Volume 13, Issue 3 , Pages e109-e111, May 2009
Isolated tricuspid valve endocarditis
Article Outline
Summary
We present two non-HIV-infected patients with isolated native non-rheumatic tricuspid valve endocarditis who were not intravenous drug abusers. The patients presented with fever and chills. Plain radiography or high-resolution computed tomography of the chest revealed consolidation or infiltrate of the left parenchyma in both patients. Large vegetation located on the tricuspid leaflets was detected by transesophageal echocardiography. Staphylococcus aureus grew in two out of three blood cultures for one patient. Tricuspid valve endocarditis imitates illnesses with fever and pulmonary symptoms or signs of acute or chronic onset, and might be present even without abnormal chest X-rays or intravenous drug addiction.
Keywords: Tricuspid valve, Endocarditis, Intravenous drug use
Introduction
Right-sided endocarditis occurs predominantly in intravenous drug abusers (IVDAs) and patients with pacemakers, central venous lines or congenital heart disease. The vast majority of cases involve the tricuspid valve.1 Tricuspid valve endocarditis (TVE) is only very rarely considered in the differential diagnosis of a febrile patient who does not use intravenous drugs. In the earlier literature, TVE accounts for 2.5–3.1% of all cases of infectious endocarditis (IE).2 One would expect a marked reduction in the incidence of TVE with the advent of effective antibiotics and a reduction in IE related to rheumatic valvular disease. Nevertheless, for a subgroup of patients who do not use intravenous drugs and have normal valves, isolated TVE continues to occur, eluding diagnosis, and is sometimes only discovered at autopsy.3
Case reports
In the first case, a 47-year-old male with a history of multiple sclerosis was admitted to hospital because of fever, chills and dyspnea. The onset of illness was two weeks before admission, with fever, headache, nausea, malaise and anorexia. Two days before admission, a physician prescribed an oral antibiotic to treat presumed acute pneumonia, with no improvement. The patient had not undergone any invasive treatment or diagnostic procedures recently. On physical examination, his temperature was 39.2
°C, his heart rate was 120 bpm and the respiratory rate was 38 breaths per minute. The patient’s blood pressure was 145/80 mmHg. A systolic murmur, grade 2 over 6, was heard at the left upper sternal border with no pericardial rub. The lungs were clear bilaterally. Peripheral stigmata of IE were absent. The patient had no peripheral venous catheters or other infectious focus (skin, genitourinary tract, gastrointestinal tract and maxillofacial area).
Laboratory findings included hemoglobin of 130g/l, a white blood cell count of 10.9×109/l, an erythrocyte sedimentation rate of 80mm/hour, and microscopic hematuria with numerous red blood cells per high power field. C-reactive protein (CRP) was in the range 20mg/l. Urine cytology and culture results were negative. Plain chest radiography was reported normal.
On the fifth day, we received a report that two out of three blood cultures were positive for Gram-positive cocci, which were later identified as methicillin-sensitive Staphylococcus aureus (MSSA). The prescribed antibiotics (ceftriaxone and vancomycin) were changed to cloxacillin. High-resolution computed tomography (HRCT) revealed consolidation in the apical segment of the lower lobe of the right lung and the apicoposterior segment of the upper lobe of the left lung. Transthoracic echocardiography (TTE) showed tricuspid regurgitation and mitral regurgitation without vegetation. A transesophageal cardiac echocardiography showed mobile, large vegetation of the tricuspid valve. Other valves appeared normal.
The patient was treated with cloxacillin for a four-week period, with negative blood culture and normal CRP levels at the end. Control echocardiographic examination and continuation of treatment by cloxacillin were not performed because of early discharge of the patient by his relatives.
In the second case, a 38-year-old female was admitted to hospital because of chills and fever for a three-week duration. The patient reported headache, vomiting, a productive cough and dyspnea two days before admission. The patient’s past history was unremarkable, other than the occurrence of type 2 diabetes mellitus for two years. On admission, the patient appeared pale and there was dullness at the base of the right lung.
Cardiac murmurs and evidence of heart failure were absent. Again, peripheral venous catheters or other infectious focus (skin, genitourinary tract, gastrointestinal tract, etc.) were absent. Laboratory findings included hemoglobin of 113g/l, a white blood cell count of 14.0×109/l, and microscopic hematuria and pyuria. CRP was in the range 15mg/l.
The results of the chest radiography and blood cultures were negative. Intravenous ceftriaxone was administered. On the third day of admission, the patient’s clinical picture and chest radiograph showed increased respiratory symptoms and pulmonary infiltrates, respectively. HRCT revealed consolidation in the lower lobe of the right lung and bilateral plural effusions. We added anti-tuberculosis drugs to the regimen, but no significant response was seen after five days. The echocardiography was done and showed large tricuspid valve vegetation (Figure 1) with regurgitation. Anti-tuberculosis drugs were discontinued, vancomycin and gentamicin were added to ceftriaxone, and she was referred to another institution for cardiac surgery. However, she died before surgery with possible massive pulmonary emboli. Autopsy was not performed after death.
Figure 1.
Large tricuspid valve vegetation caused by S. aureus in a 38-year-old patient (case 2).
Discussion
Isolated native non-rheumatic TVE is rarely diagnosed in the absence of intravenous drug use, intracardiac catheters or cardiac anomalies. In a report, 9.5% of patients who did not use intravenous drugs and 83% who did had TVE.4 Two-thirds of IVDAs had no evidence of underlying heart disease and there is a predilection for the infection to affect the tricuspid valve.5 The presence of right-sided IE might be a predicting factor of drug abuse, even if the injection sites are not clearly visible. For this reason, a toxicological analysis of patients with right-sided IE is recommended.6
S. aureus causes 50–75% of cases of endocarditis associated with intravenous drug use. Other causative organisms of TVE include Candida species, particularly Candida glabrata,7 Streptococcus bovis,8 Gemella morbillorum,9 and Pseudomonas aeruginosa.10 Fever, multiple pulmonary emboli and sustained bacteremia by S. aureus are signs of clinical alert for right-sided endocarditis.11 Symptoms related to pulmonary emboli usually force patients to seek medical attention and dominate the clinical picture. Pulmonary events occur in 80% of these cases, and vary from minor atelectases to large infiltrates, pleural exudates and cavitation, generally involving the lower lobes. Chest radiography can be normal; hence, HRCT should be performed to reveal abnormalities. Sometimes the simultaneous visualization of previously undiagnosed right-sided empyema, via transesophageal echocardiography, might lead to the diagnosis of pulmonary involvement.12 Peripheral stigmata of IE are not consistently present. There is a paucity of cardiac symptoms and signs, as is common with most cases of right-sided endocarditis. Regurgitant systolic murmurs develop late in the course of the illness. Some authors suggest that clinical suspicion of TVE should be raised in the presence of recurrent pulmonary events, anemia and microscopic hematuria – the so-called ‘tricuspid syndrome’. Some patients, such as those referred to in this study, have debility, anemia and weight loss, generating a diagnostic work-up for tuberculosis and malignancy.
In summary, TVE is an unusual cardiac event. In the absence of a history of intravenous drug use, diagnostic delays are common. We conclude that isolated TVE mimics chronic illnesses of acute or chronic onset complicated by recurrent pulmonary events, anemia and microscopic hematuria.
Acknowledgements
We thank Dr. Mohammadi and Mr Ghasemi for their assistance in the preparation of the figure.
Conflict of interest: No conflict of interest to declare
References
- . A rare localization in right-sided endocarditis diagnosed by echocardiography: a case report. Cardiovasc Ultrasound. 2003;14:10
- . Gustonian lectures on malignant endocarditis. Lancet. 1885;1:415–418
- . Isolated tricuspid valve endocarditis in nonaddicted patients: a diagnostic challenge. Am J Med Sci. 1997;314:207–212
- . Influence of vegetation size on clinical outcome of right-sided infective endocarditis. Am J Med. 1986;80:165–171
- . Endocarditis and intravascular infections. In: Mandell GL, Bennett JE, Dolin R editor. Principles and Practice of Infectious Diseases. 5th edition. New York: Churchill Livingstone; 2000;
- . Unexpected death due to right-sided infective endocarditis in a methamphetamine abuser. Leg Med (Tokyo). 2003;5:65–68
- . Fungal endocarditis: analysis of 24 cases and review of the literature. Medicine. 1975;54:331–344
- . Streptococcus bovis bacteremia requires rigorous exclusion of colonic neoplasia and endocarditis. Q J Med. 1985;56:439–450
- . Association of Gemella morbillorum endocarditis with adenomatous polyps and carcinoma of the colon: case report and review. Clin Infect Dis. 1996;22:379–380
- . Right-sided bacterial endocarditis. New concepts in the treatment of the uncontrollable infection. Ann Thorac Surg. 1973;16:136–140
- . Endocarditis in parenteral drug addicts. Right-sided endocarditis. Influence of HIV infection. Rev Esp Cardiol. 1998;51(Suppl 2):71–78
- . Diagnoses of right-sided empyema complicating tricuspid valve endocarditis during transesophageal echocardiography. J Am Soc Echocardiogr. 2004;17:464–465
PII: S1201-9712(08)01493-8
doi:10.1016/j.ijid.2008.07.018
© 2008 International Society for Infectious Diseases. Published by Elsevier Inc. All rights reserved.
Volume 13, Issue 3 , Pages e109-e111, May 2009
