Physical Address

304 North Cardinal St.
Dorchester Center, MA 02124

Prevention and Management of Procedural Complications


Introduction

Cardiac implantable electronic devices (CIEDs) have proven to be an invaluable tool in the practice of cardiology, and implantation rates continue to rise. For this reason, the number of CIEDs in use and the inevitable complications associated with these devices have also increased. The knowledge and techniques associated with both CIED implantation and the management of associated complications, including transvenous lead extraction, have advanced significantly. This chapter addresses CIED-related complications in addition to the techniques available for preventing and managing these complications. The complications addressed will be divided into two main categories: infectious and noninfectious complications.

Implantation Technique and Related Complications

Use of an appropriate implantation technique is perhaps the most important way to prevent subsequent complications. Typically, a pocket for the generator is formed, and next venous access is obtained. The formation of the pocket is a crucial part of the procedure. Proper technique and attention to detail during this step can prevent future complications. One or multiple leads are placed through the venous access, then are connected to the device and placed in the pocket. Certain implantation techniques can result in excessive stress on the leads and result in premature lead failure.

Perhaps the portion of the implant procedure with the greatest potential for acute and chronic complications is venous access. Medial subclavian vein puncture can potentially result in subclavian crush, where the lead is compressed in the space between the clavicle and the first rib leading to mechanical failure of the lead. This entrapment of the lead in the subclavius muscle, in the periosteum of the clavicle, or through the very narrow space between the clavicle and first rib, is dependent on the approach used for central venous access and thus potentially preventable. It is not uncommon that during lead extraction procedures, the leads can be seen penetrating a calcified costoclavicular ligament ( Fig. 33-1 ).

Figure 33-1, Leads penetrating a calcified costoclavicular ligament.

Accessing the venous system from a more lateral approach (where the axillary vein crosses the first rib immediately lateral to the clavicle) may eliminate the risk for this complication. However, this approach can present a different set of issues with concern to lead integrity. Axillary vein access obtained over the second or third rib can place significant stress on the lead. The axillary vein is in a more posterior location laterally, and venous access at this location results in an extreme angle of the lead on entry to the axillary vein. This creates an acute anterior bend in the lead following the trajectory of the vein and is exacerbated by the suture tie-down sleeve fixing the lead to the muscle. This places a large amount of torque and compression fatigue stress on the lead conductors. This can be of particular importance in leads with a thin body, coaxial construction, and active-fixation inner coils. For these reasons, medial axillary vein access (over the first rib) is preferable because it minimizes the risk of subclavian crush and second-rib fatigue fractures. Access can be safely obtained in this area by probing posterolaterally over the first rib with fluoroscopic guidance. If this method is unsuccessful, contrast venography or ultrasound can be employed to assist with vascular access ( ).

In cases of lead failure, it can be challenging retrospectively to determine which particular trauma compromised the integrity of the lead. However, there are a few portions of the implant procedure which deserve mention in order to prevent potential problems. The securing of suture tie-down sleeves with overly tight ligatures can damage the outer insulation, inner insulation, or conductor coils, particularly in coaxial leads with polyurethane inner insulation. Also during manipulation of the lead mechanical stress should be avoided. Overuse of the helical screw mechanism can place unnecessary stress on the conductor. Similarly, prolapsing the lead on itself should be avoided whenever possible to prevent mechanical stress. It is challenging to prove, but these practices have been associated with early lead failure, particularly with lower-profile implantable cardioverter-defibrillator (ICD) leads.

Finally, care must be exercised when connecting the leads to the CIED. Vigilance must be exercised during this seemingly innocuous portion of the procedure because no excuse exists for misconnected leads or loose set screws. Early reentry into the pocket places the patient at increased risk of infection. The introduction of the DF-4 ICD lead, in which the one IS-1 and two DF-1 connectors are replaced with a single connector, makes the potential for connection errors significantly smaller.

Noninfectious Complications

The complications associated with CIED implantation can be divided into acute and chronic complications ( Table 33-1 ).

TABLE 33-1
Acute and Chronic Device Complications
Acute Complications Chronic Complications
Dislodgement Dislodgement
Perforation Perforation
Venous thrombosis Venous thrombosis/stenosis
Pneumothorax Pain
Hemothorax Migration (twiddler syndrome)
Hematoma

Lead Dislodgement

The most common complication seen with CIED implantation is lead dislodgement (1.6% to 4.4% of cases), with atrial lead dislodgment accounting for the majority of cases. Lead dislodgement can be either in the acute or chronic setting. Acutely, the problem is commonly related to suboptimal attachment of the lead to the myocardium or excessive patient movement (raising the arm above the shoulder on the implant side too soon after the procedure). Intravascular procedures (e.g., right heart catheterization or central venous catheter placement) can result in lead dislodgement in either the acute or chronic setting. In the Mode Selection Trial in Sinus Node Dysfunction (MOST) involving over 2,000 patients, Ellenbogen et al reported atrial lead dislodgment in 1.7% of patients in the first 30 days following implantation. It is important to have an adequate intrinsic signal and to ensure sufficient contact to the myocardial wall in order to prevent dislodgement. This is assessed by viewing a modest current of injury in the unfiltered electrogram, in addition to the appearance on fluoroscopy. It cannot be over emphasized how important appropriate slack on the lead is to prevent tension on the leads and dislodgement. This allows for settling of the device when the patient is upright. Lead dislodgement comes in two varieties: microdislodgment or macrodislodgment. Microdislodgment is defined as loss of capture and sensing without radiographic evidence of dislodgment. Macrodislodgment refers to dislodgement that can be detected radiographically. In either case, the pocket must be reopened and the dislodged lead repositioned to obtain satisfactory function. It is best to reaccess the vein, remove the dislodged lead, and inspect it before repositioning. This allows for identification of damage to the lead or clot/tissue at the lead tissue interface that may preclude adequate lead fixation/function.

Perforation

Thankfully, perforation of the great vessels is quite rare during lead implantation, although it is somewhat more common with lead extraction. Ventricular perforation is also rare and has been reported to occur in <1% of CIED implantations. Perforations can occur in any chamber of the heart, including the right atrium ( Fig. 33-2 ), right ventricle ( Fig. 33-3 ), and coronary sinus ( Fig. 33-4 ). Most perforations are self-limited and have no clinically significant sequelae. It is quite possible that more implantations result in perforation than is clinically appreciated, but that these perforations go unnoticed because they do not result in symptoms, hemodynamic changes, or abnormalities of device function. Cardiac tamponade is extremely rare but should be at the forefront of any physician's mind during or immediately following device implantation if hemodynamic compromise develops. Pericardial effusion with impending tamponade must be quickly recognized and treated to avoid cardiac arrest. The diagnosis can be made with bedside echocardiography or fluoroscopy (enlarged cardiac silhouette with minimal or no movement of the left heart border). Initial management entails emergent pericardiocentesis, with surgical intervention required only if bleeding does not stop.

Figure 33-2, Right atrial lead perforation. RA, Right atrium; SVC, superior vena cava.

Figure 33-3, Right ventricular lead perforation. RV, Right ventricle.

Figure 33-4, Coronary sinus lead perforation. LV, Left ventricle; RA, right atrium; RV, right ventricle.

Perforation does not always result in tamponade and may instead present with pleuritic chest pain or extracardiac pacing. Occasionally, the only manifestation of perforation will be a change in the sensing and pacing characteristics of the lead; this may require computed tomography to confirm the diagnosis ( Fig. 33-5 ). It is worth noting that normal electrical function of a lead does not rule out perforation. It has been our experience that perforated leads that have been confirmed to be attached to the pericardium when directly visualized in the operating room may occasionally have normal sensing, impedance, and pacing threshold values. When a patient develops a chronic perforation, days to months after implantation, extraction should be performed with surgical backup at the ready in the unlikely event of acute tamponade. Although this is a risk, it has been our experience, and that reported by others, that in most cases transvenous extraction and reimplantation is typically uneventful. Right ventricular septal implantation has been associated with a lower risk of perforation, a technique that can be achieved using a stylet with a posterior angulation.

Figure 33-5, Three-dimensional reconstruction from gated cardiac computed tomography scan showing right ventricular lead perforating into the pericardial space. RV, Right ventricle.

Vein Thrombosis/Stenosis

The problems of venous stenosis and thrombosis will exist as long as CIEDs involve transvenous leads. Previous reports of the incidence of venous stenosis have varied widely. In a prospective analysis of CIED patients 6 months after implantation, 64% had some degree of venous stenosis, with the stenosis described as severe or occlusive in 21%. In cases of thrombosis alone, management with anticoagulation may suffice. The management and prevention of central venous stenosis is particularly important among patients with, or at risk for, end-stage renal disease. In these patients, central venous access is a requirement for dialysis, a life-prolonging therapy that cannot be delayed for any significant amount of time. The treatment of central venous stenosis involves multiple therapeutic options including venoplasty, stenting, and lead extraction when necessary. Although lead extraction should not be a first-line therapy, it certainly has a role in the management of these patients ( Case Study 33-1 ). For instance, trapping a transvenous lead against the vein wall when stenting open a vein should be avoided whenever possible because it eliminates the option of future transvenous extraction if necessary.

Case Study 33-1
Superior Vena Cava Syndrome

History

This 46-year-old woman was diagnosed with pulmonary and cardiac sarcoidosis 5 years before referral to our institution. She also had a history of paroxysmal atrial fibrillation and had undergone two previous catheter ablation procedures. Cardiac magnetic resonance imaging (MRI) at the time of her initial diagnosis revealed normal chamber size, as well as normal biventricular function and wall motion. The MRI also showed evidence of late gadolinium enhancement and for that reason she underwent implantable cardioverter-defibrillator (ICD) implantation for the primary prevention of sudden cardiac death. At the time of presentation to our institution, she reported sporadic swelling of her face and neck for the previous 2 years. During the preceding 4 months her symptoms had progressively worsened and eventually included morning headaches.

Current Medications

The patient was taking dabigatran 150 mg twice daily, sotalol 80 mg twice daily, diltiazem 30 mg four times daily, prednisone 20 mg daily, and oral contraceptive pills.

Physical Examination

  • Blood pressure: 102/68 mm Hg, Heart rate: 70 beats/min

  • Head/neck: Swelling/edema of the head and neck. Significant jugular venous distention.

  • Lungs/chest: Clear to auscultation and percussion bilaterally.

  • Heart: Nondisplaced point of maximal impulse (PMI). Regular rate and rhythm. No appreciable murmurs, rubs, or gallops.

  • Abdomen: Soft, normoactive bowel sounds.

  • Lower extremities: No edema. Warm and well perfused.

Laboratory Data

  • Hemoglobin: 13.2 g/dL

  • Mean corpuscular volume: 93.6 fL

  • Platelet count: 215 × 10 3 /mm 3

  • Sodium: 140 mmol/L

  • Potassium: 3.8 mmol/L

  • Creatinine: 0.85 mg/dL

  • Blood urea nitrogen: 16 mg/dL

Electrocardiogram

Her presenting electrocardiogram ( Fig. E33-1 ) showed sinus rhythm with a first degree atrioventricular block. There was also evidence of right ventricular conduction delay (rSR' pattern in the right precordial leads).

Figure E33-1, Presenting electrocardiogram.

Imaging

Preprocedure angiography ( Fig. E33-2 ) revealed complete occlusion of the superior vena cava (SVC) with flow through the bilateral azygous veins.

Figure E33-2, Preprocedure angiography revealing complete occlusion of the superior vena cava (white arrow) with flow in the bilateral azygous veins (black arrows).

Focused Clinical Questions and Discussion Points

  • Question: What are the available management options for the treatment of patients with SVC syndrome in the setting of transvenous cardiac implantable electronic device (CIED) leads?

  • Discussion: Though there is limited evidence as to the true incidence of SVC syndrome related to CIED leads, previous reports have estimated it to be less than 0.1%. 1 However, in those patients who do develop symptoms the disease can be quite debilitating and challenging to treat. The most recent multisociety consensus statement gave a class I recommendation to lead extraction in patients with symptomatic SVC stenosis/occlusion. 2 Multiple treatment modalities exist for the management of symptomatic SVC stenosis following lead extraction, including venoplasty, stenting, and surgical reconstruction. All of these are plagued by high recurrence rates. 3 Regardless of which option is employed, the use of a nontransvenous pacemaker and/or defibrillator after extraction may reduce the risk of recurrence, though this has not been proven. Options for nontransvenous approaches include epicardial lead placement, transatrial lead placement, and a subcutaneous defibrillator (in patients who do not require pacing).

Final Diagnosis

Symptomatic SVC syndrome.

You're Reading a Preview

Become a Clinical Tree membership for Full access and enjoy Unlimited articles

Become membership

If you are a member. Log in here