A Rare Cause of Respiratory Distress Syndrome in Fullterm Newborn: Obstructive Infracardiac Type Total Anomalous Pulmonary Venous Connection
Journal Title: Progressing Aspects in Pediatrics and Neonatology - Year 2018, Vol 1, Issue 5
Abstract
Total anomalous pulmonary venous connection (TAPVC) may cause clinical signs and symptoms of resistant to treatment respiratory distress syndrome (RDS) in the full-term newborn. Despite echocardiography being the basic diagnostic examination method, three-dimensional reconstructive computed tomography allows making a more precise operation plan by defining the anatomy in an excellent manner. Cardiologic evaluation should be done immediately in the case of RDS with treatment-resistant full-term newborn because a delay in the diagnosis increases operative mortality.Respiratory distress syndrome (RDS) is one of the main problems with premature infants and it develops as a result of surfactant deficiency due to lung immaturity. RDS is much rare in full-term newborns, and it usually appears in some clinical conditions causing secondary surfactant deficiency [1,2]. Particularly the obstructive type of total anomalous pulmonary venous connection (TAPVC), in which pulmonary veins drain into systemic venous structures or directly into right atrium without having any direct connection to left atrium, cause RDS by leading to severe pulmonary congestion. In this report it is reemphasized that obstructive TAPVC should be searched for an etiology of treatment resistant respiratory distress in the full-term newborn.A newborn delivered by cesarean section at 38 weeks with a birth weight of 3100 grams and an apgar score of 5 at 1 minute and 6 at 5 minutes had been admitted to the newborn intensive care unit of an outside center for post-delivery respiratory distress. Upon increasingly worsening respiratory distress under mechanic ventilation and antibiotic therapy, the patient was referred to our clinic with the diagnosis of treatment resistant respiratory distress syndrome on the 7th day of life. There was no history of maternal drug usage, premature rupture of membranes, meconium aspiration, and perinatal asphyxia. There was no history of parental consanguinity and there were no similar cases in the pedigree. On physical examination, the newborn had a body weight of 3300 grams (50th-75th percentile), height of 50cm (50th percentile), head circumference of 36cm (75th percentile), heart rate of 140 bpm, respiratory rate of 72 breaths/minute, arterial blood pressure of 44/25mmHg (mean 35mmHg), and oxygen saturation of 90% (under mechanical ventilation support). The clinical condition was extremely poor; the newborn was dyspneic, had a poor peripheral circulation, and edematous eyelids and lower extremities. No murmur was heard on auscultation but respiratory sounds were diminished and there were bilateral crackles. Liver was palpable 5cm below costal margin. Laboratory examinations revealed respiratory and metabolic acidosis, a white blood cell count of 7460/ mm3, hemoglobin count of 12.2g/dL, thrombocyte count of 251000/mm3, negative C-reactive protein, creatinine of 0.6mg/dL, alanine aminotransferase of 17 IU/L, aspartate aminotransferase of 67IL/L, prothrombin time of 12.2 seconds, and activated partial thromboplastin time of 37.6 seconds. Ground glass appearance and dilated right atrium was observed on teleradiography (Figure 1). Antibiotic treatment was started due to rule-out pneumonia. High frequency ventilation was applied because of need to high pressure support. Fluid restriction was performed due to oligury, and generalized edema.
Authors and Affiliations
Sabriye Korkut, Mustafa Argun, Hulya Halis, Ahmet Ozdemir, Osman Bastug, Levent Korkmaz, Tamer Gunes
Keywords
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- EP ID EP580500
- DOI 10.32474/PAPN.2018.01.000122
- Views 47
- Downloads 0
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