Late prematuriteit: een risicopopulatie?

Late preterm infant: a population at risk? Late preterm infants, infants born between 34 0/7 and 36 6/7 weeks of gestation, were called near term before 2005, which may lead to the assumption that they are mature and an underestimation of their risks. Late preterm infants are physiologically and metabolically immature. Compared to term infants they have increased morbidity rates, including problems such as hypothermia, hypoglycemia, hyperbilirubinemia, feeding difficulties and respiratory and immunological issues. In late preterm infants there are increased mortality rates, prolonged hospitalizations at birth, more readmissions and higher healthcare costs. The infants also have a higher risk of neurological and developmental problems and long-term respiratory, cardiovascular and metabolic difficulties. Despite their relative size and apparently mature appearance, late preterm infants should not be treated like term infants. They require careful monitoring immediately after birth, as well as during childhood and even adolescence. Child-birth should not be scheduled during the late preterm period without medical indication. The risk of continuing the pregnancy must be weighed against the risk of premature birth. The prevention and a better monitoring of late preterm infants can lead to healthcare savings.

Multiple thromboses in a late preterm infant present at birth

A late preterm infant was born to a diabetic mother on a background of reduced fetal movements and a poor CTG. It was noted immediately at birth that there was pathology in both upper limbs. Targeted investigation led to the diagnosis of bilateral upper limb arterial thromboses. Prompt assessment and multidisciplinary discussion led to an individualised management plan resulting in a positive outcome.

Valsartan exposure in pregnancy with resultant anhydramnios and chronic kidney disease in a late preterm infant

In utero exposure to angiotensin II receptor blockers (ARBs) has fetotoxic effects including renal failure, oligohydramnios and lung hypoplasia. We present the case of a 24-year-old woman who presented to the maternity services in the 34th week of her first pregnancy. She was taking valsartan for hypertension. Ultrasound showed a structurally normal fetus with anhydramnios. The patient was admitted and valsartan was discontinued. She had spontaneous preterm delivery at 35 weeks’ gestation of a baby girl. The baby’s urine output was minimal in the first week of life and she was transferred to a paediatric hospital for specialist nephrology input. At 6 months of age, she requires ongoing nephrology follow-up and she remains on treatment for hypertension and anaemia. This case demonstrates the serious adverse effects resulting from ARB exposure in utero, and highlights the importance of avoiding fetotoxic medications in women of childbearing age.

Thrombospondin domain1-related congenital chylothorax in an infant with maple syrup urine disease: a challenging case

Objectives Congenital chylothorax is a rare entity with various etiologies ranging from anatomical to genetic causes. If associated with non-immune hydrops fetalis mortality rates can reach up to 98%. Treatment is challenging and mostly supportive, with no standard guidelines. Case presentation We describe the unique and challenging course of a late preterm infant with non-immune hydrops fetalis (NIHF), and recurrent chylothorax attributed to homozygous mutations in thrombospondin domain1 (THSD1) gene. The infant was also affected with maple syrup urine disease (MSUD), which further complicated the clinical course. Treatment was supportive by means of chest tubes, intubation, mechanical ventilation, and eventually he was tracheostomized and discharged home on home BiPAP ventilation and required prolonged use of octreotide to prevent re-accumulation of chylothorax. Conclusions THSD1 gene has a role in vascular permeability and its mutation in our patient caused congenital chylothorax and NIHF and is also associated with other features such as vascular malformations.

Early-Onset Cardiomyopathy After Pacemaker Implanted in a Preterm Infant With Congenital Complete Heart Block and Anti-Ro/SSA Antibodies

Congenital complete heart block is a potentially fatal complication that can occur in neonates whose mothers have autoimmune disorders; it has rarely been reported in the presence of Sjögren syndrome. Pacemaker implantation is recommended to treat rhythm abnormalities in these neonates. We report the case of a late-preterm infant with Sjögren-syndrome-antibody–induced complete heart block who underwent temporary bipolar epicardial pacing as a bridge to permanent pacemaker implantation. Soon after the pacemaker was implanted, takotsubo cardiomyopathy developed. To our knowledge, this is the first report of reversible cardiomyopathy after pacemaker implantation in an infant.

Asymptomatic Hyperinsulinemic Hypoglycemia and Grade 4 Intraventricular Hemorrhage in a Late Preterm Infant

Hyperinsulinemic hypoglycemia (HH) has the potential to cause acute neurologic dysfunction and neurodevelopmental impairment. Parieto-occipital neuronal injuries have been reported in hypoglycemic infants, but intraparenchymal hemorrhage is rare. On day 5 of life, a late preterm infant was transferred to our care with recurrent asymptomatic hypoglycemia. Prior to arrival, plasma glucose levels were at a median of 1.25 mmol/L (22.5 mg/dL) in the first 6 hours of life, and he required a glucose infusion rate (GIR) of 22.6 mg/kg/min. Hyperinsulinism was confirmed in the presence of detectable insulin, low ketones, and fatty acid when hypoglycemic. A left grade 4 intraventricular hemorrhage (IVH) was noted in the cranial ultrasound scan during the workup for sepsis on the day of admission. However, magnetic resonance imaging of the brain on day 7 of life revealed extensive bilateral IVH. On day 9, he was initiated on diazoxide, and HH resolved within 48 to 72 hours, allowing increment of feeds while weaning GIR. Ventricular drain for post-hemorrhagic ventriculomegaly was advised but not performed. At 3 months, post-hemorrhagic ventriculomegaly was stable, and there were early signs of neurodevelopmental delay. After discontinuing diazoxide at 4 months of age, he passed an 8-hour fasting study confirming the resolution of HH. Severe hypoglycemia has been associated with cerebral hyperperfusion in preterm infants and potentially could cause IVH. Close monitoring and prompt intervention in preterm infants to prevent severe hypoglycemia are paramount. In addition to long-term neurodevelopmental follow-up, infants with recurrent hypoglycemia may benefit from neuroimaging and thereby early intervention if required.