624
September
Rrief Communications
American
6. Jensen PJ, Thomsen PEB, Bagger JP, Norgaard A, Baandrup IJ. Electrical injury causing ventricular arrhyt.hmias. Br Heart J 1987;57:279-83. 7. Oliva PB, Breckinridge JC. Acute myocardial infarction with normal or near normal coronary arteries. Am .J Cardiol 1977;40:1000-7.
Tricuspid valve endocarditis with normal hearts
in children
M. P. Tornos, MD, A. Castro, MD, N. Toran, MD.” and J. Girona, MD.b Barcelona, Spain
Tricuspid endocarditis in children with previously normal hearts is an extremely uncommondisease.(*-2) However, the diagnosisshould be ruled out in casesof bacteremia due to Staphylococcus aureus and in those with pulmonary symptoms in order to avoid delayed diagnosisand treatment. Case No. 1. A previously healthy ‘i-year-old girl wasadmitted to our hospital with a 2-week-history of fever, chills, diarrhea, and joint and chest pain. On examination, her temperature was39” C, the liver and spleenwerepalpated, there were no skin lesions,and no cardiac murmurs were heard. Chest x-ray film showedan area of consolidation in the left lower lobe. Blood test showeda white blood cell count of 12,500per cubic millimeter and marked thrombocytopenia of 40,000per cubic millimeter. Stool and blood
From Servei de Cardiologia, Anatomia Patologicaa i Clinica Infantilb. Ciutat Sanitaria Vall d’Hebron, 08035. Barcelona, Spain. Reprint requests: Dr. M. P. Tornos, Servei de Cardiologia, Hospital General Vail d’Hebron, PO Vail d’Hebron S/n, 08035 Barcelona, Spain. 4/4/13971
Heart
cultures grew Staphylococcus aureus and treatment was started with cloxacillin and gentamicin. Three days later. bilateral lung consolidationswere observedin the repeated chest x-ray. Two-dimensional echocardiography showeda large masson the tricuspid valve, consistent with vegetations (Fig. 1,A). The diagnosisof tricuspid valve endocarditis and pulmonary septic emboli was made. Antibiotic treatment was continued and the patient becameafebrile after 2 weeks.A faint systolic murmur of tricuspid incompetence appeared,but there were no further signsof pulmonary emboli or signs of heart failure. After 6 weeksof antibiotic treatment, the patient was discharged in good health, with negative blood cultures and with an echocardiogram showinga marked decreasein the size of the tricuspid vegetation (Fig. 1, B). She has remained symptomfree during 1 year of follow-up. CaseNo. 2. A 2900gm femaleinfant wasborn at 43weeks’ gestationand wasfound to bein normal health. Twenty-two days later, shewasadmitted to another hospital becauseof fever andintolerance to feeding.On admission,temperature was38.5“ C and there wasa red tender swellingon the right heel, where a routine puncture had been performed after birth. Signs of osteochondritis in the distal femoral metaphysis and a lytic lesionon the calcaneuswere seenin the x-ray examination. Culture of the aspirate and blood cultures grew Staphylococcus aureus. Treatment was started with cloxacillin and gentamicin and waschangedto vancomycin after the resultsof the antibiotic screeningwere assessed. Two days later, signsof heart failure appeared.In spite of antibiotic treatment and supportive measures,signs of heart failure persistedand after 30days of treatment the child was transferred to our hospital. At the time of admissionthe child was cyanotic and in very poor condition. The liver and spleenwere palpated to the pelvic rim. There wasa 2/6 systolic murmur and a gallop rhythm. An echocardiographicstudy revealed a large mass attached to the tricuspid valve (Fig. 2). Surgical
1. Two-dimensional echocardiographic findings in caseNo. 1. A, Parasternal long-axis view of the right ventricle showinga vegetation adherent to the tricuspid valve (arrow). B, Sameview at hospital discharge. The vegetation has disappeared.RV. Right ventricle; RA, right atrium. Fig.
1989 Journal
Volume
118
Number
3
Brief Communications
625
One of our patients treated medically survived and remains symptom-free. During the acute illness, however, she developedsevererespiratory symptomsmost likely due to pulmonary emboli.Thesesymptomsresolvedand tricuspid surgery wasnot attempted. In our secondpatient, the delay in diagnosisand consequentsurgery surely influenced the clinical outcome. Although the three casespreviously reported in the literature were all treated. surgically, we believe that even if pulmonary embolization occurs,there is a chancefor medical treatment if heart failure or major and repetitive embolization do not occur. Although the incidenceof this diseaseis probably low, it is likely to be underdiagnosed.Tricuspid endocarditis should be ruled out by meansof echocardiographyin any child with respiratory symptoms and staphylococcal septicemia. REFERENCES
2. Two-dimensional echocardiographic findings in caseNo. 2. Four-chamber apical view demonstratesa vegetation adherent to the tricuspid valve (arrow). RA, Right atrium; LA, left atrium; LV, left ventricle. Fig.
treatment wasdecidedupon. At surgery, a large vegetation was found on the tricuspid valve that spanned the valve orifice. Tricuspid resectionwasperformed. Unfortunately, the child died in the early postoperative period. Postmortem examination showeda structurally normal heart and a lesion on the right free wall extending to the tricuspid anulus. Microscopically the lesion consisted of fibrinogranulocytic depositsand patchy areasof endocardial necrosis.Other foci of acute infection were osteomyelitis on the calcaneusand tibia1 bones,panniculitis of the heel, and microabscesses in the cerebral truncus. Infective endocarditis in children is an uncommon disease,although an increasingincidence hasbeen suggested asa result of a better survival of children with severeheart malformations and the increaseduse of foreign intracardiac materials and indwelling catheters.(3-5)In neonates, endocarditis is normally related to septicemiaand invasive monitoring.6 The development of infective endocarditis in infants with sepsisbut without underlying heart diseaseis very rare. Although it has been suggestedthat the risk of infective endocarditis in Staphylococcus mre’eusbacteremia when there is a defined primary site of infection is especially low, in one of our patients a metastatic seeding from the skin clearly occurred. Our two patients were children with normal hearts who suffered from tricuspid endocarditis due to Staphylococcus aureus. To our knowlege,there are only three previous casesdescribedso far.(‘p2, In them as in ours, echocardiography wasessentialfor establishingthe correct diagnosis.
1. Goessler MC, Riggs TW, DeLeon S, Paul MH. Echocardiographic diagnosis of tricuspid valve endocarditis in a child with a normal heart. Pediatr Cardiol 1982;2:141-3. ‘2. Musewe NN, Hecht BM, Hesslein PS, Rose V, Williams WG. Tricuspid valve endocarditis in two children with normal hearts: diagnosis and therapy of an unusuai entity. J Pediatr 1987;110:735-8. 3. Schollin J, Bjarke B, Wesstriim G. Infective endocarditis in Swedish children. Acta Paediatr Stand 1986;75:993-8. 4. Stanton BF, Baltimore RS, Clemens JD. Changing spectrum of infective endocarditis in children. Am J Dis Child 1984; 138:720-5. 5. Van Hare GF, Ben-Shachar G, Liebman J, Boxerbaum B, Riemenschneider TA. Infective endocarditis in infants and children during the past10 years:adecadeof change. AM HEART J 1984;
107:1235-40.
6. McGuinness GA, Schieken RM, Maguire GF. Endocarditis the newborn. Am J Dis Child 1980;134:577-80.
Two-dimensional echocardiographic visualization of turbulent intracardiac flow across the stenotic mitral valve
in
blood
Krishnaswamy Chandrasekaran,MD, John Ross,Jr., RCPT, Veronica A. Covaiesky, MD, J. Yasha Kresh, PhD, and Gary S. Mintz, MD. Philadelphia,
Pa.
Intracavitary echoesfrom red blood cells are seen commonly on two-dimensional echocardiographic imagesin clinical conditions associatedwith low flow states and stasessuch as cardiomyopathies and ventricular aneurysms.1-5 The improved resolution of the current generation of real-time clinical ultrasonic scannershasincreased From the Likoff Cardiovascular
Institute and the Department of Medicine, Hahnemann University Hospital. Reprint requests: K. Chandrasekaran, MD, Hahnemann University, Dept. of Medicine, Likoff Cardiovascular Institute. Broad & Vine Streets, Philadelphia, PA 19102. 4/4/13970