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Asian Cardiovasc Thorac Ann 1999;7:153-155
© 1999 Asia Publishing EXchange Pte Ltd


CASE STUDY

Tricuspid Valve Endocarditis With Pulmonary Embolism Due to Postpartum Septicemia

Ashok K Srivastava, MCh, Anil Aggarwal, MS, Aditya Kapoor, DM1,

Department of Cardiovascular Surgery
1 Department of Cardiology
Sanjay Gandhi Postgraduate Institute of Medical Sciences Lucknow, India
For reprint information contact: Ashok K Srivastava, MCh Tel: 91 522 44 0963 Fax: 91 522 44 0017 or 44 0973 email: ashok{at}sgpgi.ren.nic.in Department of Cardiovascular Surgery, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Raebareli Road, Lucknow 226014, India.

    Abstract
 TOP
 Abstract
 Introduction
 Case Report
 Discussion
 References
 
Tricuspid valve endocarditis usually affects drug addicts without any preexisting heart disease. We report the successful surgical management of a case of tricuspid valve endocarditis with pulmonary artery embolism arising from postpartum septicemia.


    Introduction
 TOP
 Abstract
 Introduction
 Case Report
 Discussion
 References
 
The overall incidence of involvement of the tricuspid valve in patients with infective endocarditis is in the range of 5% to 10%. The lower frequency of right-sided endocarditis compared with the left side may be explained by the lower rates of congenital and rheumatic heart diseases affecting the right-side valves, the lower right-heart pressure with decreased stress to the tricuspid and pulmonary valves, and the lower right-heart blood oxygen content.1 Tricuspid valve endocarditis (TVE) usually affects drug addicts without any pre-existing heart disease. The relatively benign prognosis of these patients compared to those with left-sided infective endocarditis is well documented. More than 75% of these patients respond to medical treatment and only 20% to 25% require surgery.2 We describe an unusual case of TVE occurring in the postpartum period that was associated with a large embolic obstruction of the right pulmonary artery and its successful surgical management.


    Case Report
 TOP
 Abstract
 Introduction
 Case Report
 Discussion
 References
 
The patient was a 24-year-old female who had developed a high-grade fever 10 days after a full-term normal vaginal delivery at a local hospital. She was treated with various combinations of oral and intravenous antibiotics but developed progressively increasing breathlessness with a dry cough and persistence of a variable high-grade fever during the month prior to admission to our hospital. She denied any history of drug abuse, hemoptysis, acute chest pain, or pedal edema. On admission, she was febrile (40.4°C), toxic, and orthopneic. She had a pulse rate of 130 beats•min–1, blood pressure of 110/70 mm Hg, and jugular venous pressure 5 cm above the sternal angle with a prominent v wave. Cardiovascular examination revealed a grade II left parasternal heave and a grade III/IV pansystolic murmur of tricuspid regurgitation. There were diffuse end-inspiratory crackles in her chest on the right side. She had no ascites, hepatosplenomegaly, pedal edema, or features suggestive of deep-vein thrombosis of the lower limbs. Laboratory studies revealed leukocytosis and hematuria. Pseudomonas aeruginosa was isolated from blood cultures, which was reported to be sensitive to ceftazidime and amikacin. On admission, her chest radiograph revealed a wedge-shaped opacity in the right lower zone, whereas a radiograph 2 weeks earlier had been normal. Her electrocardiogram demonstrated sinus tachycardia (150 beats•min–1), right axis deviation, and small Q waves in leads II, III and aVF with inverted T waves in lead III. On echocardiography, the right atrium and right ventricle were dilated and a 16 x 5 mm highly mobile vegetation was seen attached to the posterior leaflet of the tricuspid valve. There was moderate tricuspid regurgitation and the predicted right ventricular systolic pressure was 35 mm Hg. Other valves were normal. Based on these findings, a diagnosis of tricuspid valve endocarditis with septic pulmonary embolism was entertained and a ventilation-perfusion scan performed. This revealed normal ventilation and almost no perfusion of the entire right lung, while the left lung was perfused normally. Pulmonary angiography demonstrated total occlusion of the right pulmonary artery just beyond its origin (Figure 1Go). Although the patient was started on antibiotic therapy in accordance with the blood culture and sensitivity report, it was decided to carry out urgent surgical exploration in view of the large mobile vegetation on the tricuspid valve and the septic pulmonary embolism.



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Figure 1. Main pulmonary artery angiogram (anteroposterior view) showing the obstructed proximal right pulmonary artery with normal perfusion on the left side.

 
The heart was approached via a median sternotomy. Cardiopulmonary bypass was established with moderate hypothermia using ascending aortic and bicaval cannu-lation. After a right atriotomy, a l0 x 5 mm vegetation was seen attached to the posterior leaflet of the tricuspid valve. The vegetation was excised along with part of the posterior leaflet between its annular attachment and chordal insertion. A new posterior leaflet was constructed using native pericardium in which the subvalvular apparatus was reattached, followed by De Vaga's annuloplasty. Main pulmonary arteriotomy revealed complete occlusion of the mouth of the right pulmonary artery by a septic vegetation that was removed piecemeal. As the embolus was adherent to the vessel wall, a separate incision was made over the right pulmonary artery between the superior vena cava and the ascending aorta and further vegetation was removed from the distal artery. The arteriotomy was repaired with a pericardial patch. The aortic cross-clamp time was 75 minutes and the cardiopulmonary bypass time was 120 minutes. The patient withstood the procedure well. Histopathological examination of the excised tricuspid valve leaflet showed sections lined with fibrinoid necrotic material with mixed inflammatory cell infiltration. Echocardiography 3 weeks after surgery showed a normally functioning tricuspid valve with mild regurgitation. At the one-year follow-up examination, the patient was in New York Heart Association functional class I and her echocardiogram was normal.


    Discussion
 TOP
 Abstract
 Introduction
 Case Report
 Discussion
 References
 
This patient had an unusual combination of tricuspid valve endocarditis in the setting of an intrinsically normal tricuspid valve in a non-drug user with septic pulmonary embolization involving the proximal right pulmonary artery. Although endocarditis involving the right-side valves is usually a disease of drug abusers, other conditions such as immunodeficiency states, alcoholism, extensive burns, longstanding indwelling right-side catheters, and congenital heart diseases with left-to-right shunts may give rise to TVE.3,4 Highly virulent organisms such as Staphylococcus aureus are the most commonly isolated organisms, although streptococcus, Pseudomonas aeruginosa, and candida are also frequently isolated, with polymicrobial infections being more common in drug addicts.

Our patient probably had postpartum septicemia that predisposed her to tricuspid valve endocarditis. Furthermore, she had received multiple parenteral injections and the longstanding indwelling intravenous cannula may have led to seeding of the tricuspid valve, a setting somewhat akin to that of a drug abuser. Although she denied any chest pain, the progressively increasing dyspnea was probably due to septic embolization of the vegetation in the pulmonary vasculature. The diagnosis of pulmonary embolism was provided by radiography, electrocardiography, and the ventilation-perfusion scan. Pulmonary angiography was not required for diagnosis but in view of the findings in the lung scan, it was considered necessary to locate the site of the obstruction in the right pulmonary artery prior to surgery. There was concern that the right lung might develop an abscess with secondary infection but this did not occur.

Robbin and colleagues5 suggested the major criteria for the diagnosis of TVE to be vegetation demonstrable on echocardiography and pyrexia; minor criteria comprise multiple positive blood cultures, evidence of septic pulmonary emboli, absence of systemic emboli, and a murmur compatible with tricuspid involvement. Either 2 major or one major and 3 minor criteria must be met to establish a diagnosis of TVE. However, the sensitivity and specificity of these criteria have not been established. Our patient fulfilled both of the major and 3 of the 4 minor criteria. Generally, pleuropneumonic symptoms rather than right heart failure are more common in TVE, as in our case. When present, the signs and symptoms of right heart failure indicate a poor prognosis.

Pulmonary embolism is an important complication of tricuspid valve endocarditis and emboli may continue to occur despite successful eradication of infection.6 Although recurrent pulmonary embolism may not be a indication of surgery in all cases of TVE, we decided to perform urgent surgery in this patient because of her prolonged fever and totally obstructed proximal right pulmonary artery with underlying pseudomonal infection. In tricuspid valve endocarditis with resistant or relapsing infection, surgery with excision of the tricuspid valve without immediate replacement is well tolerated so long as there is no associated pulmonary artery hypertension; if tricuspid regurgitation remains intractable and the infection has been adequately controlled, replacement of the valve can be performed later.7 A reconstructive approach for tricuspid valvuloplasty using autologous pericardial tissue (to avoid prosthetic material) has also been described in cases of TVE.8 Tricuspid valvuloplasty along with removal of the embolic vegetation from the right pulmonary artery was achieved with very satisfactory results in our patient.


    References
 TOP
 Abstract
 Introduction
 Case Report
 Discussion
 References
 

  1. Chan P, Ogibly D, Segal B. Tricuspid valve endocarditis. Am Heart J 1989;117:1140–6.[Medline]

  2. Reyes MP, Palutke WA, Wylin RF, Lerner AM. Pseudomonas endocarditis in the Detroit Medical Center, 1969–72. Medicine 1973;52:123.

  3. Baskin TW, Rosenthal A, Pruitt BA. Acute bacterial endocarditis: a silent source of sepsis in the burn patient. Ann Surg 1976;184:618.[Medline]

  4. Roweley KM, Clubb KS, Smith GJW, Cabin MS. Right-sided infective endocarditis as a consequence of flow-directed pulmonary artery catheterization. A clinicopathological study of 55 autopsied patients. N Engl J Med 1984;311:1152.[Abstract]

  5. Robbin MJ, Frater RWM, Soeiro R, Frishman WH, Storm JA. Influence of vegetation size on clinical outcome of right-sided infective endocarditis. Am J Med 1986;80:165.[Medline]

  6. Hubbell G, Cheitlin MD, Rapaport E. Presentation, management and follow-up evaluation of infective endocarditis in drug addicts. Am Heart J 1981;102:85.[Medline]

  7. Arbulu A, Asfew I. Tricuspid valvulectomy without prosthetic replacement: ten years of clinical experience. J Thorac Cardiovasc Surg 1981;82:684.[Medline]

  8. Yee ES, Ullyot DJ. Reparative approach for right-sided endocarditis. J Thorac Cardiovasc Surg 1988;96:133.[Abstract]





This Article
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Right arrow Articles by Srivastava, A. K
Right arrow Articles by Kapoor, A.


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