: presentation, management, and patient outcomes. Heart Rhythm. 2010;7:1043-1047.

31 Lekkerkerker JC, van Nieuwkoop C, Trines SA, et al. Risk factors and time delay associated with cardiac device infections: Leiden device registry. Heart. 2009;95:715-720.

32 De Oliveira JC, Martinelli M, Nishioka SA, et al. Efficacy of antibiotic prophylaxis before the implantation of pacemakers and cardioverter-defibrillators: results of a large, prospective, randomized, double-blinded, placebo-controlled trial. Circ Arrhythm Electrophysiol. 2009;2:29-34.

33 Trautmann M, Stecher J, Hemmer W, et al. Intranasal mupirocin prophylaxis in elective surgery: a review of published studies. Chemotherapy. 2008;54:9-16.

34 Sohail MR, Uslan DZ, Khan AH, et al. Management and outcome of permanent pacemaker and implantable cardioverter-defibrillator infections. J Am Coll Cardiol. 2007;49:1851-1859.

35 Klug D, Balde M, Pavin D, et al. Risk factors related to infections of implanted pacemakers and cardioverter-defibrillators: results of a large prospective study. Circulation. 2007;116:1349-1355.

36 Da Costa A, Kirkorian G, Cucherat M, et al. Antibiotic prophylaxis for permanent pacemaker implantation: a meta-analysis. Circulation. 1998;97(18):1796-1801.

37 Centers for Medicare and Medicaid Services (CMS): Specifications manual for national hospital inpatient quality measures, version 3, 2009.

38 Klug D, Wallet F, Kacet S, et al. Detailed bacteriologic tests to identify the origin of transvenous pacing system infections indicate a high prevalence of multiple organisms. Am Heart J. 2005;149(2):322-328.

39 Klug D, Wallet F, Kacet S, et al. Involvement of adherence and adhesion Staphylococcus epidermidis genes in pacemaker lead-associated infections. J Clin Microbiol. 2003;41:3348-3350.

40 Sharma S, Tleyjeh IM, Espinosa RE, et al. Pacemaker infection due to Mycobacterium fortuitum. Scand J Infect Dis. 2005;37:66-67.

41 Verghese S, Mullaseri A, Padmaja P, et al. Pacemaker implant site infection caused by atypical mycobacteria. Indian Heart J. 1998;50(2):201-202.

42 Toda H, Sato K, Iimori M, et al. [A case of Mycobacterium goodii infection with isolation from blood and a pacemaker lead]. Kansenshogaku Zasshi. 2006;80:262-266.

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47 Chrissoheris MP, Kadakia H, Marieb M, et al. Pacemaker pocket infection due to Mycobacterium goodii: case report and review of the literature. Conn Med. 2008;72:75-77.

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