Ultrasonography Causes Agitation and Pain Leading to Hemodynamic Disturbance in Neonates: A Prospective Observational Study

Background: Ultrasonography is widely used in neonatological practice and studies investigating the hemodynamic effects of various treatment protocols or clinical situations. On the other hand, pain causes changes in the cardiovascular system; so, in the case of ultrasonography leading to pain in neonates, it may cause hemodynamic alterations. In this prospective study, we evaluate whether ultrasonographic application causes pain and changes in the hemodynamic system. Methods: Newborns undergoing ultrasonographic examination were enrolled in the study. Vital signs, cerebral and mesenteric tissue oxygenation (StO2) levels, and middle cerebral artery (MCA) Doppler measurements were recorded, and NPASS scores were calculated before and after ultrasonography. Results: We enrolled 39 patients in the study. After ultrasonography, Neonatal Pain, Agitation, and Sedation Scale (NPASS) scores were significantly higher (p 2, diastolic and systolic blood pressure; p = 0.03; p p p p = 0.02, p = 0.03, respectively) were altered. Cerebral (p = 0.008) and mesenteric (p = 0.039) StO2 levels were significantly lower in the whole study group, MCA end-diastolic velocity decreased (p = 0.02), and the resistive index (p = 0.03) increased in patients whose NPASS score was >7 after ultrasonography. Conclusions: This study is the first to show that ultrasonography may cause pain in newborn patients, and alters vital signs and hemodynamic parameters. Therefore, precautions should be taken to protect newborn babies from pain during ultrasound applications, as they are already exposed to many noxious stimuli. Furthermore, pain scores should be considered in studies using ultrasonography and evaluating hemodynamic parameters to increase the reliability of the studies

Postnatal cytomegalovirus ınfection in premature infants

GİRİŞ: Prematürelerde postnatal CMV (sitomegalovirüs) enfeksiyonu en sık enfekte anne sütü alımı ile kazanılmaktadır. Diğer bulaş yolları perinatal dönemde genital sekresyonlar ve kan transfüzyonudur. Tanı postnatal 3. haftadan sonra idrar, kan ve sekresyonlarda PCR ya da kültür ile virüsün izole edilmesine dayanmaktadır. Term olgularda enfeksiyon çoğunlukla asemptomatiktir. Prematürelerde CMV ilişkili klinik bulgu ve sepsise neden olabilir. Prematüre olgularda CMV ilişkili sepsis az sayıda bildirilmiştir. OLGU SUNUMU: Olgularımızın her ikisi de 1000 gr altında prematüre idi. C/S ile doğmuşlardı. Premature formulası ile beslenmişler, lökosit filtresi kullanılarak çoklu eritrosit süspansiyonu transfüzyonu almışlardı. İzlemlerinin 2. ayında birinci olguda beslenme intoleransı ve splenomegali, ikinci olguda oksijen ihtiyacında artma ve invaziv ventilasyon ihtiyacı gelişti. Laboratuvar bulgularında her iki olguda karaciğer fonksiyon testlerinde yükselme, kolestaz, trombositopeni ve akut faz yüksekliği saptandı. Kan CMV IgM ve CMV DNA PCR pozitif bulundu. Gansiklovir başlandı. Birinci olgunun 2, ikinci olgunun altı hafta sonunda klinik ve laboratuvar bulguları düzeldi. İzlemlerinde nörolojik sekel ya da işitme kaybı gelişmedi. TARTIŞMA: Prematürelerde, 3. haftadan sonra gelişen sepsis nedeni olarak postnatal CMV enfeksiyonu akılda tutulmalıdır.INTRODUCTION: Postnatal CMV (cytomegalovirus) infection in the premature infants is most often transmitted with infected breast milk. The other routes of transmission are blood transfusion and genital secretions. Diagnosis is made by PCR or viral culture of urine, blood, or other body secretions after the first 3 weeks of life. It is mostly asymptomatic in term infants. CMV infection may cause sepsis and many clinical signs in premature infants. There are a few reports of premature infants with CMV sepsis in the literature. CASE REPORTS: Both of our cases were premature infants weighing less than 1000 g and born with ceaserean section. Since both of the mothers did not have breast milk, infants were fed with premature formula. They were transfused with erythrocyte suspension more than once. The first case has developed feeding intolerance and splenomegaly, the second case had increased oxygen demand and invasive mechanical ventilation support at the end of the second month of life. Laboratory findings showed cholestasis, thrombocytopenia, elevated transaminases and acute phase reactants. Blood CMV IgM and CMV DNA PCR were positive in both cases. Ganciclovir treatment was started. The first case had improvement in clinical and laboratory findings in 2 weeks, the second case had improvement in 6th week of the treatment. None of the patiens developed neurological sequelae or hearing loss. CONCLUSİON: We aimed to remind that postnatal CMV infection should be suspected in preterm infants who developed sepsis later than fist 3 weeks of life

Neonatology oxidative status in preterm infants with premature preterm rupture of membranes and fetal inflammatuar response syndrome

The aim of this study, to determine an index of oxidative stress index in preterm infants less than 34 weeks gestational age with premature preterm rupture of membrane (PPROM) and fetal inflammatory response syndrome (FIRS). Methods: This study was designed as a prospective study. Fifty-one premature infants less than 35 weeks of gestational age were included in the study. The umbilical cord blood concentrations of IL-6, TAC (total antioxidant capacity) and PON-1 (paraoxonase-1) levels and TOS (total oxidative stress) were studied. The oxidative stress index (OSI = TAC/TOS) was calculated in all of prematüre infants. PPROM was defined as rupture of membranes at least 24 hours before the onset of labor. FIRS was defined by an umbilical cord IL-6 level greater than 11 pg/mL. Premature infants included in the study were divided into 4 groups. Group 1 included preterm infants without FIRS and with PPROM (n = 16), while Group 2 included preterm infants without PPROM and with FIRS (n = 9), Group 3 consisted of premature infants with PPROM and FIRS (n = 21) and Group 4 included premature infants without PPROM or FIRS (n = 5). Results: Umbilical cord TOS level was found to be higher in the preterm infants without FIRS and with PPROM (36.1 μmol H2O2 Equiv./L) compared to the preterm infants without PPROM or FIRS (11.9 μmol H2O2 Equiv./L) (p = 0.03). Umbilical cord PON-1 level was found to be lower in the preterms without FIRS and with PPROM (32 U/L), preterms without PPROM and with FIRS (30. 3 U/L) and the preterm infants with both PPROM and FIRS (48.6 U/L) compared to the preterm infants having no PPROM or FIRS (85.6 U/L) (p = 0.001). Conclusion: High pro-oxidant capacity was found in PPROM and low antioxidant capacity in PPROM and FIRS

A Giant Ovarian Cyst in a Neonate with Classical 21-Hydroxylase Deficiency with Very High Testosterone Levels Demonstrating a High-Dose Hook Effect

Congenital adrenal hyperplasia (CAH) is a group of disorders affecting the adrenal steroid synthesis. The most common form, 21-hydroxylase deficiency (21-OHD), leads to decreased production of cortisol and aldosterone with increased androgen secretion. In classic CAH, glucocorticoid treatment can be life-saving and serves to bring the symptoms under control. However, the treatment challenge is to effectively control the excess androgen effect by using the lowest possible glucocorticoid dose. Previous studies suggested a relationship between ovarian cyst formation and adrenal androgen excess, but neonatal large ovarian cysts have been very rarely reported in newborns with CAH. Here, we present the unique case of a neonate with classical 21-OHD who underwent surgery for a giant (10x8x7 cm) unilateral solitary ovarian follicular cyst on the 2nd postnatal day. Hormonal evaluation of the patient revealed high-dose hook effect for serum testosterone levels for the first time by a two-site immunoradiometric assay. Possible mechanisms by which androgen excess may cause ovarian cyst formation are discussed. Conflict of interest:None declared