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Table of Contents
CASE REPORT  
Year : 2015  |  Volume : 18  |  Issue : 4  |  Page : 599-602
Unusual cause of hypoxemia after automatic implantable cardioverter-defibrillatorleads extraction


Department of Cardiothoracic Anesthesia, Freeman Hospital, High Heaton, Newcatle upon Tyne, NE7 7DN, United Kingdom

Click here for correspondence address and email

Date of Submission09-Aug-2014
Date of Acceptance14-Jul-2015
Date of Web Publication1-Oct-2015
 

   Abstract 

The indication of pacemaker/AICD removal are numerous. Serious complication can occur during their removal, severe tricuspid regurgitation is one of the complication. The occurrence of PFO is not uncommon among adult population. Shunting across PFO in most circumstance is negligible, but in some necessitates closure due to hypoxemia. We report a case of 62 year old man, while undergoing AICD removal, had an emergency sternotomy for cardiac tamponade. Postoperatively, he experienced profound hypoxemia refractory to oxygen therapy. Transthoracic Echocardiogram was performed to rule out intracardiac shunts at an early stage, but it was difficult to obtain an good imaging windows poststernotomy. A small pulmonary emboli was noted on CTPA, but was not sufficient to account for the level of hypoxemia and did not resolve with anticoagulation. Transesophageal echocardiogram showed flail septal tricuspid valve with severe TR and bidirectional shunt through large PFO. Patient was posted for surgery, tricuspid valve was replaced and PFO surgically closed. Subsequently, patient recovered well ad was discharged to home. Cause of hypoxemia might be due to respiratory or cardiac dysfunction. But for hypoxemia refractory to oxygen therapy, transoesophageal echocardiogram should be always considered and performed early as an diagnostic tool in post cardiac surgical patients.

Keywords: Automatic implantable cardioverter-defibrillator; Hypoxemia; Transesophageal echocardiogram; Patent foramen ovale; Tricuspid regurgitation

How to cite this article:
Raju D, Roysam C, Singh R, Clark SC, Plummer C. Unusual cause of hypoxemia after automatic implantable cardioverter-defibrillatorleads extraction. Ann Card Anaesth 2015;18:599-602

How to cite this URL:
Raju D, Roysam C, Singh R, Clark SC, Plummer C. Unusual cause of hypoxemia after automatic implantable cardioverter-defibrillatorleads extraction. Ann Card Anaesth [serial online] 2015 [cited 2019 Nov 18];18:599-602. Available from: http://www.annals.in/text.asp?2015/18/4/599/166484



   Introduction Top


The indications for pacemaker and automatic implantable cardioverter-defibrillator (AICD) removal are numerous, but mainly include infection or lead malfunction. [1] The treatment of choice is the extraction of the pacemaker/AICD generator and/or the leads. [1],[2],[3] The frequently used technique for lead extraction is a transvenous laser assisted approach. [2] Although the risk of this approach is low, the risk of removal of AICD leads far exceeds that for pacemaker leads. [4] Serious complications can occur, the majority of which are immediate. [1],[5],[6] There are reports of severe tricuspid regurgitation (TR) after lead removal needing surgery. [7] The occurrence of a large patent foramen ovale (PFO) with a bidirectional shunt is not uncommon in adult patients undergoing cardiac operations [8] and at times necessitates closure due to severe hypoxemia. Transesophageal echocardiogram is a highly sensitive investigation in diagnosing a PFO perioperatively in the Intensive Care Unit (ICU). [8],[9] We present a case report of severe hypoxemia after AICD lead extraction.


   Case report Top


A 62-year-old man with a history of hypertension, smoking, and AICD implant for out of hospital ventricular fibrillation arrest 13 years earlier was scheduled for AICD generator box change under general anesthesia (GA). Anesthetic pre assessment was unremarkable with a good ventricular function on echocardiogram. During the attempted removal of the AICD generator box, the cardiologist noted a break in the insulation of the AICD lead component. Because the patient was not consented for leads removal, the generator box was removed, and leads were left in situ with a plan for laser extraction at a later date. Two days later, laser extraction of leads was attempted under GA. Monitoring included standard and invasive arterial pressures. The lead extraction was complicated with pericardial tamponade due to a linear tear in the free wall of the the right ventricle, which was managed successfully by emergency surgery, and the patient was extubated later that day in the ICU. Intraoperatively, central venous pressure was noted to be around 18-22 cm of water. The following day he became intermittently hypoxemic with a PaO 2 of 6.8-13.3 kPa despite being on high inspired oxygen via continuous positive airway pressure mask. Central venous pressure was around 13-15 cm of water. Clinical examination and chest X-ray which showed some left basal collapse did not correlate with his level of hypoxemia. Transthoracic echocardiogram was not conclusive because of the poor window. Although, he remained hypoxemic, his hemodynamics and metabolic parameters were normal. So, he underwent computed tomography pulmonary angiography (CTPA), which showed a small right solitary pulmonary embolism, a small left pleural effusion and atelectasis. He was then started on heparin infusion. Despite a sufficient duration of anticoagulation and 100% oxygen he remained hypoxemic. A review of his CTPA scan suggested an aneurysmal interatrial septum. Transesophageal echocardiography was performed under GA. It demonstrated a flail tricuspid valve with severe eccentric TR, an aneurismal interatrial septum, and a large PFO with a bidirectional shunt. There was dilatation of right atrial (RA) and right ventricular (RV) with mild RV dysfunction and preserved left ventricular function. Patient was extubated, discussed with consultant cardiothoracic surgeon, and consented for surgical closure of PFO and tricuspid valve replacement [Figure 1] [Figure 2] [Figure 3]. The next day, he underwent tricuspid valve replacement and bovine pericardial patch closure of PFO. He made a good postoperative recovery and was discharged home in few days' time. At follow-up, 6 weeks later, he had returned to normal activity and had an echocardiogram which showed a well seated functioning tricuspid prosthesis and no residual shunt across the interatrial septum.
Figure 1: Mid esophageal four chamber view showing flail tricuspid valve

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Figure 2: Mid esophageal four chamber view showing severe tricuspid regurgitation

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Figure 3: Mid esophageal bi-caval view showing shunt across large patent foramen ovale

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   Discussion Top


Lead extraction is not without complications; though much reduced with effective current techniques. [3] Implantable cardioverter-defibrillator (ICD) lead replacement complications were 8.1%, of which 5.8% were major complications. [6] Many reports favor lead extraction for infective complications to reduce systemic sepsis. Risk factors for complications include younger patients, [4],[10] implantation site, female gender, [11] physician experience, and the duration of lead implantation. [11] Lead extraction can be difficult due to the encasement of the leads in fibrotic tissue. The process of fibrotic encapsulation is by activation of different cellular and humoral mechanisms. [12] Because fibrous attachments to surrounding structures may involve the tricuspid valve, valvular damage may be provoked by lead removal. [7] Methods to extract leads range from a transvenous approach to open procedures. Of the many transvenous approaches the laser assisted technique has been shown to have least complications. Laser sheaths reduce the duration and magnitude of the force applied and aids in disrupting fibrous tissues, although the possibility of serious complications still exists. [2],[13]

The incidence of PFO ranges from 14.6% to 35% in postmortem examinations. [14],[15],[16] Morphologically findings of hypermobility of septum primum and enlargement of fossa ovalis can occur in the presence of PFO. [17] Transient right to left shunting through a PFO causing refractory hypoxemia is less recognized and should be considered in the differential diagnosis of severe hypoxemia. This kind of shunting can also occur in pulmonary embolism, RV infarction, [14] heart failure with left ventricular assist device, [18] pneumonectomy, [19] chronic obstructive pulmonary disease, [20] and application of positive end-expired pressure during intermittent positive pressure ventilation. [8],[21] Detection of the interatrial shunt is essential for the diagnosis of PFO in the absence of atrial septal defect. Among the various modern methods of PFO detection, transesophageal echocardiogram (TOE) is generally considered to be the "gold standard." [22] This report describes a middle aged man presenting with refractory hypoxemia after ICD leads removal. Transthoracic echocardiogram was performed to rule out intracardiac shunts at an early stage, but it was inconclusive because of poor window poststernotomy. A small pulmonary embolism was noted on CTPA, which did not account for the level of hypoxemia and did not resolve with anticoagulation. Transesophageal echocardiogram was performed under GA and patient was woken up immediately after the procedure, primarily to obtain consent. Accentuation of the shunt across PFO results when RA pressure exceeds more than left atrial pressure or when the anatomic relationship of the interatrial septum to the inferior vena cava is altered. [14] In this case, although the RV perforation had been dealt with immediately, the injury to the tricuspid valve and ensuing severe TR went unrecognized. In our opinion, the raised RA pressures and severe TR jet toward the septum may have opened the PFO significantly accounting for the shunt.


   Conclusion Top


PFO is not uncommon in the adult population. In situations where right sided pressure exceeds the left sided pressure, the right to left intracardiac shunt may result in hypoxemia. Hypoxemia is common in post cardiac surgical/cardiology patients and is either due to respiratory dysfunction or congestive heart failure. We conclude that TOE is a vital investigating tool, which should be considered early for the diagnosis of suspected postoperative hypoxemia refractory to oxygen therapy.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Rusanov A, Spotnitz HM. A 15-year experience with permanent pacemaker and defibrillator lead and patch extractions. Ann Thorac Surg 2010;89:44-50.  Back to cited text no. 1
    
2.
Milla F, Mack CA, Girardi LN. Arteriovenous fistula after laser-assisted pacemaker lead extraction. Ann Thorac Surg 2006;81:2304-6.  Back to cited text no. 2
    
3.
Bracke FA, Meijer A, van Gelder LM. Pacemaker lead complications: When is extraction appropriate and what can we learn from published data? Heart 2001;85:254-9.  Back to cited text no. 3
    
4.
Kennergren C, Bucknall CA, Butter C, Charles R, Fuhrer J, Grosfeld M, et al. Laser-assisted lead extraction: The European experience. Europace 2007;9:651-6.  Back to cited text no. 4
    
5.
Smith HJ, Fearnot NE, Byrd CL, Wilkoff BL, Love CJ, Sellers TD. Five-years experience with intravascular lead extraction. U.S. Lead Extraction Database. Pacing Clin Electrophysiol 1994;17:2016-20.  Back to cited text no. 5
    
6.
Gould PA, Krahn AD, Canadian Heart Rhythm Society Working Group on Device Advisories. Complications associated with implantable cardioverter-defibrillator replacement in response to device advisories. JAMA 2006;295:1907-11.  Back to cited text no. 6
    
7.
Franceschi F, Thuny F, Giorgi R, Sanaa I, Peyrouse E, Assouan X, et al. Incidence, risk factors, and outcome of traumatic tricuspid regurgitation after percutaneous ventricular lead removal. J Am Coll Cardiol 2009;53:2168-74.  Back to cited text no. 7
    
8.
Tabry I, Villanueva L, Walker E. Patent foramen ovale causing refractory hypoxemia after off-pump coronary artery bypass: A case report. Heart Surg Forum 2003;6:E74-6.  Back to cited text no. 8
    
9.
Chen WJ, Kuan P, Lien WP, Lin FY. Detection of patent foramen ovale by contrast transesophageal echocardiography. Chest 1992;101:1515-20.  Back to cited text no. 9
    
10.
Centella T, Oliva E, García-Andrade I, Martín-Dávila P, Cobo J, Moya JL, et al. Percutaneous extraction of pacemaker and defibrillator leads. Rev Esp Cardiol 2007;60:607-15.  Back to cited text no. 10
    
11.
Kay GN, Brinker JA, Kawanishi DT, Love CJ, Lloyd MA, Reeves RC, et al. Risks of spontaneous injury and extraction of an active fixation pacemaker lead: Report of the Accufix Multicenter Clinical Study and Worldwide Registry. Circulation 1999;100:2344-52.  Back to cited text no. 11
    
12.
Esposito M, Kennergren C, Holmström N, Nilsson S, Eckerdal J, Thomsen P. Morphologic and immunohistochemical observations of tissues surrounding retrieved transvenous pacemaker leads. J Biomed Mater Res 2002;63:548-58.  Back to cited text no. 12
    
13.
Wilkoff BL, Byrd CL, Love CJ, Hayes DL, Sellers TD, Schaerf R, et al. Pacemaker lead extraction with the laser sheath: Results of the pacing lead extraction with the excimer sheath (PLEXES) trial. J Am Coll Cardiol 1999;33:1671-6.  Back to cited text no. 13
    
14.
Fedullo AJ, Swinburne AJ, Mathew TM, Ryan GF, Dvoretsky PM, Davidson KH. Hypoxemia from right to left shunting through patent foramen ovale. Am J Med Sci 1985;289:164-6.  Back to cited text no. 14
    
15.
Hagen PT, Scholz DG, Edwards WD. Incidence and size of patent foramen ovale during the first 10 decades of life: An autopsy study of 965 normal hearts. Mayo Clin Proc 1984;59:17-20.  Back to cited text no. 15
    
16.
Penther P. Patent foramen ovale: An anatomical study. Apropos of 500 consecutive autopsies. Arch Mal Coeur Vaiss 1994;87:15-21.  Back to cited text no. 16
    
17.
Louie EK, Konstadt SN, Rao TL, Scanlon PJ. Transesophageal echocardiographic diagnosis of right to left shunting across the foramen ovale in adults without prior stroke. J Am Coll Cardiol 1993;21:1231-7.  Back to cited text no. 17
    
18.
Baldwin RT, Duncan JM, Frazier OH, Wilansky S. Patent foramen ovale: A cause of hypoxemia in patients on left ventricular support. Ann Thorac Surg 1991;52:865-7.  Back to cited text no. 18
    
19.
Bakris NC, Siddiqi AJ, Fraser CD Jr, Mehta AC. Right-to-left interatrial shunt after pneumonectomy. Ann Thorac Surg 1997;63:198-201.  Back to cited text no. 19
    
20.
Soliman A, Shanoudy H, Liu J, Russell DC, Jarmukli NF. Increased prevalence of patent foramen ovale in patients with severe chronic obstructive pulmonary disease. J Am Soc Echocardiogr 1999;12:99-105.  Back to cited text no. 20
    
21.
Cujec B, Polasek P, Mayers I, Johnson D. Positive end-expiratory pressure increases the right-to-left shunt in mechanically ventilated patients with patent foramen ovale. Ann Intern Med 1993;119:887-94.  Back to cited text no. 21
    
22.
Sukernik MR, Bennett-Guerrero E. The incidental finding of a patent foramen ovale during cardiac surgery: Should it always be repaired? A core review. Anesth Analg 2007;105:602-10.  Back to cited text no. 22
    

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Correspondence Address:
Dinesh Raju
Department of Anesthesia, Narayana Health, Bommasandra Industrial Area, Anekal Taluk, Bengaluru - 560 099, Karnataka
United Kingdom
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9784.166484

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