18 research outputs found
Respiratory Distress and Management Strategies in the Newborn
Approximately 10% of neonates require respiratory support immediately after delivery due to transitional problems or respiratory disorders, and up to 1% of neonates are in need of resuscitation. Respiratory distress is the most frequent cause of neonatal intensive care unit (NICU) admission, and the individual management strategies should be the main task in NICUs for these infants. Regardless of the cause, if not recognized and managed in advance, respiratory distress can escalate to respiratory failure and cardiopulmonary arrest. This chapter explores the evaluation and differential diagnosis of respiratory distress in neonates and presents an update on management strategies according to the protocol of Ankara University Children’s Hospital Neonatal Intensive Care Unit
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Editorial: Management of Patent Ductus Arteriosus in Preterm Infants
Current Controversy on Platelets and Patent Ductus Arteriosus Closure in Preterm Infants.
Platelets are critically involved in murine patent ductus arteriosus (PDA) closure. To date, the clinical significance of these findings in human preterm infants with PDA is still controversial. We discuss the available study data on the role of platelets for PDA closure in preterm infants: Several mostly retrospective studies have yielded conflicting results on whether thrombocytopenia contributes to failed spontaneous ductal closure. The same applies to investigations on the role of thrombocytopenia as a risk factor for unsuccessful ductus arteriosus closure by pharmacological treatment with cyclooxygenase inhibitors. Nonetheless, recent meta-analyses have concluded that thrombocytopenia constitutes an independent risk factor for both failed spontaneous and pharmacological PDA closure in preterm infants. However, the available investigations differ in regard to patient characteristics, diagnostic strategies, and treatment protocols. Several studies suggest that impaired platelet function rather than platelet number is critically involved in failure of ductus arteriosus closure in the preterm infant. A recent randomized-controlled trial on platelet transfusions in preterm infants with PDA failed to show any benefit for liberal vs. restrictive transfusion thresholds on PDA closure rates. Importantly, liberal transfusions were associated with an increased rate of intraventricular hemorrhage, and thus should be avoided. In conclusion, the available evidence suggests that thrombocytopenia and platelet dysfunction contribute to failure of spontaneous and pharmacological PDA closure in preterm infants. However, these platelet effects on PDA seem to be of only moderate clinical significance. Furthermore, platelet transfusions in thrombocytopenic preterm infants in order to facilitate PDA closure appear to cause more harm than good
Placenta, Secret Witness of Infant Morbidities: The Relationship Between Placental Histology and Outcome of the Premature Infant
Objective: The microscopic and macroscopic features of the placenta can contribute to the clinical understanding of premature delivery. The aim of our study was to figure out the relationship between the histopathological findings of the placentas of premature deliveries and its effects on neonatal morbidity and mortality.
Material and Method: The placentas of 284 singleton preterm infants with <35 weeks of gestation were examined. three groups created as the normal, chorioamnionitis and vasculopathy according to histopathological findings in placentas subjects.
Results: The mean gestational age of the infants in the study group was 30.5 ± 3.2 weeks, and the mean birth weight was 1588 ± 581 g. The pathology was normal in ninety-six (33.8%), vasculopathy in 153 (53.9%) and chorioamnionitis in 35 (12.3%). The gestation age of the infants was lower in the chorioamnionitis group. Moreover, retinopathy of prematurity, early onset neonatal sepsis, and duration of respiratory support were found to be higher in the chorioamnionitis group. In the vasculopathy group, preeclampsia and small for gestational age were found to be significantly higher.
Conclusion: Histopathological findings of the placentas from preterm deliveries provided important data in determining the etiology of preterm delivery and outcomes of infants. Infants delivered by mothers with chorioamnionitis were particularly found to be more preterm, and these preterm infants would have a longer hospital stay, higher respiratory support requirement, and more serious morbidities
Congenital Isolated Adrenocorticotropin Deficiency: An Underestimated Cause Of Neonatal Death, Explained By Tpit Gene Mutations
Tpit is a T box transcription factor important for terminal differentiation of pituitary proopiomelanocortin-expressing cells. We demonstrated that human and mouse mutations of the TPIT gene cause a neonatal-onset form of congenital isolated ACTH deficiency (IAD). In the absence of glucocorticoid replacement, IAD can lead to neonatal death by acute adrenal insufficiency. This clinical entity was not previously well characterized because of the small number of published cases. Since identification of the first TPIT mutations, we have enlarged our series of neonatal IAD patients to 27 patients from 21 unrelated families. We found TPIT mutations in 17 of 27 patients. We identified 10 different TPIT mutations, with one mutation found in five unrelated families. All patients appeared to be homozygous or compound heterozygous for TPIT mutations, and their unaffected parents are heterozygous carriers, confirming a recessive mode of transmission. We compared the clinical and biological phenotype of the 17 IAD patients carrying a TPIT mutation with the 10 IAD patients with normal TPIT-coding sequences. This series of neonatal IAD patients revealed a highly homogeneous clinical presentation, suggesting that this disease may be an underestimated cause of neonatal death. Identification of TPIT gene mutations as the principal molecular cause of neonatal IAD permits prenatal diagnosis for families at risk for the purpose of early glucocorticoid replacement therapy.Wo
sj-docx-1-cat-10.1177_10760296241231944 - Supplemental material for Investigating the Impact on Long-Term Outcomes and the Necessity of Hereditary Thrombophilia Screening in Presumed or Perinatal Arterial Ischemic Stroke
Supplemental material, sj-docx-1-cat-10.1177_10760296241231944 for Investigating the Impact on Long-Term Outcomes and the Necessity of Hereditary Thrombophilia Screening in Presumed or Perinatal Arterial Ischemic Stroke by Ömer Bektaş, MD, Özben Akinci GÖktaş, MD, Begüm Atasay, MD, and Serap Teber, MD in Clinical and Applied Thrombosis/Hemostasis</p
A newborn with congenital glucose-galactose malabsorption and recurrent episodes of sepsis
Konjenital glukoz ve galaktoz malabsorbsiyonu absorbe edilemeyen glukoz ve galaktoz nedeniyle ortaya çıkan kronik osmotik bir ishal durumudur. Burada, yenidoğan döneminde ishal nedeniyle başvuran ve konjenital glukoz ve galaktoz malabsorbsiyonu tanısı alan, takibinde tekrarlayan Candida albicans, Klebsiella pneumoniae ve Enterococcus faecalis etkenleri ile sepsis atakları geçiren fakat altta yatan hücresel ve humoral immün yetmezlik tespit edilmeyen bir olgu sunulmaktadır. Nadir görülen konjenital glukoz ve galaktoz malabsorbsiyonunda, erken tanı ve uygun tedavinin yaşamı tehdit eden komplikasyonların önüne geçebileceği, büyüme ve gelişmenin normal olabileceği bilinmektedir. Konjenital glukoz ve galaktoz malabsorbsiyonu tanısı alıp tekrarlayan fırsatçı mikroorganizmalarla enfeksiyon geçiren literatürde bizim olgumuz dışında yalnızca bir olgu daha tanımlanmaktadır.Congenital glucose-galactose malabsorption is a chronic osmotic diarrhea due to defective absorption of glucose and galactose in the intestine. Here, we present a newborn that was admitted to our hospital for neonatal diarrhea and was diagnosed as congenital glucosegalactose malabsorption. He had recurrent sepsis with Candida albicans, Klebsiella pneumoniae and Enterococcus faecalis during follow-up without having any underlying cellular or humoral immune deficiency.Early diagnosis and appropriate treatment of this rare disease can prevent life-threatening complications, and normal growth and development can be achieved. To our knowledge, the present case will be the second glucose-galactose malabsorption case with recurrent infectious due to opportunistic microorganisms after only one similar case in the literature
Aquired cytomegalovirus ınfection of extremely low birth weight ınfant
Anne sütü, özellikle prematürelerde kazanılmış sitomegalovirüs (CMV) enfeksiyonu için majör kaynaktır ve anne sütünden kazanılan CMV enfeksiyonu seropozitif anne bebeklerinde görülmektedir. Türkiye’de annelerin çoğunluğunun seropozitif olmasına karşın prematüre bebeklerde yaşamı tehdit eden akkiz CMV enfeksiyonu yalnızca vaka sunumları şeklinde çok az olguda bildirilmektedir. Preterm semptomatik anne sütü kaynaklı CMV enfeksiyonunun tedavisi klinik bulguların ağırlığına göre yapılmalıdır. Postnatal 111. gününde menenjit-sepsis tanısı alan, anne sütünden kazanılan CMV enfeksiyonu tanımlanan ancak yaşamı tehdit eden çoklu organ yetmezliği gelişmemesi nedeniyle antiviral tedavi verilmeyen prematüre bir bebek literatür bilgileri eşliğinde sunulmuştur. Preterm bebeklerde etken saptanmayan sepsis kliniği, açıklanamayan trombositopeni, karaciğer enzim yüksekliği ve direkt bilirübinemi varlığında kazanılmış CMV enfeksiyonu akla getirilmelidir.Breast milk is a major source for acquired cytomegalovirus infection especially in premature infants and acquired CMV infection occurs in infants whose mothers were seropositive for CMV. Although most of mothers of premature infants are seropositive in Turkey, acquired life-threatening breast milk acquired CMV infection was reported occasionally. Treatment of preterm with symptomatic breast milk acquired CMV infection should be done according to the severity of clinical signs. In this report, a preterm case with a diagnosis of breast milkacquired CMV meningitis and sepsis without multiorgan failure on the 111th day of life, who did not require antiviral therapy was presented and discussed in the context of the acquired CMV literature. In preterm babies, when there is sepsis with no apparent causes, unexplained thrombocytopenia, elevated liver transaminases and direct hyperbilirubinemia acquired CMV infection should be suspected