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Valvar vegetations in the neonate due to fetal endocarditis
International Journal of Cardiology, 32 (1991) 103-105 0 1991 Elsevier Science Publishers B.V. 0167-5273/91/$03.50 ADONIS 0167527391001647
CARD10
103
12821
Brief Reports
Valvar vegetations in the neonate due to fetal endocarditis
*
Samuel Menahem, Melissa J. Robbie and V. Samuel Rajadurai Departments
of Cardiology, Paediatries and Pathology, Monash Medical Centre, Melbourne, Australia
(Received 4 December 1990; revision accepted 3 January 1991)
.
Mass lesions were observed on the tricuspid valve by cross-sectional ecboeanhogrppb yin5neonateq4ofwhom presented with fetal distress. Four went on to develop severe respiratory distress, 3 from meconhnn aspkation and 1 from hyaline membrane disease, with 2 deaths despite intensive treatment. Autopsy confii meeoaium aspiration pneumonia. Sterile, unorganised vegetations were seen on the tricuspid valve (and in 1 infant the m&al valve too). Perinatal factors such as hypoxia, ‘haemodynamic and coagulation disturbances may have contrfbute4l to the formation of the vegetations and may reflect the severity and refractoriness of persistent pulmonary hypertension. Key words: Fetal/neonatal
valvar vegetation; Persistent pulmonary hypertension
Introduction Valvar vegetations are rarely seen in the newborn and previously have been described as findings at autopsy [l-3]. We have now observed 5 neonates having such lesions identified by cross-sectional echocardiography carried out to exclude a cardiac cause for persistent pulmonary hypertension and mild duskiness in 1 infant. Subjects and Results Valvar vegetations were seen in 5 neonates. Four were post-term infants, 2 delivered by urgent Caesarian section and 2 by forceps, all for foetal distress. Three developed fetal bradycardia and thick meconium liquor. All 3 required early ventilation because of severe respiratory distress and meconium aspiration. Inotropic support and vasodilators were instituted because of fairly rapid deterioration. Cross-sectional echocardiography done on day 1 or 2 confirmed persistent fetal circulation but also showed mass lesions on the triCorrespondence to; A/Prof. S. Menahem, Monash Medical Centre, 246 Clayton Rd, Clayton, Vie 3168, Australia. * Presented in part to the Cardiac Society of Australia and New Zealand, May 1990.
cuspid valve measuring 4 to 7 mm in diameter (Fig. 1). Despite intensive treatment, 2 infants died at 46 and 51 hours. Autopsy confirmed meconium aspiration pneumonia. The tricuspid lesions (Fig. 2a), revealed on histology, unorganised laminated platelet and fibrin thrombus (Fig. 2b). A smaller thrombus was also present on the mitral valve in one infant and in the abdominal aorta where an umbilical arterial catheter had been present in the other. The early development of hypotension and increasing cyanosis despite ventilation in the third infant led to the institution of extracorporeal membrane oxygenation at the Royal Children’s Hospital. Melbourne, with a successful outcome. The fourth infant who only had meconium staining of the liquor remained pale, slightly dusky with mild respiratory distress and developed a temperature of 37S” C on day 3. Her cultures remained negative but cross-sectional echocardiography on day 7 revealed normal anatomy, a dilated right ventricle and a vegetation on the tricuspid valve. The final infant was delivered by Caeserian section at 36 weeks because of maternal toxaemia and falling oestriols. He developed severe hyaline membrane disease and required inotropic support for hypotension, and vasodilators for persistent pulmonary hypertension. Echocardiography on day 2 confirmed the latter but in
survived, one with the help of extracorporeal membrane oxygenation. In the 3 SUrviVOrS, follow-up echocardiography revealed gradual decrease in the size of the vegetations. Discussion
Fig. 1. Vegetation noted on tricuspid leaflet on cross-sectional echocardiography (parastemal short axis view of right ventricle. RA = right atrium; RV = right ventricle; TV = tricuspid valve; veg = vegetations.
addition showed a tricuspid lesion. He gradually improved over the course of a week. Thrombocytopaenia and consumptive coagulopathy were noted in only 2 of the 5 infants, both of whom
The presence of vegetations at or shortly after birth suggests perinatal factors contributing to their formation. The infants experienced fetal and neonatal hypoxia together with haemodynamic and metabolic disturbances. Recent studies have attempted to look at physiological and biochemical changes affecting the endothelium and pulmonary vascular bed in neonatal pulmonary hypertension [4]. This may provide a more rational explanation for the formation of the vegetations, rather than implication of infective or rheumatic causes as suggested by earlier reports which tried to explain incidental autopsy findings [l]. All infants had negative blood cultures, and the vegetations themselves were found to be sterile at autopsy. No infant had a central venous line that could have traumatized the tricuspid valve. Blood cysts [5] may be found on the closure lines of the tricuspid valve, and occasionally on the mitral and arterial valves. They tend to be single though may be multiple. Usually in the neonate they are quite small, reaching a size of 1 to 2 mm in diameter and need not be confused with the larger, uniformly dense vegetations noted on cross-sectional echocardiography and confirmed histologically. The presence of such vegetations in the ill neonate with persistent pulmonary hypertension may indicate a pOOr prognosis and suggest the possible development of pulmonary vascular changes which are refractory to treatment. One infant, however, seemed not as severely affected. These observations warrant a further search of such lesions in the newborn, together with a clearer elucidation of their pathogenesis.
Fig. 2. (a) Vegetation
as seen at autopsy.
(b) Photomicrograph
of vegetation thrombus
References 1 McDonald RH. Valvular thrombotic vegetations in the newborn (fetal endocarditis). Arch Path01 1950;50:538-544. 2 Plaut A, Shamoff G. Acute valvular endocarditis in the newborn. Arch Pathol 1935;20:582-586. 3 Plaut A. Active endocarditis in the newborn (report of 2 cases). Am J Pathol 1939;15:649-650.
consisting
of unorganised
layers of platelet
and fibrin
S. Pulmonary vascular remodelling in neonatal 4 Haworth pulmonary hypertension. Chest 1988;93(suppl):127S-132s. KG, Paplanus SH. Dong S, Nagle RB. Con5 Zimmerman genital blood cysts of the heart valves. Hum Path01 1983;14:699-703.
CARD10
103
12821
Brief Reports
Valvar vegetations in the neonate due to fetal endocarditis
*
Samuel Menahem, Melissa J. Robbie and V. Samuel Rajadurai Departments
of Cardiology, Paediatries and Pathology, Monash Medical Centre, Melbourne, Australia
(Received 4 December 1990; revision accepted 3 January 1991)
.
Mass lesions were observed on the tricuspid valve by cross-sectional ecboeanhogrppb yin5neonateq4ofwhom presented with fetal distress. Four went on to develop severe respiratory distress, 3 from meconhnn aspkation and 1 from hyaline membrane disease, with 2 deaths despite intensive treatment. Autopsy confii meeoaium aspiration pneumonia. Sterile, unorganised vegetations were seen on the tricuspid valve (and in 1 infant the m&al valve too). Perinatal factors such as hypoxia, ‘haemodynamic and coagulation disturbances may have contrfbute4l to the formation of the vegetations and may reflect the severity and refractoriness of persistent pulmonary hypertension. Key words: Fetal/neonatal
valvar vegetation; Persistent pulmonary hypertension
Introduction Valvar vegetations are rarely seen in the newborn and previously have been described as findings at autopsy [l-3]. We have now observed 5 neonates having such lesions identified by cross-sectional echocardiography carried out to exclude a cardiac cause for persistent pulmonary hypertension and mild duskiness in 1 infant. Subjects and Results Valvar vegetations were seen in 5 neonates. Four were post-term infants, 2 delivered by urgent Caesarian section and 2 by forceps, all for foetal distress. Three developed fetal bradycardia and thick meconium liquor. All 3 required early ventilation because of severe respiratory distress and meconium aspiration. Inotropic support and vasodilators were instituted because of fairly rapid deterioration. Cross-sectional echocardiography done on day 1 or 2 confirmed persistent fetal circulation but also showed mass lesions on the triCorrespondence to; A/Prof. S. Menahem, Monash Medical Centre, 246 Clayton Rd, Clayton, Vie 3168, Australia. * Presented in part to the Cardiac Society of Australia and New Zealand, May 1990.
cuspid valve measuring 4 to 7 mm in diameter (Fig. 1). Despite intensive treatment, 2 infants died at 46 and 51 hours. Autopsy confirmed meconium aspiration pneumonia. The tricuspid lesions (Fig. 2a), revealed on histology, unorganised laminated platelet and fibrin thrombus (Fig. 2b). A smaller thrombus was also present on the mitral valve in one infant and in the abdominal aorta where an umbilical arterial catheter had been present in the other. The early development of hypotension and increasing cyanosis despite ventilation in the third infant led to the institution of extracorporeal membrane oxygenation at the Royal Children’s Hospital. Melbourne, with a successful outcome. The fourth infant who only had meconium staining of the liquor remained pale, slightly dusky with mild respiratory distress and developed a temperature of 37S” C on day 3. Her cultures remained negative but cross-sectional echocardiography on day 7 revealed normal anatomy, a dilated right ventricle and a vegetation on the tricuspid valve. The final infant was delivered by Caeserian section at 36 weeks because of maternal toxaemia and falling oestriols. He developed severe hyaline membrane disease and required inotropic support for hypotension, and vasodilators for persistent pulmonary hypertension. Echocardiography on day 2 confirmed the latter but in
survived, one with the help of extracorporeal membrane oxygenation. In the 3 SUrviVOrS, follow-up echocardiography revealed gradual decrease in the size of the vegetations. Discussion
Fig. 1. Vegetation noted on tricuspid leaflet on cross-sectional echocardiography (parastemal short axis view of right ventricle. RA = right atrium; RV = right ventricle; TV = tricuspid valve; veg = vegetations.
addition showed a tricuspid lesion. He gradually improved over the course of a week. Thrombocytopaenia and consumptive coagulopathy were noted in only 2 of the 5 infants, both of whom
The presence of vegetations at or shortly after birth suggests perinatal factors contributing to their formation. The infants experienced fetal and neonatal hypoxia together with haemodynamic and metabolic disturbances. Recent studies have attempted to look at physiological and biochemical changes affecting the endothelium and pulmonary vascular bed in neonatal pulmonary hypertension [4]. This may provide a more rational explanation for the formation of the vegetations, rather than implication of infective or rheumatic causes as suggested by earlier reports which tried to explain incidental autopsy findings [l]. All infants had negative blood cultures, and the vegetations themselves were found to be sterile at autopsy. No infant had a central venous line that could have traumatized the tricuspid valve. Blood cysts [5] may be found on the closure lines of the tricuspid valve, and occasionally on the mitral and arterial valves. They tend to be single though may be multiple. Usually in the neonate they are quite small, reaching a size of 1 to 2 mm in diameter and need not be confused with the larger, uniformly dense vegetations noted on cross-sectional echocardiography and confirmed histologically. The presence of such vegetations in the ill neonate with persistent pulmonary hypertension may indicate a pOOr prognosis and suggest the possible development of pulmonary vascular changes which are refractory to treatment. One infant, however, seemed not as severely affected. These observations warrant a further search of such lesions in the newborn, together with a clearer elucidation of their pathogenesis.
Fig. 2. (a) Vegetation
as seen at autopsy.
(b) Photomicrograph
of vegetation thrombus
References 1 McDonald RH. Valvular thrombotic vegetations in the newborn (fetal endocarditis). Arch Path01 1950;50:538-544. 2 Plaut A, Shamoff G. Acute valvular endocarditis in the newborn. Arch Pathol 1935;20:582-586. 3 Plaut A. Active endocarditis in the newborn (report of 2 cases). Am J Pathol 1939;15:649-650.
consisting
of unorganised
layers of platelet
and fibrin
S. Pulmonary vascular remodelling in neonatal 4 Haworth pulmonary hypertension. Chest 1988;93(suppl):127S-132s. KG, Paplanus SH. Dong S, Nagle RB. Con5 Zimmerman genital blood cysts of the heart valves. Hum Path01 1983;14:699-703.