| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Letters |
1
Pediatric Neonatal Intensive Care Unit and
2
Clinical Chemistry and Hematology Laboratory, Hospital of Verona, Piazzale A. Stefani 1, 37126 Verona, Italy
aAuthor for correspondence. Fax 39-045-8073481; e-mail claudio.cavalli{at}mail.azosp.vr.it.
To the Editor:
The measurement of cardiac troponin I (cTnI) is pivotal in the biochemical diagnosis of myocardial damage in adults and in infants as well (1). cTnI could also be used in other pathologies that may affect the neonatal heart, such as birth asphyxia, primary pulmonary hypertension, sepsis, and multiple organ system failure (2)(3).
A newly born term male suffered a mild episode of asphyxia at birth (Apgar scores: 3 and 9 at 1st and 5th min, respectively) and needed a short resuscitation course at our Neonatal Intensive Care Unit. Blood tests 30 min after delivery showed metabolic acidosis, an arterial lactate concentration of 4.9 mmol/L, and a cTnI concentration of 0.18 µg/L (Dimension RxL-HM; Dade Behring) (4). The cTnI was below the 99th percentile (0.73 µg/L; Fig. 1
) (5). As part of routine care, we positioned an umbilical venous catheter (UVC) and checked the correct position of its tip in the inferior vena cava by chest x-ray. In the next few hours, both clinical and biochemical indices improved, but a marked increase of cTnI (1.03 µg/L) was detected at 80 h despite the infant’s stable clinical conditions and normal electrocardiogram. Echocardiography demonstrated a normal cardiac contractility but, unexpectedly, revealed that the UVC tip had moved through the foramen ovale into the left atrium. The catheter was immediately removed. At 120 h, a marked decrease in the cTnI concentration (0.36 µg/L) was observed, and echocardiographic and electrocardiographic findings were normal. On day 6, the patient was discharged in good clinical condition.
|
In newborns suffering episodes of asphyxia at birth, we routinely measure cTnI concentrations to detect signs of myocardial injury (3). The management of these patients includes oxygen therapy, cannulation of the umbilical vein, and cardiorespiratory monitoring (2). In the patient described here, despite marked clinical improvement already apparent a few hours after birth, transient myocardial ischemia complicating birth asphyxia was suspected after a nearly sixfold increase in cTnI on the 4th day of life. We confirm previous reports of higher concentrations of cTnI in newborns compared with adults measured on another analyzer (Immuno1; Bayer) (6). However, the well-known standardization problems of cTnI assays (7) hamper the comparison of absolute results from different assays.
The mechanical injury attributable to the UVC tip hitting the endocardium wall during each cardiac cycle could explain the increase in cTnI, a specific and sensitive marker of cardiac injury, and its almost threefold decrease 40 h after removal of the UVC. Increased cTnI has been reported after difficult positioning of intracardiac catheters in adults and, similarly, after atriotomy performed in children undergoing cardiac surgery (8). Our observation suggests that increases in cTnI without clinical explanation in a newborn having an UVC should raise suspicion of accidental intracardiac displacement of the catheter.
References
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
