| Optimal Treatment of Native and Prosthetic Aortic Valve Endocarditis |
Advanced Therapy in Cardiac Surgery, 1999 26:245-249Book Chapter written by John D. Oswalt, M.D.
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| Clinical Summary of Patients | ||||
|---|---|---|---|---|
| Age | Sex | Organism | Infection | Preoperative Complications |
| 29 | M | Enterococcus | Active | Stroke-speech |
| 53 | M | Streptococcus viridans | Active | |
| 34 | F | S. viridans | Inactive | |
| 32 | M | Unknown | Inactive | SBE 8-90/healed |
| 58 | M | S. viridans | Active | |
| 23 | M | S. viridans | Active | |
| 32 | M | Staphylococcus aureus Enterococcus | Active | |
| 39 | M | S. viridans | Active | |
| 50 | M | Enterococcus | Active | |
| 39 | IM | S. viridans | Inactive | Stroke-speech |
| 61 | M | Streptococcus bovis | Active | >P-R Interval |
| 59 | M | S. viridans | Active | |
| 31 | IM | S. viridans | Active | Previous freehand homograft |
| 53 | M | Unknown | Inactive | |
| 46 | M | S. aureus | Active | Peripheral emboli |
| 37 | IM | S. aureus Candida albicans | Active | |
| 34 | F | Unknown | Inactive | |
| 31 | F | Grp B Streptococcus agalactlae | Active | Hypotensive, pulmonary edema, sepsis |
| 38 | M | S. aureus | Active | Sepsis |
| 32 | M | Haemophilus influenzae | Active | |
| 33 | F | Brucellosis | Active | CHF |
| 28 | IM | S. viridans | Inactive | Cerebral emboli with seizures |
| 27 | M | S. aureus | Active | |
| 38 | M | S. viridans | Active | |
| 19 | M | S. viridans | Inactive | |
| 27 | M | S. aureus S. viridans | Inactive | |
| 39 | IM | S. viridans | Active | |
| 31 | M | Enterococcus | Active | |
| 39 | M | S. viridans | Active | |
| 54 | M | Alpha streptococcus | Inactive | |
| 50 | F | Enterococcus | Active | End-stage renal disease with dialysis |
| 25 | M | S. aureus | Active | Septic emboli-cerebral, renal, and peripheral |
| 50 | M | S. aureus | Active | End-stage renal disease with dialysis, multivegetations on mitral valve |
| 36 | F | S. virldans | Active | |
| 38 | M | Unknown | Inactive | CHF, massive LVH, 4+ mitral regurgitation, ruptured chordae |
| SBE = subacute bacterial endocarditis; CHF = congestive heart failure, LVH = left ventricular hypertrophy. | ||||
Surgical Technique
The Ross procedure has been described in other sources, but it is appropriate to discuss some of the surgical principles that should be employed during the management of aortic valve endocarditis. Complete debridement should be the order of the day, and this includes resection of all infected or marginally infected material to viable tissue. This often involves total excision of the annulus to the left ventricular outflow tract and the unroofing and exposure of all annular abscesses. Complete exteriorization of all infection away from the reconstructed circulation is important as it allows for healing of the ongoing infection. The autograft facilitates reconstruction by its pliability, allowing for viable tissue to be anastomosed accurately to viable tissue. The proximal suture line is reinforced with a strip of autologous pericardium, thereby placing no foreign material in the reconstruction of the root. All fistulas and other areas requiring repair (i.e., mitral valve or mitral valve annulus) are repaired with viable autologous pericardium or with extended right ventricular subannular muscle of the autograft taken as the autograft is harvested. Previously, we reported the harvesting of the pulmonary autograft prior to exposing the aortic root so that reconstruction of the right ventricular outflow tract with the homograft could be completed prior to exposure of the infected area. We now debride the infected area first. After the debridement, we can harvest more right ventricular muscle with the autograft if we have ascertained that additional tissue will be needed in the repair and reconstruction.
Results
Follow-up has been 77% at 7 years (mean 3 years). All 35 patients were cured of their infections. Antibiotics were administered for 3 to 6 weeks, depending on culture results it the time of surgery. If the culture was negative on tissue submitted at surgery, the shorter course was chosen, with subsequent cessation of antibiotics at 3 weeks. There was no operative mortality and there has been zero recurrence of infection on the aortic valve. One patient, at 48 months postoperatively, contracted endocarditis on his pulmonary homograft. This patient is HIV positive and a drug abuser. He was managed medically and cured of his recurrence. Postoperative complications have occurred in 20% (See table below). Postoperative bleeding occurred in 3 patients. One of these patients also required later reoperation for a false aneurysm at the proximal aortic anastomosis. Tissue from this area grew Candida, and the patient was placed on antifungal agents with no recurrence. The aortic valve was not involved. There have been 2 reoperations for valve failures; both of these patients had myxomatous changes in the autogr4ft valve leaflets at the time of mechanical replacement. Prior to their endocarditis, they both must have had myxomatous disease of their aortic valves, and this, likewise, affected the pulmonary valve. There have been 2 late deaths, I from myocardial infarction and I from congestive heart failure. Actuarial 5-year survival is 94%, and freedom from recurrent aortic endocarditis is 100%. Thromboembolic events have not been seen in late follow-up, and no patient- receives anticoagulation with the exception of the 2 patients who eventually received mechanical prostheses. The mean length of stay in the ICU was 5 days, and the hospital length of stay from procedure to discharge was 9 days.
| Operative Morbidity | |
|---|---|
| Renal | 2 |
| G1 reoperation | 1 |
| Cardiac arrest | 1* |
| Tamponade | 1 |
| Reoperation bleed | 3 |
| Infection | 1 |
| Valve failure | 2 |
| Pulmonary | 2 |
| Pacemaker | 1 |
| *Resuscitated | |
Summary
Aortic endocarditis is a difficult disease process that is increasing rather than declining. One may conclude from the reviewed data that delaying surgery is best. The author would submit that retrospective studies subselect patients so that those that were managed with antibiotics and cured prior to their surgical repair naturally would do better than those requiring urgent operation. The complications that require our urgent intervention (i.e., emboli, heart block, fistula, and continued sepsis) often arise because of our delay in treating the disease process. Placing a patient on the appropriate antibiotics does not necessarily stop the advancement of the disease process. It is important for us to educate our Cardiology and Infectious Disease colleagues that the management of endocarditis should be medical antibiotic therapy only as long as there is a normally functioning aortic valve or as long as there are no complications pushing one to surgical intervention (i.e., emboli or persistent sepsis). Once the endocarditis has destroyed the valve so that it will require replacement, the therapy should then become surgical and the operation performed for the replacement of the diseased valve. This, in turn, will treat the active infection. It is the delay after the valve needs replacement that often creates a more difficult surgical experience.
Prosthetic valve endocarditis is a different disease process from that of native valve endocarditis primarily due to the organisms. The literature certainly supports that management with antibiotics is rarely going to be successful. Should echocardiographic data show that there is a perivalvular abscess or periprosthetic insufficiency, surgical replacement as soon as possible certainly improves the outcomes. Likewise, the literature is replete with suggestions that complete debridement is essential. The aortic root is a complex structure, and once the annulus is destroyed, root resection is likely to yield the best results. Once a complete and thorough debridement is done, the replacement valve choice probably becomes less critical. Of the choices of valves used in the repair following the debridement, the literature again would suggest that choosing a valve that completely exteriorizes the infection may yield better results. Mechanical and bioprosthetic valves yield more perivalvular leaks. The accurate fixation of a nonpliable valve in a diseased root is more difficult than reconstruction with a pliable valve. The techniques of freehand subcoronary or inclusion cylinder homograft valve replacement create potential spaces between the native diseased aorta and the graft. This does not allow for exteriorization of all abscesses and is a source of recurrent endocarditis. With simple endocarditis involving only the valve leaflets, it is likely that any valve selection will yield good results. However, in complex endocarditis involving the annulus with abscesses, best results appear to favor the root replacement. Root replacement allows for total debridement of all infected material and exteriorizes any remaining infection. One must remember that the aortic leaflets and annulus are a continuum of the entire root structure. Should any part of the annulus become infected or abscessed, complete debridement probably means resection of the root. In choosing a valve, one must consider the longevity and the availability of a valve. As the disease process primarily affects the younger age group, consideration of longevity is important but it is the control of the infection and repair of the insufficiency that should the primary concern over that of longevity of the valve.
The urgency with which one must perform a curative operation for the endocarditis also requires availability of valves. The aortic homograft is becoming more and more difficult to obtain, a fact that is a consideration in choosing this tissue. Mechanical valves obviously are always available, and pulmonary homografts to replace the harvested autograft continue to be readily available. However, in the not so distant future, there could be an insufficient supply of pulmonary homografts.
Finally, there are several key points in the management of aortic infective endocarditis, for either native or prosthetic valve endocarditis. Management of prosthetic valve endocarditis with antibiotics is likely to be unsuccessful, and early operation is recommended. Once the diseased valve becomes incompetent, surgical resection and replacement should be achieved as soon as possible regardless of the infective state. The surgical operation should employ complete debridement of all infected material and the unroofing and exteriorization of all abscessed areas. The replacement valve should be meticulously implanted, ensuring good coaptation of structures, and provide the best longevity against replacement. We strongly believe that the pulmonary autograft as a root replacement is the valve that best suits all of the essential characteristics needed to achieve a cure for aortic endocarditis.
The author appreciates the assistance of Suzi Nelson, R.N., and Sharon Koch, R.N., in the preparation of this manuscript.
References
- Hufnagel CA. Surgical techniques ill the treatment of infected valvular prostheses. Baltimore: University Park Press. p. 143-60.
- Hayclock D, Barratt-Boyes B, Macedo T, et al. Aortic valve replacement for active infectious endocarditis in 108 patients. J Thorac Cardiovasc Surg 1997; 113:285-91.
- Petrou M, Wong K, Albertuci M, et al. Evaluation of unstented aortic homografts for the treatment of prosthetic aortic valve endocarditis. Circulation 1994;90(part 2): 198-204.
- Aranki S, Santini F, Adams D, et al. Aortic valve endocarditis: determinants of early Survival – and late morbidity.Circulation 1994;90(part 2): 175-82.
- Ralph-Edwards R, David T, Box J. Infective endocarditis in patients who had replacement of the aortic root. Ann Thorac Surg 1994;58:429-33.
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- Dearani J, Orszulak T, Schaff H, et al. Results of allograft aortic valve replacement for complex endocarditis. J Thorac Cardiovasc Surg 1997; 113:285-91.
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- Joyce F, Oswalt J, Tingleff J, et al. The Ross operation: treatment of choice for aortic endocarditis? Twenty Third Annual Meeting Western Surgical Association, June, 1997.
