Surgical management of prosthetic valve endocarditis

J THORAC CARDIOVASC SURG 86:112-114, 1983

Surgical management of prosthetic valve endocarditis Operative mortality in patients with prosthetic valve endocarditis (PVE). who already have severe hemodynamic failure. is extremely high (35% to 84%). Over a period of 10 years. between 1972 and 1981. fourteen consecutive urgent operations were performed for PVE in 12 patients. On thirteen occasions the patients were in severe hemodynamic failure (NYHA Functional Class IV). and five of them had early PVE (within 60 days of previous operation). In all patients at least two of the other recognized risk factors. such as presence of non-streptococcal organisms. detachment of the prosthesis. and myocardial invasion. were present. All of the patients but one were operated upon within 48 hours of their hemodynamic deterioration, and there was one postoperative death (operative mortality ·7%). Our results indicate that an acceptable surgical mortality in patients with intractable heart failure due to early and late PVE can be achieved by prompt surgical intervention despite the presence of multiple risk factors.

Tapas Raychaudhury, F.R.C.S.(Eng.), F.R.C.S.Ed., E. W. J. Cameron, F.R.C.S.Ed., and P. R. Wa1baum, F.R.C.S.Ed., Edinburgh, Scotland

DesPite improvement in antimicrobial therapy, surgical technique, and myocardial preservation, the operative mortality for patients having severe heart failure because of prosthetic valve endocarditis (PVE) remains high and has been reported as 35% to 84% in recent publications. 1-6 Various risk factors, such as early presentation (within 60 days of previous valve replacement), presence of non-streptococcal organisms, new or increased regurgitant murmur, myocardial invasion, severe hemodynamic failure, and aortic prosthetic replacement have been identified, and urgent surgical intervention has been proposed for patients in whom these risk factors are detectable." However, no report is available so far which shows the degree of success which can be achieved by such an approach. We describe here our surgical experience of 14 urgent prosthetic valve replacements for bacterial endocarditis in 12 severely ill patients. Patients and method

The names of all the patients who required prosthetic valve replacement for bacterial endocarditis, admitted From the Regional Cardiothoracic Centre, The Royal Infirmary, Edinburgh, Scotland. Received for publication Sept.9, 1982. Accepted for publication Oct. 8, 1982. Address for reprints: T. Raychaudhury, Department of Cardiothoracic Surgery, Wythenshawe Hospital, Manchester M23 9LT, England.

112

Table I. Presence of recognized risk factors in 14 prosthetic valve replacements (PVR) Risk factors New regurgitant murmur NYHA Functional Class IV Aortic prosthesis replacement Non-streptococcal organisms Myocardial invasion Presentation within 60 days Combination Combination Combination Combination

of of of of

three of the above four of the above five of the above all of the above

No.ofPVR 14

13 12 10

9

5 2 5 6

1

Legend: NYHA, New York Heart Association.

between 1972 and 1981, were drawn from the Central Computer Service of our hospital. Their medical records were reviewed and current follow-up data have been obtained from clinic visits, letter and telephone contact with the general practitioner responsible, and from questionnaires sent directly to the patients. The diagnosis of PVE required at least two of the following criteria to be present: (l) at least two positive preoperative blood cultures; (2) clinical features of PVE (fever with leukocytosis in the presence of a new cardiac murmur, peripheral embolism, or splenomegaly); (3) the presence of vegetation or periprosthetic dehiscence with granulation tissue, noncalcific bioprosthetic leaflet destruction, or annular abscess formation, as observed at operation; (4) histologic or bacteriologic evidence of

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Prosthetic valve endocarditis

113

Table II. Prostheses, bacteriology, and results of operation Case no.

2 3

4

5 6

7

s 9 10 II 12

Original prosthesis Fascia lata aortic "No. 10 Starr Fascia lata aortic No. 10 Starr No.9 Starr Hancock, 25 mm No. 10 Starr NO.9 Starr "Carpentier, 23 mm Bjork, 25 mm No.3 Starr Bjork, 25 mm Carpentier, 25 mm Bjork, 31 mm

Organism responsible Staph. Staph. Staph. Staph.

albus albus albus aureus

Diphtheroides

Staph. aureus Strep. viridans Strep. viridans Strep. viridans plus Staph. albus No growth

Staph. albus No growth Pseudomonas Diphtheroides plus enterococci

Replacement prosthesis

Outcome

No. 10 Starr No. 10 Starr No. 10 Starr Hancock, 25 mm Hancock, 25 mm Bjork, 27 mm Bjork, 27 mm Carpentier, 23 mm Carpentier. 23 mm

Reinfection, seventh wk Alive. 10 yr Late death, 2 yr, cause unknown Alive,6 yr Alive, 6 yr Late death, 3 yr, CY A Alive, 5 yr Reinfection, 3 yr Alive, 2 yr

Hancock, 25 mm Carpentier, 31 mm Carpentier, 31 mm Hancock, 25 mm Bjork, 31 mm

Alive, 3 yr Alive, 3 yr Alive, 2 1/ , yr Died 3 wk postop., cardiac arrest Late death 3 mo postop., pneumonia

Legend: CV 1\. Cerebrovascular accident. "Rcopcration.

infection in the excised prosthesis. The operative mortality was defined as death occurring within 30 days of operation, and the degree of heart failure was assessed according to the New York Heart Association (NYHA) functional classification." The term "hemodynamic deterioration" refers to deterioration from NYHA Functional Class I or II to Class III or IV. Seven male patients with an average age of 46.2 years (range 24 to 56) and five female patients with average age of 49.2 years (range 24 to 62) underwent prosthetic valve replacement. Two patients required reoperation for reinfection of their prostheses; therefore, 14 prosthetic valve replacements were performed in 12 patients. On fiveoccasions patients presented within 60 days of their previous valve or prosthesis replacements, and on nine occasions the average asymptomatic period following the previous valve replacement was 28.5 months (range 7 to 63). At presentation all patients were febrile, having had a rectal temperature of over 38.5° C for 48 hours or more. The fever persisted-even after appropriate antibiotic treatment, on eight occasions, and six patients had atrioventricular conduction defects suggesting myocardial invasion. New regurgitant cardiac murmurs were present in all patients, and four patients had peripheral embolic episodes. On thirteen occasions, patients exhibited severe hemodynamic failure (Class IV) while on medical management and were operated upon within 48 hours of their hemodynamic deterioration. One patient who presented 5 weeks after mitral valve replacement, with heart failure (Class III), fever, and a regurgitant murmur, showed progressive deterioration and was operated upon in the third week of her illness.

Results The presence of risk factors and the surgical outcome are detailed in Tables I and II, respectively. Staphylococcus was the most COmmon organism isolated in the preoperative blood cultures, and nonstreptococcal organisms were isolated on ten of fourteen occasions. Small periprosthetic leak and flail bioprosthetic valve leaflet were the causes of regurgitant murmur in two patients, whereas on twelve other occasions the infected prostheses were detached from the anulus by one third to two thirds of their circumference. The myocardium was invaded by annular or subannular abscess formation in nine patients, and in five of them there was complete loss of supporting tissue because of multiple interconnections between the abscess cavities. There was one postoperative death, for an operative mortality of 7% (95% confidence limit range: 0.2% to 34%). In the patient who died (Patient 11 in Table 11), who presented 8 months after aortic valve replacement, both the preoperative and postoperative blood cultures grew Pseudomonas. At operation there was extensive subannular abscess around the aortic prosthesis, and there was a transient atrioventricular conduction defect postoperatively. The patient remained critically ill and had a cardiac arrest in the third postoperative week. At autopsy the aortic suture line was found to be grossly infected and there was mediastinal abscess formation; however, the prosthetic valve was satisfactory. There were three late deaths (Table II). Autopsy was carried out in two of them. There was no evidence of reinfection in either, and in both the prostheses were intact. Currently there are eight survivors (out of 12

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The Journal of Thoracic and Cardiovascular Surgery

Raychaudhury, Cameron, Walbaum

patients) with a mean follow up of 5.6 years (range 2 to 10). Six are in NYHA Class I and two are in Class II. Discussion The continuing high and unacceptable mortality of PVE has prompted several authors to review their own experience. So far, the operative mortality has ranged from 35% to 84% in the patients having severe hemodynamic failure.'? Various other risk factors, such as presentation within 60 days of previous valve replacement (early PVE), presence of non-streptococcal organisms, new regurgitant murmur, evidence of myocardial invasion, and aortic prosthetic replacement, have also been identified." In recent reports the presence of any of the above was associated with a mortality of over 75%,5 and the combination of two of the above increased the mortality by up to 90%.6 Although urgent surgical intervention has been proposed for patients in whom these risk factors are demonstrable, no report is available so far which would show that urgent prosthetic valve replacement in such circumstances can be successful. In Edinburgh, a policy has been observed whereby emergency prosthesis replacements have been performed on patients with suspected PVE in whom severe heart failure developed in the presence of a new regurgitant murmur. No criterion apart from those listed herein was taken into consideration for the selection of our patients. However, in retrospect, on all fourteen occasions at least three of the recognized risk factors were present, and on seven occasions nearly all of the risk factors were present (Table I). On all but one occasion the patients were operated upon within 48 hours of their hemodynamic deterioration, and our operative mortality of 7% clearly shows the feasibility and success of an aggressive surgical approach, which has already been recommended by others." Saffle and associates in 1977 reported on six patients in whom urgent prosthetic valve replacement was performed electively, irrespective of their hemodynamic status. There was one late postoperative death. However, their patients are not comparable to the patients in this series, because none of their patients had significant heart failure at the time of operation. In our patients, on the other hand, the presence of severe and intractable hemodynamic failure and advanced infection of the aortic anulus constituted a considerable threat. In six patients the femoral vessels were exposed under local anesthesia, and in five of them femoro-femoral bypass was established before the sternotomy incision was reopened. In three severely ill patients partial bypass was

established before the induction of general anesthesia. At operation all abscess cavities were curetted and obliterated by using buttressed sutures, which were subsequently used to secure the new prosthesis. Whenever the aortic anulus was partially destroyed, stitches were applied to the base of the anterior leaflet of the mitral valve and to the muscles of the left ventricular outflow tract without any complication. We did not feel any necessity to replace the aortic root or to translocate the prosthesis, as described by Danielson," Wilson," Reitz, 12 and their associates. Finally, in all but one patient (Patient 1, Table II) the appropriate antibiotic was continued intrayenously for at least 4 weeks. REFERENCES Wilson WR, Jaumin PR, Danielson GK, Giuliani ER, Washington JH, Geraci JE: Prosthetic valve endocarditis. Ann Intern Med 82:751-755,1976 2 Quenzer RW, Edwards 10, Levin S: A comparative study of 48 host valve and 24 prosthetic valve endocarditis cases. Am Heart J 92: 15-22, 1976 3 Rossiter SJ, Stinson EB, Oyer PE, Miller DC, Schapira IN, Martin RP, Shumway NE: Prosthetic valve endocarditis. J THORAC CARDIOVASC SURG 76:795-803, 1978 4 Richardson JV, Karp RB, Kirklin JW, Dismukes WE: Treatment of infective endocarditis. Circulation 58:589597, 1978 5 Masur H, Johnson WD: Prosthetic valve endocarditis. J THORAC CARDIOVASC SURG 80:31-37,1980 6 Karchmer A W, Dismukes WE, Buckley MJ, Austen WG: Late prosthetic valve endocarditis. Clinical features influencing therapy. Am J Med 64:199-206, 1978 7 Saffle JR, Gardner P, Schoenbaum SC, Wild W: Prosthetic valve endocarditis. The case for prompt valve replacement. J THORAC CARDIOVASC SURG 73:416-420, 1977 8 Arnett EN, Roberts WC: Prosthetic valve endocarditis. Clinicopathological analysis of 22 necropsy patients with active infective endocarditis involving natural left sided cardiac valves. Am J Cardiol 38:281-296, 1976 9 Braunwald E: Heart Disease I, Philadelphia, 1980, W. B. Saunders Company, p 501 10 Danielson GK, Titus JL, DuShane JW: Successful treatment of aortic valve endocarditis and aortic root abscesses by insertion of prosthetic valve in the ascending aorta and placement of bypass grafts to coronary arteries. J THORAC CARDIOVASC SURG 67:443-449, 1974 11 Wilson WR, Danielson GK, Giuliani ER, Washington JA, Jaumin PM, Geraci JE: Valve replacement in patients with active infective endocarditis. Circulation 58:585-588, 1978 12 Reitz BA, Stinson EB, Watson DC, Baumgartner WA, Jamieson MB: Translocation of the aortic valve for prosthetic valve endocarditis. J THORAC CARDIOVASC SURG 81:212-218,1981