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[Myocardial damage following neonatal severe asphyxia]
A Bancalari1, C Otero, P Bello
1Hospital Guillermo Grant Benavente, Concepción.
Insights
Severe asphyxia in newborns can cause secondary myocardial damage, detected by serial electrocardiograms. This cardiac dysfunction may be missed, presenting as respiratory distress syndrome.
Area of Science:
- Neonatal cardiology
- Perinatal medicine
- Pediatric critical care
Context:
- Severe birth asphyxia poses significant risks to newborns.
- Secondary myocardial damage is a potential complication.
- Clinical presentation can be complex, mimicking other conditions.
Purpose:
- To investigate the incidence and clinical manifestations of secondary myocardial damage in newborns with severe asphyxia.
- To evaluate the utility of electrocardiography (ECG) and cardiac biomarkers in diagnosing myocardial damage.
- To highlight the importance of cardiac monitoring in asphyxiated neonates.
Summary:
- Serial ECGs identified myocardial damage in 18.7% of term newborns with severe asphyxia.
- Damage included subendocardial ischemia and left ventricular wall necrosis.
- Creatine-phosphokinase and its MB isoenzyme were not useful for diagnosis.
- Affected neonates developed respiratory distress syndrome; one mortality occurred with histopathological evidence of myocardial hemorrhage.
Impact:
- Serial ECGs are crucial for detecting occult myocardial damage in asphyxiated newborns.
- Cardiac dysfunction can be present despite a primary diagnosis of respiratory distress syndrome.
- Early identification of myocardial damage may guide clinical management and improve outcomes.
Abstract:
Sixteen newborn infants with severe asphyxia were prospectively studied for evidence of secondary myocardial damage and, in that case, their clinical findings. Myocardial damage was diagnosed in three term newborn infants of adequate weight for gestational age (18.7%) by means of serial electrocardiograms taken in the first 72 hours of life. Two of them showed evidence of diffuse subendocardial ischemia and a third one showed electrocardiographic signs suggesting necrosis of the left ventricular posteroinferior wall. Neither creatine-phosphokinase serum activity nor its muscle brain MB isoenzyme were useful in the identification of myocardial damage. All three affected neonates developed respiratory distress syndrome without signs of cardiac failure and one of them died. The histopathological study of this late one showed localized hemorrhage of the papillary muscles and interventricular septum. These finding underscore the need for serial electrocardiographic recordings in newborns with severe asphyxia, since cardiac dysfunction may inadvertently occur under the appearance of respiratory distress syndrome.