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Anesthesia & Analgesia:
doi: 10.1213/ANE.0000000000000195
Cardiovascular Anesthesiology: Echo Didatics

Infective Endocarditis: The Importance of Intraoperative Transesophageal Echocardiography

Methangkool, Emily MD; Howard-Quijano, Kimberly MD; Ho, Jonathan K. MD; Mahajan, Aman MD, PhD

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From the Department of Anesthesiology, University of California, Los Angeles, Los Angeles, California.

Accepted for publication January 24, 2014.

Funding: Not funded.

The authors declare no conflicts of interest.

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s Web site.

Reprints will not be available from the authors.

Address correspondence to Aman Mahajan, MD, PhD, Department of Anesthesiology, University of California, 757 Westwood Plaza, Box 957403, 3302 RRMC, Los Angeles, CA 90095-7403. Address e-mail to amahajan@mednet.ucla.edu.

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CLINICAL CASE

A 72-year-old man with end-stage renal disease is admitted with fatigue, fever, leukocytosis, and Staphylococcus aureus positive blood cultures. He presents to the operating room with new onset severe mitral regurgitation and infective endocarditis (IE).

Endocarditis carries a 6-month mortality of 14% to 33%.1 Risk factors include IV drugs, hemodialysis, congenital heart disease, or valve lesions. The Duke criteria established major and minor criteria for the diagnosis of IE; diagnosis by echocardiography is a major criterion.2,3 Transesophageal echocardiography (TEE) is more sensitive than transthoracic echocardiography (TTE) in diagnosis of IE and is recommended for surgical cases4,6 (Table 1). Surgery is necessary in up to 50% of cases.5 Indications in native valve endocarditis include heart failure, pulmonary hypertension, heart block, abscess, and fistula formation as well as infection caused by highly resistant or fungal organisms. Indications for surgery in prosthetic valve endocarditis include heart failure, dehiscence, worsening obstruction or regurgitation, and abscess6 (Table 2).

Table 1
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Table 2
Table 2
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Echocardiographic Evaluation of Infective Endocarditis

Intraoperative TEE confirms the IE diagnosis, identifies the extent of tissue damage, and guides surgical repair. Major echocardiographic features are (1) vegetations, (2) abscess, (3) prosthetic valve dehiscence, and (4) new or worsening valvular regurgitation (Table 3, Figs. 1–4, Videos 1–4, see Supplemental Digital Content 1–4, http://links.lww.com/AA/A887, http://links.lww.com/AA/A888, http://links.lww.com/AA/A889, http://links.lww.com/AA/A890).3 Close examination of indwelling catheters and pacemaker leads, as well as nonvalvular structures should be performed, as all structures can serve as nidi for infection; while rare, even cases of Eustachian valve endocarditis have been reported.7 High resolution and zoom settings improve visualization of small vegetations. Risk factors for vegetation embolization determined by TEE are (1) large (>10 mm), (2) pedunculated, (3) multiple, (4) prolapsing, (5) noncalcified, or (6) rapidly increasing in size. Systemic embolization may occur in up to 34% of patients, with a higher risk associated with mitral valve origin.8,9

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Table 3
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Native Valve Endocarditis

Native valve endocarditis most frequently involves the mitral or aortic valves; in IV drug users, however, it is the tricuspid valve.10 Endocarditis rarely affects the pulmonary valve. A 2-dimensional examination of the mitral valve can be completed using the midesophageal 4-chamber, midcommissural, 2-chamber, and long-axis views. The aortic valve is imaged from the midesophageal short-axis and long-axis views. All valves should be examined for leaflet thickening, vegetations, regurgitation, and spread of infection. Three-dimensional imaging more specifically localizes vegetations and leaflet damage. Compared with other intracardiac masses, vegetations are (1) oscillating masses, (2) lobulated or amorphous, (3) moving independently of the valve, and (4) usually located on the proximal flow side (Fig. 1, Video 1, see Supplemental Digital Content 1, http://links.lww.com/AA/A887).

Vegetations cause destruction of valvular structures, leading to valve aneurysm, perforation, prolapse, and chordal or papillary muscle rupture. Vegetation location, regurgitation mechanism, and severity can be assessed by color flow Doppler. Vegetations on leaflet tips prevent leaflet coaptation, resulting in central regurgitation, whereas leaflet perforations are characterized by noncentral jets. Vegetations from the aortic valve can also prolapse into the left ventricular outflow tract, seeding the mitral valve.11 The degree of valve involvement and damage to surrounding tissues, as determined by echocardiography and direct visual inspection, guide the surgical approach. Extensive destruction of the native annulus or large perforations not amenable to patching may favor valve replacement; valve repair, if feasible, leads to improved outcomes with decreased risk of recurrent infection.6,12

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Prosthetic Valve Endocarditis

Prosthetic valve endocarditis comprises 22.2% of all cases of endocarditis, with the mitral valve more affected than the aortic valve.13 Left-sided endocarditis has the worst prognosis, with mortality from 20% to 40%.14 In the absence of overt vegetations and continued clinical suspicion for IE, examination for abscesses and perivalvular extension as well as prosthetic valve dehiscence (Fig. 2, Video 2, see Supplemental Digital Content 2, http://links.lww.com/AA/A888) should be performed.4

TEE examination of mitral and aortic prosthetic valves is complicated by acoustic shadowing of the valve apparatus. Deep transgastric views with lower frequency settings optimize image quality and overcome shadowing artifacts. In mechanical valve endocarditis, infection is usually localized to the junction between the sewing ring and the annulus, leading to perivalvular abscess, dehiscence, and fistula formation (Fig. 3, Video 3, see Supplemental Digital Content 3, http://links.lww.com/AA/A889). In contrast, bioprosthetic valve endocarditis is usually localized on the leaflets, leading to cusp rupture and perforation.15 Aortic valve endocarditis can be complicated by perivalvular extension into the aortic root with abscess or pseudoaneurysm. An abscess will appear as echo-dense abnormal thickening, with a tendency for invasion of the aortic-mitral intervalvular fibrosa, given the relative avascularity of this area (Fig. 4, Video 4, see Supplemental Digital Content 4, http://links.lww.com/AA/A890).16,17 Abscess can have a similar echocardiographic appearance to a hematoma and may be distinguished by evidence of systemic infection (elevated white blood cell count, fevers, positive blood cultures). In both native and prosthetic valve endocarditis, perforations of the anterior mitral leaflet caused by aortic regurgitant jets can occur, leading to mitral regurgitation, and fistula formation between the aorta and left atrium can also occur.11,18

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Differential Diagnosis

IE vegetations must be distinguished from Libman-Sacks endocarditis, papillary fibroelastomas, Lambl’s excrescences, small tumors, thrombi, prolapsing valvular structures, or imaging artifacts. The vegetations of Libman-Sacks present as valve thickening or verrucous vegetations, with a smooth appearance compared with the rough and ragged borders of bacterial vegetation.19 These vegetations can resolve or worsen intermittently over time, and bacterial endocarditis can be superimposed. Surgical intervention depends on the degree of valvular dysfunction as well as risk of systemic embolization, with the caveat that surgery may not always prevent recurrent vegetations.20 Papillary fibroelastomas are small pedunculated structures with “frond-like” appearances; Lambl’s excrescences are thin, fibrous strands on the contact surfaces of the valve.21 Pannus or thrombus formation can be difficult to differentiate from one another and is another area where TEE may be more useful than TTE; while the degree of mechanical valve obstruction may be similar, thrombi tend to be larger and to extend into the left atrium. In addition, thrombi often have an echodensity similar to myocardium, and measurements of ultrasound intensity have been used to differentiate between pannus and thrombi.22 As has been detailed, identification of valvular masses can be difficult, and definitive diagnosis relies on clinical suspicion, culture data, as well as echocardiography. E

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Teaching Points

* IE most frequently involves the mitral and aortic valves, except in the case of IV drug users when it is the tricuspid valve. The pulmonary valve is least often affected.

* TEE is more sensitive than TTE in the diagnosis of IE and is recommended for surgical cases.

* Major echocardiographic features of IE include (1) an oscillating mass or vegetation on the valve or supporting structures, (2) abscess, (3) prosthetic valve dehiscence, and (4) new or worsening valvular regurgitation.

* IE vegetations must be distinguished from Libman-Sacks endocarditis, papillary fibroelastomas, Lambl’s excrescences, small tumors, pannus, thrombi, prolapsing valvular structures, or imaging artifacts.

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DISCLOSURES

Name: Emily Methangkool, MD.

Contribution: This author helped design and conduct the study, analyze the data, and write the manuscript.

Attestation: Emily Methangkool approved the final manuscript.

Name: Kimberly Howard-Quijano, MD.

Contribution: This author helped design and conduct the study, analyze the data, and write the manuscript.

Attestation: Kimberly Howard-Quijano approved the final manuscript.

Name: Jonathan K. Ho, MD.

Contribution: This author helped design and conduct the study, analyze the data, and write the manuscript.

Attestation: Jonathan K. Ho approved the final manuscript.

Name: Aman Mahajan, MD, PhD.

Contribution: This author helped design and conduct the study, analyze the data, and write the manuscript.

Attestation: Aman Mahajan approved the final manuscript.

This manuscript was handled by: Martin J. London, MD.

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REFERENCES

1. Tleyjeh IM, Steckelberg JM, Murad HS, Anavekar NS, Ghomrawi HM, Mirzoyev Z, Moustafa SE, Hoskin TL, Mandrekar JN, Wilson WR, Baddour LM. Temporal trends in infective endocarditis: a population-based study in Olmsted County, Minnesota. JAMA. 2005;293:3022–8

2. Durack DT, Lukes AS, Bright DK. New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Duke Endocarditis Service. Am J Med. 1994;96:200–9

3. Li JS, Sexton DJ, Mick N, Nettles R, Fowler VG Jr, Ryan T, Bashore T, Corey GR. Proposed modifications to the Duke criteria for the diagnosis of infective endocarditis. Clin Infect Dis. 2000;30:633–8

4. Kini V, Logani S, Ky B, Chirinos JA, Ferrari VA, St John Sutton MG, Wiegers SE, Kirkpatrick JN. Transthoracic and transesophageal echocardiography for the indication of suspected infective endocarditis: vegetations, blood cultures and imaging. J Am Soc Echocardiogr. 2010;23:396–402

5. Tornos P, Iung B, Permanyer-Miralda G, Baron G, Delahaye F, Gohlke-Bärwolf Ch, Butchart EG, Ravaud P, Vahanian A. Infective endocarditis in Europe: lessons from the Euro heart survey. Heart. 2005;91:571–5

6. Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD, Gaasch WH, Lytle BW, Nishimura RA, O’Gara PT, O’Rourke RA, Otto CM, Shah PM:e1–142

7. Skubas N, Slepian RL, Lee LY, Tortolani AJ. Tricuspid regurgitation caused by eustachian valve endocarditis. Anesth Analg. 2006;103:1410–1

8. Thuny F, Di Salvo G, Disalvo G, Belliard O, Avierinos JF, Pergola V, Rosenberg V, Casalta JP, Gouvernet J, Derumeaux G, Iarussi D, Ambrosi P, Calabró R, Calabro R, Riberi A, Collart F, Metras D, Lepidi H, Raoult D, Harle JR, Weiller PJ, Cohen A, Habib G. Risk of embolism and death in infective endocarditis: prognostic value of echocardiography: a prospective multicenter study. Circulation. 2005;112:69–75

9. Vilacosta I, Graupner C, San Román JA, Sarriá C, Ronderos R, Fernández C, Mancini L, Sanz O, Sanmartín JV, Stoermann W. Risk of embolization after institution of antibiotic therapy for infective endocarditis. J Am Coll Cardiol. 2002;39:1489–95

10. Carozza A, De Santo LS, Romano G, Della Corte A, Ursomando F, Scardone M, Caianiello G, Cotrufo M. Infective endocarditis in intravenous drug abusers: patterns of presentation and long-term outcomes of surgical treatment. J Heart Valve Dis. 2006;15:125–31

11. Karalis DG, Bansal RC, Hauck AJ, Ross JJ Jr, Applegate PM, Jutzy KR, Mintz GS, Chandrasekaran K. Transesophageal echocardiographic recognition of subaortic complications in aortic valve endocarditis. Clinical and surgical implications. Circulation. 1992;86:353–62

12. Feringa HH, Shaw LJ, Poldermans D, Hoeks S, van der Wall EE, Dion RA, Bax JJ. Mitral valve repair and replacement in endocarditis: a systematic review of literature. Ann Thorac Surg. 2007;83:564–70

13. Murdoch DR, Corey GR, Hoen B, Miró JM, Fowler VG Jr, Bayer AS, Karchmer AW, Olaison L, Pappas PA, Moreillon P, Chambers ST, Chu VH, Falcó V, Holland DJ, Jones P, Klein JL, Raymond NJ, Read KM, Tripodi MF, Utili R, Wang A, Woods CW, Cabell CHInternational Collaboration on Endocarditis-Prospective Cohort Study (ICE-PCS) Investigators. . Clinical presentation, etiology, and outcome of infective endocarditis in the 21st century: the International Collaboration on Endocarditis-Prospective Cohort Study. Arch Intern Med. 2009;169:463–73

14. Wang A, Athan E, Pappas PA, Fowler VG Jr, Olaison L, Paré C, Almirante B, Muñoz P, Rizzi M, Naber C, Logar M, Tattevin P, Iarussi DL, Selton-Suty C, Jones SB, Casabé J, Morris A, Corey GR, Cabell CHInternational Collaboration on Endocarditis-Prospective Cohort Study Investigators. . Contemporary clinical profile and outcome of prosthetic valve endocarditis. JAMA. 2007;297:1354–61

15. Horstkotte D, Piper C, Niehues R, Wiemer M, Schultheiss HP. Late prosthetic valve endocarditis. Eur Heart J. 1995;16(Suppl B):39–47

16. Stechert MM, London MJ. Native aortic root endocarditis with invasion of the right outflow tract. Anesth Analg. 2010;110:36–8

17. Stechert MM, Kellermeier JP. Aorto-atrial fistula: an important complication of aortic prosthetic valve endocarditis. Anesth Analg. 2007;105:332–3

18. Rao SL, Campbell DB, Haouzi-Judenherc AR. Echocardiographic recognition of mitral valve involvement in primary aortic valve endocarditis. Anesth Analg. 2011;112:59–61

19. Shroff H, Benenstein R, Freedberg R, Mehl S, Saric M. Mitral valve Libman-Sacks endocarditis visualized by real time three-dimensional transesophageal echocardiography. Echocardiography. 2012;29:E100–1

20. Roldan CA, Shively BK, Crawford MH. An echocardiographic study of valvular heart disease associated with systemic lupus erythematosus. N Engl J Med. 1996;335:1424–30

21. Daveron E, Jain N, Kelley GP, Luer WH, Fermin C, Helmcke F, Kerut EK. Papillary fibroelastoma and Lambl’s excrescences: echocardiographic diagnosis and differential diagnosis. Echocardiography. 2005;22:285–7

22. Barbetseas J, Nagueh SF, Pitsavos C, Toutouzas PK, Quiñones MA, Zoghbi WA. Differentiating thrombus from pannus formation in obstructed mechanical prosthetic valves: an evaluation of clinical, transthoracic and transesophageal echocardiographic parameters. J Am Coll Cardiol. 1998;32:1410–7

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